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20,300 | Endomyocardial Biopsy via the Femoral Vein Using a Long, Curved Sheath. | Endomyocardial biopsy (EMB) has been defined as the gold standard method for surveillance of rejection after heart transplantation, and it has also been used in the diagnosis of myocarditis and the unknown causes of cardiomyopathies. The procedure, however, is not free from complications. Access through the jugular vein or the femoral vein is the standard approach. In this study, we performed biopsies by using a long, curved sheath and evaluated the rate of complications with this technique.</AbstractText>In this descriptive case series study, 97 EMBs were performed in 72 patients who were referred to a cardiovascular and medical research center in Tehran, Iran, between October 2011 and May 2013. The procedures were performed via the femoral approach by using a long bioptome with a long, curved sheath.</AbstractText>Adequate specimens were obtained in 97.9% of the total EMBs, with an average of 5 fragments per procedure. No deaths occurred, and there were no cases of pericardial effusion, myocardial rupture, papillary muscle rupture, increase in the severity of tricuspid regurgitation, atrioventricular block, sustained and nonsustained ventricular tachycardia, or atrial fibrillation. There was one case of persistent right bundle branch block.</AbstractText>Using a long, curved sheath can facilitate access to the interventricular septum compared with common sheaths and can be used safely in EMB via the femoral approach.</AbstractText>Copyright © 2017 Elsevier Inc. All rights reserved.</CopyrightInformation> |
20,301 | Clinical and Echocardiographic Correlates of Left Atrial Function Index: The Framingham Offspring Study. | Left atrial (LA) remodeling is a predictor of cardiovascular disease (CVD). We performed measurement of the LA function index (LAFI), a composite measure of LA structure and function, in a community-based cohort and here report the distribution and cross-sectional correlates of LAFI.</AbstractText>In 1,719 Framingham Offspring Study participants (54% women, mean age 66 ± 9 years), we derived LAFI from the LA emptying fraction, left ventricular (LV) outflow tract velocity time integral, and indexed maximal LA volume. We used multivariable linear regression to assess the clinical and echocardiographic correlates of LAFI adjusting for age, sex, anthropometric measurements, and CVD risk factors.</AbstractText>The average LAFI was 35.2 ± 12.1. Overall, LAFI declined with advancing age (β = -0.27, P < .001). LAFI was significantly higher (37.5 ± 11.6) in a subgroup of participants free of CVD and CVD risk factors compared with those with either of these conditions (34.5 ± 12.2). In multivariable models, LAFI was inversely related to antihypertensive use (β = -1.26, P = .038), prevalent atrial fibrillation (β = -4.46, P = .001), heart failure (β = -5.86, P = .008), and coronary artery disease (β = -2.01, P = .046). In models adjusting for echocardiographic variables, LAFI was directly related to LV ejection fraction (β = 14.84, P < .001) and inversely related to LV volume (β = -7.03, P < .001).</AbstractText>LAFI was inversely associated with antihypertensive use and prevalent CVD and was related to established echocardiographic traits of LV remodeling. Our results offer normative ranges for LAFI in a white community-based sample and suggest that LAFI represents a marker of pathological atrial remodeling.</AbstractText>Copyright © 2017 American Society of Echocardiography. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
20,302 | Arrhythmias after left ventricular assist device implantation: Incidence and management. | The use of mechanical circulatory support has become an increasingly common practice in patients with heart failure, whether used as bridge to transplantation or as destination therapy. The last couple of decades has seen a drastic change in the functioning of the left ventricular assist devices (LVAD), changing from the first generation devices running on pulsatile flow to the current continuous flow devices. Atrial and ventricular arrhythmias are common among heart failure patients, and though the systematic circulation is well supported in patients on mechanical circulatory support, these arrhythmias can still be the cause of detrimental symptoms and lead to potentially fatal outcomes. Several studies have shown that mortality rates in LVAD recipients secondary to lethal arrhythmias are uncommon, and newer generation continuous flow devices particularly seem to support hemodynamic support well. While it is common practice to implant ICDs in patients with LVADs and a history of ventricular arrhythmias, the efficacy behind this practice at preventing sudden death in this population is unknown. In this review, we highlight what is already known about the complications, management and treatment of atrial and ventricular arrhythmias in patients with LVAD devices. |
20,303 | Intensive Exercise Training Improves Cardiac Electrical Stability in Myocardial-Infarcted Rats. | Moderate exercise training has been shown to decrease sudden cardiac death post myocardial infarction. However, the effects of intensive exercise are still controversial.</AbstractText>Fourteen myocardial-infarcted rats were divided into sedentary (n=8) and intensive training groups (n=6) and 18 sham control rats to sedentary (n=10) and intensive training groups (n=8). Heart rate variability was obtained at weeks 1 and 8. The inducibility of ventricular tachycardia/fibrillation was assessed in a Langendorff system. Fast Fourier transforms were applied on the recorded ventricular tachycardia/fibrillations. Training reduces low to high frequency ratio of heart rate variability at week 8 compared with that at week 1 (P</i><0.05). In isolated hearts, the probability for ventricular tachycardia/fibrillation was decreased from 4.5±0.8% in sedentary controls to 1.56±0.2% in intensive training controls (P</i><0.05) and from 13.5±2.1% in the sedentary group to 5.4±1.2% in the intensive training group (P</i><0.01). Moreover, the pacing current required for ventricular fibrillation induction in the trained groups was increased following exercise (P</i><0.05). Fast Fourier transform analysis of ECG findings revealed an exercise-induced ventricular fibrillation transition from a narrow, single-peak spectrum at 17 Hz in sedentary controls to a broader range of peaks ranging from 13 to 22 Hz in the intensive training controls.</AbstractText>Intensive exercise in infarcted rats leads to reduced ventricular fibrillation propensity and is associated with normalization of refractoriness and intrinsic spatiotemporal electrical variations.</AbstractText>© 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.</CopyrightInformation> |
20,304 | Effects of local cardiac denervation on cardiac innervation and ventricular arrhythmia after chronic myocardial infarction. | Modulation of the autonomic nervous system (ANS) has already been demonstrated to display antiarrhythmic effects in patients and animals with MI. In this study, we investigated whether local cardiac denervation has any beneficial effects on ventricular electrical stability and cardiac function in the chronic phase of MI.</AbstractText>Twenty-one anesthetized dogs were randomly assigned into the sham-operated, MI and MI-ablation groups, respectively. Four weeks after local cardiac denervation, LSG stimulation was used to induce VPCs and VAs. The ventricular fibrillation threshold (VFT) and the incidence of inducible VPCs were measured with electrophysiological protocol. Cardiac innervation was determined with immunohistochemical staining of growth associated protein-43 (GAP43) and tyrosine hydroxylase (TH). The global cardiac and regional ventricular function was evaluated with doppler echocardiography in this study.</AbstractText>Four weeks after operation, the incidence of inducible VPC and VF in MI-ablation group were significantly reduced compared to the MI dogs (p<0.05). Moreover, local cardiac denervation significantly improved VFT in the infarcted border zone (p<0.05). The densities of GAP43 and TH-positive nerve fibers in the infarcted border zone in the MI-ablation group were lower than those in the MI group (p<0.05). However, the local cardiac denervation did not significantly improve cardiac function in the chronic phase of MI, determined by the left ventricle diameter (LV), left atrial diameter (LA), ejection fraction (EF).</AbstractText>Summarily, in the chronic phase of MI, local cardiac denervation reduces the ventricular electrical instability, and attenuates spatial heterogeneity of sympathetic nerve reconstruction. Our study suggests that this methodology might decrease malignant ventricular arrhythmia in chronic MI, and has a great potential for clinical application.</AbstractText> |
20,305 | Inappropriate implantable cardioverter defibrillator shocks-incidence, effect, and implications for driver licensing. | Patients with implantable cardioverter defibrillators (ICDs) have an ongoing risk of sudden incapacitation that may cause traffic accidents. However, there are limited data on the magnitude of this risk after inappropriate ICD therapies. We studied the rate of syncope associated with inappropriate ICD therapies to provide a scientific basis for formulating driving restrictions.</AbstractText>Inappropriate ICD therapy event data between 1997 and 2014 from 50 Japanese institutions were analyzed retrospectively. The annual risk of harm (RH) to others posed by a driver with an ICD was calculated for private driving habits. We used a commonly employed annual RH to others of 5 in 100,000 (0.005%) as an acceptable risk threshold.</AbstractText>Of the 4089 patients, 772 inappropriate ICD therapies occurred in 417 patients (age 61 ± 15 years, 74% male, and 65% secondary prevention). Patients experiencing inappropriate therapies had a mean number of 1.8 ± 1.5 therapy episodes during a median follow-up period of 3.9 years. No significant differences were found in the age, sex, or number of inappropriate therapies between patients receiving ICDs for primary or secondary prevention. Only three patients (0.7%) experienced syncope associated with inappropriate therapies. The maximum annual RH to others after the first therapy in primary and secondary prevention patients was calculated to be 0.11 in 100,000 and 0.12 in 100,000, respectively.</AbstractText>We found that the annual RH from driving was far below the commonly cited acceptable risk threshold. Our data provide useful information to supplement current recommendations on driving restrictions in ICD patients with private driving habits.</AbstractText> |
20,306 | Cardiac Subtype-Specific Modeling of K<sub>v</sub>1.5 Ion Channel Deficiency Using Human Pluripotent Stem Cells. | The ultrarapid delayed rectifier K<sup>+</sup> current (I<sub>Kur</sub>), mediated by K<sub>v</sub>1.5 channels, constitutes a key component of the atrial action potential. Functional mutations in the underlying <i>KCNA5</i> gene have been shown to cause hereditary forms of atrial fibrillation (AF). Here, we combine targeted genetic engineering with cardiac subtype-specific differentiation of human induced pluripotent stem cells (hiPSCs) to explore the role of K<sub>v</sub>1.5 in atrial hiPSC-cardiomyocytes. CRISPR/Cas9-mediated mutagenesis of integration-free hiPSCs was employed to generate a functional <i>KCNA5</i> knockout. This model as well as isogenic wild-type control hiPSCs could selectively be differentiated into ventricular or atrial cardiomyocytes at high efficiency, based on the specific manipulation of retinoic acid signaling. Investigation of electrophysiological properties in K<sub>v</sub>1.5-deficient cardiomyocytes compared to isogenic controls revealed a strictly atrial-specific disease phentoype, characterized by cardiac subtype-specific field and action potential prolongation and loss of 4-aminopyridine sensitivity. Atrial K<sub>v</sub>1.5-deficient cardiomyocytes did not show signs of arrhythmia under adrenergic stress conditions or upon inhibiting additional types of K<sup>+</sup> current. Exposure of bulk cultures to carbachol lowered beating frequencies and promoted chaotic spontaneous beating in a stochastic manner. Low-frequency, electrical stimulation in single cells caused atrial and mutant-specific early afterdepolarizations, linking the loss of <i>KCNA5</i> function to a putative trigger mechanism in familial AF. These results clarify for the first time the role of K<sub>v</sub>1.5 in atrial hiPSC-cardiomyocytes and demonstrate the feasibility of cardiac subtype-specific disease modeling using engineered hiPSCs. |
20,307 | A review of rate control in atrial fibrillation, and the rationale and protocol for the RATE-AF trial. | Atrial fibrillation (AF) is common and causes impaired quality of life, an increased risk of stroke and death as well as frequent hospital admissions. The majority of patients with AF require control of heart rate. In this article , we summarise the limited evidence from clinical trials that guides prescription, and present the rationale and protocol for a new randomised trial. As rate control has not yet been shown to reduce mortality, there is a clear need to compare the impact of therapy on quality of life, cardiac function and exercise capacity. Such a trial should concentrate on the long-term effects of treatment in the largest proportion of patients with AF, those with symptomatic permanent AF, with the aim of improving patient well-being.</AbstractText>The RAte control Therapy Evaluation in permanent Atrial Fibrillation (RATE-AF) trial will enrol 160 participants with a prospective, randomised, open-label, blinded end point design comparing initial rate control with digoxin or bisoprolol. This will be the first head-to-head randomised trial of digoxin and beta-blockers in AF.</AbstractText>Recruited patients will be aged ≥60 years with permanent AF and symptoms of breathlessness (equivalent to New York Heart Association class II or above), with few exclusion criteria to maximise generalisability to routine clinical practice.</AbstractText>The primary outcome is patient-reported quality of life, with secondary outcomes including echocardiographic ventricular function, exercise capacity and biomarkers of cellular and clinical response. Follow-up will occur at 6 and 12 months, with feasibility components to inform the design of a future trial powered to detect a difference in hospital admission. The RATE-AF trial will underpin an integrated approach to management including biomarkers, functions and symptoms that will guide future research into optimal, personalised rate control in patients with AF.</AbstractText>East Midlands-Derby Research Ethics Committee (16/EM/0178); peer-reviewed publications.</AbstractText>Clinicaltrials.gov: NCT02391337; ISRCTN: 95259705. Pre-results.</AbstractText>© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.</CopyrightInformation> |
20,308 | Contemporary Outcomes in Patients With Long QT Syndrome. | Long QT syndrome (LQTS) is a potentially lethal cardiac channelopathy with a 1% to 5% annual risk of LQTS-triggered syncope, aborted cardiac arrest, or sudden cardiac death.</AbstractText>This study sought to evaluate LQTS outcomes from a single center in the contemporary era.</AbstractText>The authors conducted a retrospective study comprising the 606 patients with LQTS (LQT1 in 47%, LQT2 in 34%, and LQT3 in 9%) who were evaluated in Mayo Clinic's Genetic Heart Rhythm Clinic from January 1999 to December 2015. Breakthrough cardiac events (BCEs) were defined as LQTS-attributable syncope or seizures, aborted cardiac arrest, appropriate ventricular fibrillation-terminating implantable cardioverter-defibrillator shocks, and sudden cardiac death.</AbstractText>There were 166 (27%) patients who were symptomatic prior to their first Mayo Clinic evaluation. Median age at first symptom was 12 years. Treatment strategies included no active therapy in 47 (8%) patients, beta-blockers alone in 350 (58%) patients, implantable cardioverter-defibrillators alone in 25 (4%) patients, left cardiac sympathetic denervation alone in 18 (3%) patients, and combination therapy in 166 (27%) patients. Over a median follow-up of 6.7 (IQR: 3.9 to 9.8) years, 556 (92%) patients have not experienced an LQTS-triggered BCE. Only 8 of 440 (2%) previously asymptomatic patients have experienced a single BCE. In contrast, 42 of 166 (25%) previously symptomatic patients have experienced ≥1 BCE. Among the 30 patients with ≥2 BCEs, 2 patients have died and 3 LQT3 patients underwent cardiac transplantation.</AbstractText>Although outcomes have improved markedly, further optimization of treatment strategies is still needed given that 1 in 4 previously symptomatic patients experienced at least 1 subsequent, albeit nonlethal, LQTS-triggered cardiac event.</AbstractText>Copyright © 2017 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
20,309 | Can the electrocardiogram distinguish foci from rotors during ventricular fibrillation?<Pagination><StartPage>1167</StartPage><EndPage>1168</EndPage><MedlinePgn>1167-1168</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/jce.13293</ELocationID><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Roth</LastName><ForeName>Bradley J</ForeName><Initials>BJ</Initials><Identifier Source="ORCID">0000-0003-4321-9806</Identifier><AffiliationInfo><Affiliation>Department of Physics, Oakland University, Rochester, MI, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016421">Editorial</PublicationType><PublicationType UI="D016420">Comment</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>08</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Cardiovasc Electrophysiol</MedlineTA><NlmUniqueID>9010756</NlmUniqueID><ISSNLinking>1045-3873</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentOn"><RefSource>J Cardiovasc Electrophysiol. 2017 Oct;28(10):1158-1166</RefSource><PMID Version="1">28670858</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D004562" MajorTopicYN="Y">Electrocardiography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D022062" MajorTopicYN="N">Electrophysiologic Techniques, Cardiac</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014693" MajorTopicYN="Y">Ventricular Fibrillation</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">electrocardiogram</Keyword><Keyword MajorTopicYN="N">focus</Keyword><Keyword MajorTopicYN="N">rotor</Keyword><Keyword MajorTopicYN="N">ventricular fibrillation</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>7</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>5</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>7</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28727199</ArticleId><ArticleId IdType="doi">10.1111/jce.13293</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Curated"><PMID Version="1">28726654</PMID><DateCompleted><Year>2017</Year><Month>09</Month><Day>19</Day></DateCompleted><DateRevised><Year>2018</Year><Month>12</Month><Day>02</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1512-0112</ISSN><JournalIssue CitedMedium="Internet"><Issue>267</Issue><PubDate><Year>2017</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Georgian medical news</Title><ISOAbbreviation>Georgian Med News</ISOAbbreviation></Journal>THE SAFETY AND EFFICACY OF AMIODARONE AND CARVEDILOL COMBINATION IN TREATMENT OF PATIENTS WITH SEVERE CARDIAC RHYTHM DISORDERS. | Different arrhythmias are cause of sudden death in many patients with heart failure. Amiodarone is usually used for prevent this arrhythmias, but it is not drug of choice for treatment the patients with heart failure. We retrospectively analyzed 142 patients with moderate and severe heart failure and history of myocardial infarction. These patients have received amiodarone, carvedilol or combination of these two medications together with standard therapy. In our retrospective analysis, the combination therapy with Amiodarone and Carvedilol had highly significant decrease arrhythmic death compare with carvedilol and amiodarone groups. This therapy is more effective in recovering of sinus rhythm in patients with atrial fibrillation and for control ventricular arrhythmias. The effects of carvedilol on left ventricular remodeling, systolic function and symptomatic status are not affected adversly by concurrent treatment with amiodarone. Carvedilol is an effective additional therapy for the patients with chronic heart failure already receiving Amiodarone. Carvedilol can be added to Amiodarone in patients with severe ventricular rhythm disorders and increased risk of sudden death without expecting of increase adverse events (than either drug alone) or loss of clinical efficacy. |
20,310 | Thyrotoxic Valvulopathy: Case Report and Review of the Literature. | We report a 42-year-old female who was admitted for abdominal pain, and also endorsed dyspnea, fatigue and chronic palpitations. Past medical history included asthma, patent ductus arteriosus repaired in childhood and ill-defined thyroid disease. Physical examination revealed blood pressure of 136/88 mm Hg and heart rate of 149 beats per minute. Cardiovascular exam revealed an irregularly irregular rhythm, and pulmonary exam revealed mild expiratory wheezing. Abdomen was tender. Electrocardiogram revealed atrial fibrillation with rapid ventricular response which responded to intravenous diltiazem. Labs revealed TSH of < 0.1 mU/L and free T4 of 2.82 ng/dL, a positive TSH-receptor and thyroid peroxidase antibodies suggesting Grave's thyrotoxicosis. A transthoracic echocardiogram reported an ejection fraction of 55-60%, with mild to moderate mitral regurgitation (MR) and moderate to severe tricuspid regurgitation (TR) and dilated right heart chambers. Pulmonary artery systolic pressure was 52 mm Hg. Transesophageal echocardiogram revealed a myxomatous tricuspid valve with thickening and malcoaptation of the leaflets and moderate to severe TR, mild to moderate MR with mild thickening of the mitral valve leaflets. Abdominal ultrasound revealed wall thickening of the gall bladder concerning for acute cholecystitis. She underwent laparoscopic cholecystectomy and was discharged in stable condition on methimazole for her thyroid disease, and on oral diltiazem for rate control and anticoagulation for atrial fibrillation. Follow-up visit with her cardiologist few months later documented absence of cardiac symptoms, and no murmurs were reported on physical examination. This case underscores the importance of maintaining a high index of suspicion for hyperthyroidism when faced with significant newly diagnosed pulmonary hypertension and TR, as treatment of the thyroid abnormalities can reverse these cardiac findings. |
20,311 | Comparison of Clopidogrel With Prasugrel and Ticagrelor in Patients With Acute Coronary Syndrome: Clinical Outcomes From the National Cardiovascular Database ACTION Registry. | We aimed to compare the clinical outcomes of clopidogrel, prasugrel, and ticagrelor in clinical practice using the National Cardiovascular Database ACTION Registry®</sup>. Treatment guidelines for patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention recommend dual antiplatelet therapy (DAPT) for 12 months. Few clinical trials have compared the safety and efficacy of clopidogrel with that of newer antiplatelet therapies.</AbstractText>A retrospective study of patients hospitalized for ACS at Cleveland Clinic Akron General was conducted. Data elements included detailed medical history and clinical outcomes during hospital stay. The primary outcome was a composite of major clinical events (cardiogenic shock, atrial fibrillation, ventricular fibrillation, ventricular tachycardia, heart failure, bleeding, and mechanical ventilation). The independent variable was the type of DAPT. Statistical analyses were performed using Chi-square and Mann-Whitney U tests. A post-hoc</i> analysis was performed to compare between the antiplatelet drugs head-to-head.</AbstractText>Subjects (n = 1,388) admitted between January 2011 and March 2016 with ACS and treated with clopidogrel, prasugrel, or ticagrelor were included in the study. Mean age was 65 ± 14 years and 46% had ST-segment elevation myocardial infarction. Prasugrel administration within 24 h was associated with a lower incidence of the composite outcome (P = 0.049), bleeding (P = 0.028), and heart failure (P = 0.002).</AbstractText>There was a significant difference between the type of antiplatelet drug and clinical outcomes in ACS patients who were treated with DAPT. Observations from current study may provide important information for prescribers in clinical decision-making.</AbstractText> |
20,312 | Left Atrial Appendage Volume and Plasma Docosahexaenoic Acid Levels Are Associated With Atrial Fibrillation Recurrence After Catheter Ablation. | Risk factors for atrial fibrillation (AF) recurrence in patients who have undergone AF catheter ablation have not been fully clarified. The objective of this study was to assess whether the left atrium (LA) and LA appendage (LAA) volumes, and cardio-metabolic markers such as polyunsaturated fatty acids (PUFAs) levels were associated with AF recurrence.</AbstractText>Seventy-seven consecutive patients with AF (mean age, 59 ± 8 years; male, 81%; paroxysmal AF, 64%) undergoing catheter ablation were enrolled. Using contrast-enhanced cardiac multi-detector computed tomography (MDCT) scan, the LA and LAA volume and orifice area were assessed. Radiofrequency ablation was performed by an irrigation catheter, initially targeting the pulmonary veins with a wide area circumferential ablation.</AbstractText>Patients with AF recurrence (36%) exhibited both larger LAA volumes and an LAA orifice area than those without AF recurrence, whereas the LA diameter and LA volumes were not significantly different. Notably, AF recurrence occurred in all patients with a large LAA (≥ 25 mL), and the LAA volume was significantly and negatively associated with docosahexaenoic acid (DHA) levels (β = -0.33, P = 0.003). A multiple regression analysis revealed that the log N-terminal proB-type natriuretic peptide and plasma DHA levels were independent factors for the LAA volume when adjusted for age, AF detected age, left ventricular (LV) ejection fraction, end-systolic LV diameter.</AbstractText>These results suggest that the association between LAA volume and low plasma DHA levels may be an important factor for post-ablation AF recurrence.</AbstractText> |
20,313 | Effect of Recurrent Mitral Regurgitation After Mitral Valve Repair in Patients With Degenerative Mitral Regurgitation. | This study investigated the consequences of recurrent mitral regurgitation (MR) after mitral valve (MV) repair in patients with degenerative MR and risk factors for recurrence.Methods and Results:From January 1990 to December 2015, 792 patients underwent MV repair due to degenerative MR. Recurrent MR was defined as moderate-to-severe MR on follow-up echocardiography. Mean follow-up duration was 8.71±5.58 years. During the follow-up period, MR recurred in 133 (16.8%) patients, and the MR recurrence-free rate at 20 years was 77.5±2.0%. In the recurrence group, the degree of MR decreased in 8 (6.0%) patients and was aggravated in 46 (34.6%) patients. Recurrent MR was associated with increased mortality and adverse left ventricular (LV) remodeling. Independent risk factors for MR recurrence were MV repair performed before 2000, preoperative atrial fibrillation, high LV end-diastolic dimension (LVEDD), prolapse of the isolated anterior leaflet or multiple segments, and absence of ring annuloplasty. Predictors of MR progression were high LVEDD and repair without artificial chordae implantation.</AbstractText>Recurrent MR after MV repair in patients with degenerative MR showed a tendency to progress and was associated with increased mortality and adverse LV remodeling. Early referral for MV repair before development of atrial fibrillation and LV enlargement may reduce the risk of MR recurrence. Moreover, artificial chordae implantation and ring annuloplasty may assure the long-term durability of MV repair.</AbstractText> |
20,314 | Prognostic implication of early ventricular fibrillation among patients with ST elevation myocardial infarction. | The aim of this study was to analyze the prognosis of patients presenting early ventricular fibrillation (VF) in the setting of ST elevation myocardial infarction (STEMI).</AbstractText>Among patients included in the ARIAM (Análisis del Retraso en el Infarto Agudo de Miocardio) registry with the diagnosis of STEMI, those who received primary revascularization and were admitted in the first 12 h were analyzed retrospectively.</AbstractText>From January 2007 to January 2012, 8340 patients were included in the STEMI cohort and 680 (8.2%) of them presented with VF before admission to the ICU (VF). This group comprised younger patients with fewer comorbidities. They received more often primary angioplasty (33.7 vs. 24.9%; P<0.001), had more prevalence of Killip class greater than or equal to 2 at admission (37.5 vs. 17.8%; P<0.001), and suffered more often cardiogenic shock (18.5 vs. 5.9%, P<0.001). By logistic regression analysis, VF was associated with a greater in-hospital mortality [odds rate (OR): 2.08, 95% confidence interval (CI): 1.57-2.81, P<0.001]. After a propensity score matching process, VF was associated with in-hospital mortality (OR: 1.53, 95% CI: 1.05-2.25, P=0.028). However, when analyzing patients treated by primary angioplasty, the mortality was not significantly related to VF (OR: 0.86, 95% CI: 0.45-1.61, P=0.628).</AbstractText>Our results show that VF before ICU admission was an independent predictor of in-hospital outcome in a cohort of patients in whom fibrinolysis was the most used revascularization therapy. However, this prognostic value was not found in patients treated with primary angioplasty.</AbstractText> |
20,315 | Structured pain management reduces patient discomfort after catheter ablation and rhythm device surgery. | The goal was to test the effectiveness of a structured pain management programme after invasive electrophysiological interventions in cardiology including ablation of atrial fibrillation (AF) or ventricular tachycardia (VT) and implantation, or explantation, of pacemakers or implantable cardioverter defibrillators.</AbstractText>This was a prospective study with a pre-/post-design where a post-intervention group (116 consecutive patients) was compared to a pre-intervention group (102 consecutive patients) after implementation of a structured pain-management programme using the numeric rating scale (NRS 0-10) and classified as moderate-to-severe if NRS > 3. Measurements were recorded every two hours during the first 24 h post-operatively. The location of the pain and the amount of analgesic used were also recorded.</AbstractText>The proportion of patients who experienced moderate-to-severe pain after the procedure decreased after initiation of the pain-management program: 47% versus 61%; p = 0.048. This difference was driven primarily by reduced pain late (8-24 h) after the procedure; 16% versus 39%; p < 0.001. The risk to develop late (8-24 h) post-procedural pain was reduced approximately three-fold after implementation of the pain-management programme (OR = 0.32, 95% CI 0.16-0.64, p = 0.001). Multivariate analysis indicated chronic pain, early pain (0-6 h), and type of intervention were associated with late post-interventional pain. In contrast, age, diabetes mellitus, BMI, gender and procedure time were not related.</AbstractText>The findings illustrate the potential value of a structured pain-management programme. The proportion of patients who experienced moderate-to-severe pain after these electrophysiological procedures decreased significantly.</AbstractText>This is the first exploratory study that evaluates the impact of a multidisciplinary pain-management programme after cardiac electrophysiological interventions. It demonstrates that significant quality improvement is achievable following simple rules together with patient and staff education. The programme reduces the proportion of patients with moderate-to-severe pain after electrophysiological procedures significantly.</AbstractText>© 2017 European Pain Federation - EFIC®.</CopyrightInformation> |
20,316 | Free Fatty Acid Is Associated with Thrombogenicity in Cardioembolic Stroke. | Recently, the role of free fatty acids (FFAs) in thromboembolism has re-emerged in the context of cardioembolic stroke. Therefore, we attempted to determine the role of FFAs in embolic risk in various potential sources of cardioembolism (PSCE). We hypothesized that if elevated FFA levels in stroke patients are associated with thrombogenesis, then patients with a well-known high risk of embolic sources would have high FFA levels.</AbstractText>Data collected from 2 hospital-based stroke registries were analyzed to investigate the association between FFA and PSCE.</AbstractText>A total of 2,770 acute stroke patients, including 539 with cardioembolic stroke, were selected for analysis. FFA was an independent predictor for cardioembolism (OR 2.755, 95% CI 2.221-3.417, p < 0.001). Among the PSCE, FFA levels were significantly associated with high risk of atrial fibrillation (AF), valvular heart disease, congestive heart failure with low ejection fraction, left atrial thrombus, left ventricular thrombus, left atrial smoke, and ventricular wall motion abnormality. FFA levels increased with the number of PSCE per patient without interaction with the presence of AF.</AbstractText>Among acute stroke patients, FFA levels increased in groups with higher risk of cardioembolic stroke irrespective of the presence of AF. These results suggest that enhanced thrombogenicity could be the main mechanism to explain the elevated FFA levels in patients with cardioembolic stroke.</AbstractText>© 2017 S. Karger AG, Basel.</CopyrightInformation> |
20,317 | Echocardiographic parameters versus CHA2DS2-VASc score in prediction of overall cardiac events, heart failure, and stroke in non-valvular atrial fibrillation. | Apart from stroke, atrial fibrillation (AF) is associated with higher mortality and heart failure (HF), in which risk stratification scheme is lacking. Therefore this investigation examined the prognostic value of echocardiographic predictors against CHA2DS2-VASc score in permanent non- -valvular AF (NVAF).</AbstractText>In 252 asymptomatic or mildly symptomatic consecutive patients with NVAF, comprehensive echocardiography was performed. Left atrial deformation parameters were also obtained by two-dimen-sional speckle tracking echocardiography. End-points pertaining to HF deterioration, ischemic stroke and cardiac death were recorded.</AbstractText>There were 74 cardiovascular events, including 44 deterioration of HF, 22 ischemic strokes and 8 cardiovascular deaths during an average follow-up period of 20.8 ± 13.5 months (interquartile range, 8-31 months). For prediction of overall prognosis and HF, left ventricular mass index, peak early filling velocity (E), and E to tissue Doppler mitral annular early diastolic velocity ratio (E/e') outper-formed CHA2DS2-VASc score in multivariate analysis, area under curve, and stepwise nested regression models. Left ventricular hypertrophy and E/e' > 8 showed worse overall and heart-failure free survival in Kaplan-Meier curves. For prediction of ischemic stroke, the addition of E or E/e' to CHA2DS2-VASc score provides extra prognostic value.</AbstractText>Echocardiographic parameters offer incremental value over CHA2DS2-VASc score for prediction of future cardiac events in NVAF. (Cardiol J 2018; 25, 1: 60-71).</AbstractText> |
20,318 | Impact of percutaneous mitral valvuloplasty on left ventricular function in patients with mitral stenosis assessed by 3D echocardiography. | The status of intrinsic left ventricular (LV) contractility in patients with isolated rheumatic mitral stenosis (MS) has been debated. The acute changes in loading conditions after percutaneous mitral valvuloplasty (PMV) may affect LV performance. We aimed to examine the acute effects of PMV on LV function and identify factors associated with LV ejection fraction (LVEF) changes, and determinants of long-term events following the procedure.</AbstractText>One hundred and forty-two patients who underwent PMV for symptomatic rheumatic MS (valve area of 0.99±0.3cm2</sup>) were prospectively enrolled. LV volumes and LVEF were measured by three-dimensional (3D) echocardiography. Long-term outcome was a composite endpoint of death, mitral valve (MV) replacement, repeat PMV, new onset of atrial fibrillation, and stroke.</AbstractText>The mean age was 42.3±12.1years, and 125 patients were women (88%). After PMV, LVEF increased significantly (51.4 vs 56.5%, p<0.001), primary due to a significant increase in LV end-diastolic volume (65.8mL vs 67.9mL, p=0.002), and resultant increase in the stroke volume (33.9mL vs 39.6mL, p<0.001). Changes in cardiac index and systolic pulmonary artery pressure were associated with LVEF changes after PMV. During a mean follow-up period of 30.8months, 28 adverse clinical events were observed. Postprocedural mitral regurgitation, MV area, and mean gradient were independent predictors of composite endpoints.</AbstractText>In patients with rheumatic MS, PMV resulted in a significant improvement in LV end-diastolic volume, stroke volume and consequently increased in LVEF. Changes in cardiac index and systolic pulmonary artery pressure were associated with LVEF changes after PMV. The predictors of long-term adverse events following PMV were post-procedural variables, including mitral regurgitation, valve area, and mean gradient.</AbstractText>Copyright © 2017 Elsevier B.V. All rights reserved.</CopyrightInformation> |
20,319 | Catheter ablation of accessory pathway: 14-year trends in utilization and complications in adults in the United States. | The aim of this study was to determine the temporal trends in utilization of catheter ablation of accessory pathways in the United States.</AbstractText>All patients from the Nationwide Inpatient Sample (NIS) ≥18years of age with a primary diagnosis of anomalous atrioventricular excitation syndrome (International Classification of Diseases, Ninth Edition, Clinical Modification [ICD-9-CM] code 426.7) were included in the study. Patients who underwent catheter ablation were identified using ICD-9-CM procedure code 37.34. Patients with a concomitant diagnosis of atrial fibrillation, atrial flutter, atrial tachycardia or ventricular arrhythmias were excluded from the analysis. Annual hospital volume was identified using unique hospital identification number and was divided into tertiles for further analysis.</AbstractText>A total of 11,601 catheter ablations for anomalous atrioventricular excitation syndrome were studied from 1998 to 2011. The mean length of stay was 1.8days (median 1day). The utilization trends of accessory pathway ablation have steadily declined from 3.9 ablation procedures/million US population in 1998-1999 to 2.5 ablation procedures/million US population in 2010-2011. The second tertile (adjusted OR 0.41; 95% CI 0.20-0.83, p=0.01) and third tertile (adjusted OR 0.39; 95% CI 0.18-0.85, p=0.02) of hospital volume were associated with reduction in cardiac complications as compared to first tertile of hospital volume. Advanced age (OR 1.02, 95% CI 1.01-1.04, p=0.002) was independent predictor of cardiac complications. There were no in-hospital deaths.</AbstractText>Despite decline in ablation trends, it still remains a relatively safe procedure associated with low morbidity and no mortality.</AbstractText>Copyright © 2017 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
20,320 | Ischemic Stroke with Cardiac Pacemaker Implantation: Comparison of Physiological and Ventricular Pacing Modes. | The clinical characteristics of ischemic stroke in patients with a pacemaker (PM) are not well understood.</AbstractText>Forty-six ischemic stroke patients with a PM were investigated retrospectively, and the impact of different pacing modes was compared.</AbstractText>The patients were divided into a physiological pacing group (n = 22) and a ventricular pacing group (n = 24). The prevalence of atrial fibrillation (AF) was significantly higher in the ventricular pacing group (36% versus 75%; P = .008). The mean left atrial dimension was relatively large in the ventricular pacing group than in the physiological pacing group (44.5 ± 6.7 mm versus 39.1 ± 8.5 mm, respectively; P = .071). Twenty-four percent of the patients were receiving anticoagulants, whereas 41% of the patients were receiving antiplatelet drugs. Cardioembolism was the most common stroke subtype in both groups. Although there was no statistically significant difference, neurological severity on admission was higher in the ventricular pacing group than in the physiological pacing group (P = .061). Functional outcomes, excluding patients with transient ischemic attack or prior stroke, significantly declined in the ventricular pacing group compared with the physiological pacing group (P = .044).</AbstractText>The avoidance of the ventricular pacing mode may result in improved clinical outcomes. In patients without persistent AF, it may be important to select physiological pacing instead of ventricular pacing to decrease potential stroke severity.</AbstractText>Copyright © 2017 National Stroke Association. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
20,321 | Spectrum of Cardiac Arrhythmias in Isolated Ventricular Non-Compaction. | A wide spectrum of cardiac arrhythmias has been observed in patients with isolated ventricular non-compaction, which is defined by hypertrabeculated ventricular myocardium with deep intertrabecular recesses, in the absence of concomitant congenital heart disease. In this genetically diverse phenotype, the development of fibrosis contributes to an arrhythmogenic substrate underlying atrioventricular conduction diseases, supraventricular tachycardias and ventricular tachycardias. Within this spectrum, monomorphic ventricular tachycardia is the most frequently observed arrhythmia, and this prevalence has important implications for sudden cardiac death risk. |
20,322 | Rationale and design of the AdaptResponse trial: a prospective randomized study of cardiac resynchronization therapy with preferential adaptive left ventricular-only pacing. | The AdaptResponse trial is designed to test the hypothesis that preferential adaptive left ventricular-only pacing with the AdaptivCRT<sup>®</sup> algorithm reduces the incidence of the combined endpoint of all-cause mortality and intervention for heart failure (HF) decompensation, compared with conventional cardiac resynchronization therapy (CRT), among patients with a CRT indication, left bundle branch block (LBBB) and normal atrioventricular (AV) conduction. The AdaptResponse study is a prospective, randomized, controlled, single-blinded, multicentre, clinical trial (ClinicalTrials.gov Identifier: NCT02205359), conducted at up to 200 centres worldwide. Following enrolment and baseline assessment, eligible subjects will be implanted with a CRT system containing the AdaptivCRT algorithm, and randomized in a 1:1 fashion to either a treatment ('AdaptivCRT') or control ('Conventional CRT') group. The study is designed to observe a primary endpoint in 1100 patients ('event-driven') and approximately 3000 patients will be randomized. The primary endpoint is the composite of all-cause mortality and intervention for HF decompensation; secondary endpoints include all-cause mortality, intervention for HF decompensation, clinical composite score (CCS) at 6 months, atrial fibrillation, quality of life measured by the Kansas City Cardiomyopathy Questionnaire (KCCQ), health outcome measured by the EQ-5D instrument, all-cause readmission after a HF admission, and cost-effectiveness. The AdaptResponse clinical trial is powered to assess clinical endpoints and is expected to provide definitive evidence on the incremental utility of AdaptivCRT-enhanced CRT systems. |
20,323 | Risk stratification personalised model for prediction of life-threatening ventricular tachyarrhythmias in patients with chronic heart failure. | The development of prognostic factors of life-threatening ventricular tachyarrhythmias (VTA) and sudden cardiac death (SCD) continues to maintain its priority and relevance in cardiology. The development of a method of personalised prognosis based on multifactorial analysis of the risk factors associated with life-threatening heart rhythm disturbances is considered a key research and clinical task.</AbstractText>To design a prognostic and mathematical model to define personalised risk for life-threatening VTA in patients with chronic heart failure (CHF).</AbstractText>The study included 240 patients with CHF (mean-age of 50.5 ± 12.1 years; left ventricular ejection fraction 32.8 ± 10.9%; follow-up period 36.8 ± 5.7 months). The participants received basic therapy for heart failure. The elec-trocardiogram (ECG) markers of myocardial electrical instability were assessed including microvolt T-wave alternans, heart rate turbulence, heart rate deceleration, and QT dispersion. Additionally, echocardiography and Holter monitoring (HM) were performed. The cardiovascular events were considered as primary endpoints, including SCD, paroxysmal ventricular tachycardia/ventricular fibrillation (VT/VF) based on HM-ECG data, and data obtained from implantable device interrogation (CRT-D, ICD) as well as appropriated shocks.</AbstractText>During the follow-up period, 66 (27.5%) subjects with CHF showed adverse arrhythmic events, including nine SCD events and 57 VTAs. Data from a stepwise discriminant analysis of cumulative ECG-markers of myocardial electrical instability were used to make a mathematical model of preliminary VTA risk stratification. Uni- and multivariate Cox logistic regression analysis were performed to define an individualised risk stratification model of SCD/VTA. A binary logistic regression model demonstrated a high prognostic significance of discriminant function with a classification sensitivity of 80.8% and specificity of 99.1% (F = 31.2; c2 = 143.2; p < 0.0001).</AbstractText>The method of personalised risk stratification using Cox logistic regression allows correct classification of more than 93.9% of CHF cases. A robust body of evidence concerning logistic regression prognostic significance to define VTA risk allows inclusion of this method into the algorithm of subsequent control and selection of the optimal treatment modality to treat patients with CHF.</AbstractText> |
20,324 | Frontiers in non-invasive cardiac mapping: future implications for arrhythmia treatment. | Electrocardiographic mapping (ECM) is a noninvasive technique using body surface potentials and CT geometry to reconstruct epicardial maps. ECM is emerging as an important tool not only for diagnostic mapping, but also as a guide for trans-catheter ablation of complex arrhythmias such as atrial fibrillation. It provides the clinician with an immediate global view of the substrate, allowing easier pre-procedural planning, potentially improving clinical outcomes. Panoramic mapping of ventricular fibrillation (VF) is helping to develop a better understanding of its physiology, with future implications for the identification of therapeutic targets in patients with structural heart disease, as well as in idiopathic VF. |
20,325 | Non-functional tricuspid valve disease. | Only 75% of severe tricuspid regurgitation is classified as functional, or related primarily to pulmonary hypertension, right ventricular dysfunction, or a combination of both. Non-functional tricuspid regurgitation occurs when there is damage to the tricuspid leaflets, chordae, papillary muscles, or annulus, independent of right ventricular dysfunction or pulmonary hypertension. The entities that cause non-functional tricuspid regurgitation include rheumatic and myxomatous disease, acquired and genetic connective tissue disorders, endocarditis, sarcoid, pacing, RV biopsy, blunt trauma, radiation, carcinoid, ergot alkaloids, dopamine agonists, fenfluramine, cardiac tumors, atrial fibrillation, and congenital malformations. Over time, severe tricuspid regurgitation that is initially non-functional, can blend into functional tricuspid regurgitation, related to progressive right ventricular dysfunction. Symptoms and signs, including a falling right ventricular ejection fraction, cardiac cirrhosis, ascites, esophageal varices, and anasarca, may occur insidiously and late, but are associated with substantial morbidity and mortality. Attempted valve repair or replacement at late stages carries a high mortality. Crucial to following patients with severe non-functional tricuspid regurgitation is attention to echo quantification of the tricuspid regurgitation and right ventricular function, patient symptoms, and the physical examination. |
20,326 | When Is the Optimal Timing of Surgical Intervention for Severe Functional Tricuspid Regurgitation? | Functional tricuspid regurgitation (TR) is a serious pathology to be noted for severe right heart failure (HF) and poor prognosis; however, the conventional assessment of TR has some limitations and the optimal timing of surgical intervention remains unclear. A 79-year-old Japanese female was admitted to our hospital to undergo cardiac surgery, because edema gradually got worse despite the increase in diuretics. She had a history of atrial fibrillation (AF) and chronic HF due to severe TR and had been treated with a furosemide for leg edema 4 years ago. A transthoracic echocardiogram (TTE), transesophageal echocardiogram, cardiac magnetic resonance imaging, and cardiac pool scintigraphy demonstrated severe functional TR with tricuspid annular dilation, insufficient tricuspid valve coaptation, and reduced right ventricular ejection fraction (EF) but preserved left ventricular EF. In addition, Swan-Ganz catheter study showed normal pulmonary arterial wedge pressure and mean pulmonary arterial pressure. Tricuspid ring annuloplasty was performed with MC3 ring. Postoperative TTE showed trivial TR, and she had no edema with normal sinus rhythm two months later. Annuloplasty to severe functional TR caused by tricuspid annular dilation due to AF dramatically improved right HF. Cardiologist should pay strict attention to the optimal timing of surgical intervention for TR. |
20,327 | Cardiac damage in athlete's heart: When the "supernormal" heart fails! | Intense exercise may cause heart remodeling to compensate increases in blood pressure or volume by increasing muscle mass. Cardiac changes do not involve only the left ventricle, but all heart chambers. Physiological cardiac modeling in athletes is associated with normal or enhanced cardiac function, but recent studies have documented decrements in left ventricular function during intense exercise and the release of cardiac markers of necrosis in athlete's blood of uncertain significance. Furthermore, cardiac remodeling may predispose athletes to heart disease and result in electrical remodeling, responsible for arrhythmias. Athlete's heart is a physiological condition and does not require a specific treatment. In some conditions, it is important to differentiate the physiological adaptations from pathological conditions, such as hypertrophic cardiomyopathy, arrhythmogenic dysplasia of the right ventricle, and non-compaction myocardium, for the greater risk of sudden cardiac death of these conditions. Moreover, some drugs and performance-enhancing drugs can cause structural alterations and arrhythmias, therefore, their use should be excluded. |
20,328 | Modeling Atrial Fibrillation using Human Embryonic Stem Cell-Derived Atrial Tissue. | Since current experimental models of Atrial Fibrillation (AF) have significant limitations, we used human embryonic stem cells (hESCs) to generate an atrial-specific tissue model of AF for pharmacologic testing. We generated atrial-like cardiomyocytes (CMs) from hESCs which preferentially expressed atrial-specific genes, and had shorter action potential (AP) durations compared to ventricular-like CMs. We then generated confluent atrial-like CM sheets and interrogated them using optical mapping techniques. Atrial-like CM sheets (~1 cm in diameter) showed uniform AP propagation, and rapid re-entrant rotor patterns, as seen in AF could be induced. Anti-arrhythmic drugs were tested on single atrial-like CMs and cell sheets. Flecainide profoundly slowed upstroke velocity without affecting AP duration, leading to reduced conduction velocities (CVs), curvatures and cycle lengths of rotors, consistent with increased rotor organization and expansion. By contrast, consistent with block of rapid delayed rectifier K+ currents (Ikr) and AP prolongation in isolated atrial-like CMs, dofetilide prolonged APs and reduced cycle lengths of rotors in cell sheets without affecting CV. In conclusion, using our hESC-derived atrial CM preparations, we demonstrate that flecainide and dofetilide modulate reentrant arrhythmogenic rotor activation patterns in a manner that helps explain their efficacy in treating and preventing AF. |
20,329 | Automated Quantification of Low-Amplitude Abnormal QRS Peaks From High-Resolution ECG Recordings Predicts Arrhythmic Events in Patients With Cardiomyopathy. | Cardiomyopathy patients are at risk of sudden death, typically from scar-related abnormalities of electrical activation that promote ventricular tachyarrhythmias. Abnormal intra-QRS peaks may provide a measure of altered activation. We hypothesized that quantification of such QRS peaks (QRSp) in high-resolution ECGs would predict arrhythmic events in implantable cardioverter-defibrillator (ICD)-eligible cardiomyopathy patients.</AbstractText>Ninety-nine patients with ischemic or non-ischemic dilated cardiomyopathy undergoing prophylactic ICD implantation were prospectively enrolled (age 62±11 years, left ventricular ejection fraction 27±7%). High-resolution (1024 Hz) digital 12-lead ECGs were recorded during intrinsic rhythm. QRSp was quantified for each precordial lead as the total number of low-amplitude deflections that deviated from their respective naive QRS template. The primary end point of arrhythmic events was defined as appropriate ICD therapy or sustained ventricular tachyarrhythmias. After a median follow-up of 24 (15-43) months, 20 (20%) patients had arrhythmic events. Both QRSp and QRS duration were greater in those with arrhythmic events (both P</i><0.001) and this was consistent for QRSp for both cardiomyopathy types. In a multivariable Cox regression model that included age, left ventricular ejection fraction, QRS duration, and QRSp, only QRSp was an independent predictor of arrhythmic events (hazard ratio, 2.1; P</i><0.001). Receiver operating characteristic analysis revealed that a QRSp ≥2.25 identified arrhythmic events with greater sensitivity (100% versus 70%, P</i><0.05) and negative predictive value (100% versus 89%, P</i><0.05) than QRS duration ≥120 ms.</AbstractText>QRSp measured from high-resolution digital 12-lead ECGs independently predicts ventricular tachyarrhythmias in ICD-eligible cardiomyopathy patients. This novel QRS morphology index has the potential to improve sudden death risk stratification and patient selection for prophylactic ICD therapy.</AbstractText>© 2017 American Heart Association, Inc.</CopyrightInformation> |
20,330 | Ventricular fibrillation induced by high-output ICD shock: report of cases and review of literature. | This report highlights the importance of realising that even the modern-day implantable cardioverter defibrillators (ICDs) with R wave synchronised appropriate shocks have a potential proarrhythmic effect. We present two cases of ventricular fibrillation induction resulting from an appropriate ICD shock observed in two different patients at our institution. Such cases have not been reported before. We discuss the possible reasons for our observations and are also submitting a pertinent literature review with our reports. |
20,331 | Brugada syndrome in a patient with amyotrophic lateral sclerosis: a case report. | Amyotrophic lateral sclerosis is a fatal neuromuscular disorder characterized by progressive death of the upper and lower motor neurons in the central nervous system. Patients with this disease die mostly as a result of respiratory failure; however, owing to prolonged survival through assisted ventilation, cardiovascular causes are increasingly responsible for mortality. We report what is to the best of our knowledge the first case of type 2 Brugada syndrome causing ventricular tachyarrhythmia and cardiac arrest in a patient with upper limb onset amyotrophic lateral sclerosis.</AbstractText>A 48-year-old Caucasian woman with a significant past medical history of papillary thyroid carcinoma status postresection, pulmonary embolism on anticoagulation, and a recent diagnosis of right upper limb-onset amyotrophic lateral sclerosis presented to the emergency department of our hospital with acute on chronic shortness of breath. On further evaluation, she was found to have hypoxic and hypercapnic respiratory failure and was placed on bilevel positive airway pressure ventilation. Her 12-lead electrocardiogram showed sinus rhythm with J-point elevation, saddle-shaped ST segment elevation, predominantly in V1 and V2 with no significant QTc prolongation. No troponin elevation was noted in her laboratory workup. Because she was unable to protect her airway, a decision was made to intubate her. After 1 minute of induction with etomidate and succinylcholine, she went into pulseless ventricular tachycardia and fibrillation requiring three cycles of cardiopulmonary resuscitation with high-quality chest compressions, three doses of epinephrine, and a loading dose of amiodarone prior to return of spontaneous circulation. She was further evaluated by cardiology services and was diagnosed with type 2 Brugada syndrome, for which she was started on quinidine. Her respiratory failure and the drugs she received for intubation likely caused her ventricular tachycardia to occur in conjunction with an underlying Brugada pattern seen on an electrocardiogram. The results of evaluation of her genetic panel for Brugada syndrome were negative. She was subsequently discharged to home in stable condition after a 10-day hospital stay.</AbstractText>Amyotrophic lateral sclerosis is a progressive neuromuscular disorder with significant mortality. Respiratory failure is the leading cause of death, but lately, owing to increased survival associated with early tracheostomy and positive pressure ventilation, there has been an increasing trend in the identification of cardiovascular causes of mortality, especially arrhythmias, that may need periodic electrocardiographic surveillance.</AbstractText> |
20,332 | Characteristic features of patients with multiple accessory pathways. | Objective Only limited clinical and electrophysiological data concerning patients (pts) with multiple accessory pathways (MAP) in comparison to large control groups are available. The aim of our study was to analyse these data from the largest cohort of patients with multiple accessory pathways and a large control group. Method and results We analysed data from pts with MAP (group 1) and pts with a single accessory pathway (AP) (group 2) referred for radiofrequency catheter ablation (RFCA) at our tertiary centre. Group 1 consisted of 124 pts (M 62.10%, mean age 33.00 ± 5.26) with MAP and RFCA. Group 2 consisted of 376 pts (M 51.20%, mean age 35.87 ± 16.15) with a single accessory pathway and RF ablation. Group 1 exhibited a higher incidence of overt APs (P < 0.0001), Ebstein anomaly (P = 0.001), ventricular fibrillation (P = 0.012), antidromic atrioventricular re-entrant tachycardia (A AVRT) (P = 0.025) and male gender (P = 0.038). The mean age at the first documented atrioventricular re-entrant tachycardia (AVRT) episode was lower in pts with MAP than in pts with single APs: 16.79 ± 13.41 vs 20.84 ± 14.29, respectively (P = 0.001). Concealed accessory pathways (P < 0.0001) occurred more frequently in the control group. Group 1 had more right-lateral (P = 0.0001), mid-septal (P = 0.0001), left-posterior (P = 0.01), left-anterior (P = 0.013) and left-lateral localizations of AP (P < 0.037). Conclusions The MAP group included statistically significantly more men, Ebstein anomaly and overt APs. The mean age of the first episode of atrioventricular re-entrant tachycardia was lower in pts with MAP. Certain distribution patterns are apparent for single and MAP. Pts with MAP are at higher risk of VF and antidromic atrioventricular re-entrant tachycardia. |
20,333 | Galectin-3 correlates with arrhythmogenic right ventricular cardiomyopathy and predicts the risk of ventricular -arrhythmias in patients with implantable defibrillators. | Background Arrhythmogenic right ventricular dysplasia (ARVD) is a heritable disorder characterized by fibro-fatty replacement of right ventricular myocytes, increased risk of ventricular arrhythmias, and sudden cardiac death. Galectin-3 (GAL3) is known to play an important role in a number of fibrotic conditions, including cardiac fibrosis. Many studies have focused on the association between GAL3 levels and cardiac fibrosis in heart failure. However, the role of GAL3 in the pathogenesis of ARVD and ventricular arrhythmias has not yet been evaluated thoroughly. The aim of this study was to explore GAL3 levels in patients with ARVD and its association with ventricular arrhythmias. Methods Twenty-nine patients with ARVD and 24 controls were included. All patients with ARVD had an implantable cardiac defibrillator (ICD) for primary or secondary prevention. Ventricular arrhythmia history was obtained from a chart review and ICD data interrogation. Galectin-3 levels were measured using an enzyme-linked immunosorbent assay. Results Patients with ARVD had higher plasma GAL3 levels (16.9 ± 2.6 ng/mL vs 11.3 ± 1.8 ng/mL, P < 0.001) than the control group. Ten patients had sustained or non-sustained ventricular arrhythmias during follow-up. In the multivariable analysis, left ventricular disease involvement (HR: 1.05; 95% CI: [1.01-1.12]; P = 0.03); functional capacity >2 (HR: 1.21; 95% CI: [1.13-1.31]; P < 0.005); and GAL3 levels (HR: 1.05; 95% CI: [1.00-1.11]; P = 0.01) independently predicted VT/VF. Conclusion We demonstrated that serum GAL3 was significantly elevated in patients with ARVD. Also, serum GAL 3 levels could be regarded as a candidate biomarker in the diagnosis of ARVD which needs to be tested in larger prospective studies. In addition, GAL3 levels were higher in patients with VT/VF as compared with those without VT/VF. |
20,334 | Cardiovascular Histopathology of a 11-Year Old with Mucopolysaccharidosis VII Demonstrates Fibrosis, Macrophage Infiltration, and Arterial Luminal Stenosis. | Mucopolysaccharidosis type VII (MPS VII) is caused by β-glucuronidase deficiency, resulting in lysosomal accumulation of glycosaminoglycans (GAGs) and multisystemic disease. We present cardiovascular gross and histopathology findings from a 11-year-old MPS VII male, who expired after developing ventricular fibrillation following anesthesia induction. Gross anatomic observations were made at autopsy; postmortem formalin-fixed paraffin-embedded samples of the carotid artery, aorta, myocardium, and valves were sectioned and stained with hematoxylin-eosin, Verhoeff-Van Gieson, CD68, and trichrome stains. Gross heart findings include an enlarged, dilated heart, mitral valve prolapse with thick, shortened chordae tendinae, and thickened aortic valve cusps. The aorta contained raised intimal plaques mimicking conventional atherosclerosis. Cardiac myocytes included hypertrophic nuclei, subendocardial fibrosis, and increased interfascicular collagen. Coronary lumens were 40-70% stenosed by fibrointimal hyperplasia containing storage material-laden cells, CD68<sup>+</sup> macrophages, and fragmented elastin laminae. Similar findings were visualized in aortic intimal plaques. We confirm that arterial plaques, elastin fragmentation, and activated CD68<sup>+</sup> macrophage infiltration occur in human MPS VII, consistent with previously observed findings in murine and canine MPS VII. We also confirm ultrasonographically observed carotid intimal-medial thickening is an in vivo correlate of histopathologic vascular fibrointimal hyperplasia. MPS VII patients should be regularly monitored for cardiac disease, with methods such as Holter monitors and stress testing; MPS VII-directed treatments should effectively address cardiovascular disease. |
20,335 | Regulation of cardiac Ca<sup>2+</sup> and ion channels by shear mechanotransduction. | Cardiac contraction is controlled by a Ca<sup>2+</sup> signaling sequence that includes L-type Ca<sup>2+</sup> current-gated opening of Ca<sup>2+</sup> release channels (ryanodine receptors) in the sarcoplasmic reticulum (SR). Local Ca<sup>2+</sup> signaling in the atrium differs from that in the ventricle because atrial myocytes lack transverse tubules and have more abundant corbular SR. Myocardium is subjected to a variety of forces with each contraction, such as stretch, shear stress, and afterload, and adapts to those mechanical stresses. These mechanical stimuli increase in heart failure, hypertension, and valvular heart diseases that are clinically implicated in atrial fibrillation and stroke. In the present review, we describe distinct responses of atrial and ventricular myocytes to shear stress and compare them with other mechanical responses in the context of local and global Ca<sup>2+</sup> signaling and ion channel regulation. Recent evidence suggests that shear mechanotransduction in cardiac myocytes involves activation of gap junction hemichannels, purinergic signaling, and generation of mitochondrial reactive oxygen species. Significant alterations in Ca<sup>2+</sup> signaling and ionic currents by shear stress may be implicated in the pathogenesis of cardiac arrhythmia and failure. |
20,336 | National Institutes of Health-Funded Cardiac Arrest Research: A 10-Year Trend Analysis. | Cardiac arrest (CA) is a leading cause of death in the United States, claiming over 450 000 lives annually. Improving survival depends on the ability to conduct CA research and on the translation and implementation of research findings into practice. Our objective was to provide a descriptive analysis of annual National Institutes of Health (NIH) funding for CA research over the past decade.</AbstractText>A search within NIH RePORTER for the years 2007 to 2016 was performed using the terms: "cardiac arrest" or "cardiopulmonary resuscitation" or "heart arrest" or "circulatory arrest" or "pulseless electrical activity" or "ventricular fibrillation" or "resuscitation." Grants were reviewed and categorized as CA research (yes/no) using predefined criteria. The annual NIH funding for CA research, number of individual grants, and principal investigators were tabulated. The total NIH investment in CA research for 2015 was calculated and compared to those for other leading causes of death within the United States. Interrater reliability among 3 independent reviewers for fiscal year 2015 was assessed using Fleiss κ. The search yielded 2763 NIH-funded grants, of which 745 (27.0%) were classified as CA research (κ=0.86 [95%CI 0.80-0.93]). Total inflation-adjusted NIH funding for CA research was $35.4 million in 2007, peaked at $76.7 million in 2010, and has decreased to $28.5 million in 2016. Per annual death, NIH invests ≈$2200 for stroke, ≈$2100 for heart disease, and ≈$91 for CA.</AbstractText>This analysis demonstrates that the annual NIH investment in CA research is low relative to other leading causes of death in the United States and has declined over the past decade.</AbstractText>© 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.</CopyrightInformation> |
20,337 | Inpatient rehabilitation for adult patients with Marfan syndrome: an observational pilot study. | Advances in medical, interventional and surgical treatment have increased average life expectancy of patients with congenital heart defects. As a result a new group of adult patients with congenital cardiac defects requires medical rehabilitation. Patients with Marfan syndrome (MFS) are a relevant group among these patients. So far, no reports on the effectiveness of specialized rehabilitation programmes for MFS patients exist. We implemented an inpatient 3-week rehabilitation program for MFS patients at the Muehlenberg-Clinic for rehabilitation and assessed the medical safety as well as the impact of the program on physical fitness and psychological wellbeing of participants by means of an observational pilot study. The comprehensive multidisciplinary program included medical, physiotherapeutic, psychological and social issues. Two groups including 8 and 10 individuals with verified MFS attended the programme. Medically adverse events that occurred during the rehabilitation were registered. Adverse events were defined as: any new cardiac arrhythmias such as atrial fibrillation, ventricular tachycardia, cardiac syncope or any complications located at the aorta. Psychological assessment was performed using Short Form-36 (SF-36), hospital anxiety and depression scale and other psychometric questionnaires. Medical examinations included assessment of maximum power in bicycle ergometry. All assessments were performed at the beginning and at the end of the rehabilitation. Psychometric assessments were repeated 1 year after the end of the programme for both groups, respectively.</AbstractText>Patients were highly satisfied with the programme and improved in almost all psychological and physical fitness assessments. The pre-post-comparison resulted in significant positive changes for mental health (p < .001 for SF-36 Mental Health), fatigue (p < .05 for Fatigue Severity Scale), nociception (p < .05 for SF-36 Pain) and vitality (p < .05 for SF-36 Vitality). Physical fitness improved from admission to discharge (p < .001 for maximum power in bicycle ergometry, p < .05 for maximum nordic walking distance). Considerable improvements persisted through 1 year follow-up. Medical assessments excluded medical problems or adverse events caused by participation in the programme.</AbstractText>In our study, inpatient rehabilitation was both safe and helpful for MFS patients. They benefited in terms of physical fitness, health related quality of life and in terms of psychological wellbeing. An evaluation of the efficacy of the programme in a controlled design as well as further conceptual improvements of our current program is desirable.</AbstractText> |
20,338 | Association of ventricular arrhythmia and in-hospital mortality in stroke patients in Florida: A nonconcurrent prospective study. | Stroke remains one of the leading causes of death in the United States. Current evidence identified electrocardiographic abnormalities and cardiac arrhythmias in 50% of patients with an acute stroke. The purpose of this study was to assess whether the presence of ventricular arrhythmia (VA) in adult patients hospitalized in Florida with acute stroke increased the risk of in-hospital mortality.Secondary data analysis of 215,150 patients with ischemic and hemorrhagic stroke hospitalized in the state of Florida collected by the Florida Agency for Healthcare Administration from 2008 to 2012. The main outcome for this study was in-hospital mortality. The main exposure of this study was defined as the presence of VA. VA included the ICD-9 CM codes: paroxysmal ventricular tachycardia (427.1), ventricular fibrillation (427.41), ventricular flutter (427.42), ventricular fibrillation and flutter (427.4), and other - includes premature ventricular beats, contractions, or systoles (427.69). Differences in demographic and clinical characteristics and hospital outcomes were assessed between patients who developed versus did not develop VA during hospitalization (χ and t tests). Binary logistic regression was used to estimate unadjusted and adjusted odds ratios and 95% confidence intervals (CIs) between VA and in-hospital mortality.VA was associated with an increased risk of in-hospital mortality after adjusting for all covariates (odds ratio [OR]: 1.75; 95% CI: 1.6-1.2). There was an increased in-hospital mortality in women compared to men (OR: 1.1; 95% CI: 1.1-1.14), age greater than 85 years (OR: 3.9, 95% CI: 3.5-4.3), African Americans compared to Whites (OR: 1.1; 95% CI: 1.04-1.2), diagnosis of congestive heart failure (OR: 2.1; 95% CI: 2.0-2.3), and atrial arrhythmias (OR: 2.1, 95% CI: 2.0-2.2). Patients with hemorrhagic stroke had increased odds of in-hospital mortality (OR: 9.0; 95% CI: 8.6-9.4) compared to ischemic stroke.Identifying VAs in stroke patients may help in better target at risk populations for closer cardiac monitoring during hospitalization. The impact of implementing methods of quick assessment could potentially reduce VA associated sudden cardiac death. |
20,339 | Arterial switch operation in patients with transposition and a left-sided aorta. | Arterial switch operation is the treatment of choice in infants with transposed arterial trunks. It is technically challenging to perform in patients having usual atrial arrangement and concordant atrioventricular connections but having a left-sided aorta. Correction in this setting requires surgical expertise and precision. Here we review our experience with such patients.</AbstractText>Between January, 2002 and October, 2013, the arterial switch operation was performed in 20 patients in the combination emphasised above. Patient records were analysed in detail for coronary arterial patterns, and for the techniques used for transfer of the coronary arteries and reconstruction of the great arteries. Outcomes were recorded in terms of in-hospital survival and left ventricular function at the most recent follow-up.</AbstractText>All patients survived the procedure. Ages ranged from 3 days to 18 months, with a median of 75 days; the weight of the patients ranged from 3 to 8.8 kg, with a median of 3.85 kg. The LeCompte manoeuvre was performed in only nine patients. The mean cardiopulmonary bypass time was 157.5±24.9, with a median of 161 minutes, and the mean aortic cross-clamp time was 101.2±23.8, with a median of 102 minutes. Subsequently, two patients died: the first due to a sudden onset of ventricular fibrillation and the second during a crisis of severe pulmonary hypertension. At the last follow-up, which ranged from 23 to 41 months, with a mean of 38.04±2.32 and a median of 38.4 months, all 18 survivors were in NYHA class I, with none requiring cardiac medications and all having normal bi-ventricular function without residual defects.</AbstractText>With appropriate technical modifications, patients with concordant atrioventricular and discordant ventriculo-arterial connections with a left-sided aorta can undergo successful anatomical repair.</AbstractText> |
20,340 | [Digoxin and atrial fibrillation in 2016]. | Various properties of digoxin have been exploited for decades, amongst which are its positive inotropy used in the treatment of heart failure, and its vagotonic effect used to slow ventricular response to atrial fibrillation. Pharmacologic properties of digoxin are however characterised by a narrow therapeutic interval, and recent observational studies suggest a potential association with increased mortality in patients with atrial fibrillation. As a result and because of available alternative therapeutic strategies, current guidelines do not recommend digoxin as first line treatment of atrial fibrillation. Digoxin may be considered in patients with heart failure and atrial fibrillation with rapid ventricular response when other therapeutic options cannot be pursued.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Théone</LastName><ForeName>Sarah</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Service de médecine interne générale, HUG, 1211 Genève 14.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Carballo</LastName><ForeName>Sebastian</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Service de médecine interne générale, HUG, 1211 Genève 14.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Carballo</LastName><ForeName>David</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Service de cardiologie, HUG, 1211 Genève 14.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Marti</LastName><ForeName>Christophe</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Service de médecine interne générale, HUG, 1211 Genève 14.</Affiliation></AffiliationInfo></Author></AuthorList><Language>fre</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><VernacularTitle>Utilisation de la digoxine dans la fibrillation auriculaire.</VernacularTitle></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Rev Med Suisse</MedlineTA><NlmUniqueID>101219148</NlmUniqueID><ISSNLinking>1660-9379</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000889">Anti-Arrhythmia Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>73K4184T59</RegistryNumber><NameOfSubstance UI="D004077">Digoxin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000889" MajorTopicYN="N">Anti-Arrhythmia Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001281" MajorTopicYN="N">Atrial Fibrillation</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004077" MajorTopicYN="N">Digoxin</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006333" MajorTopicYN="N">Heart Failure</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017410" MajorTopicYN="N">Practice Guidelines as Topic</DescriptorName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="fre">Depuis de nombreuses années, la digoxine est utilisée dans le traitement de l’insuffisance cardiaque en raison de son inotropisme positif, et pour contrôler la réponse ventriculaire en présence de fibrillation auriculaire (FA) via ses propriétés vagotoniques. Caractérisée par une marge thérapeutique étroite, des études observationnelles récentes suggèrent que la digoxine pourrait être associée à une surmortalité chez les patients avec FA. Pour ces raisons, et du fait de nombreuses alternatives thérapeutiques, la digoxine n’est actuellement plus recommandée en première intention lors de FA. Elle peut être envisagée chez les patients présentant une insuffisance cardiaque et une FA à réponse ventriculaire rapide lorsque des traitements alternatifs ne peuvent être poursuivis. |
20,341 | Impact of Chronic Kidney Disease on the Presentation and Outcome of Patients Hospitalized With Atrial Fibrillation: Insights From Qatar. | Atrial fibrillation (AF) with coexistent chronic kidney disease (CKD) is poorly described in the literature. We compared the presenting symptoms, clinical characteristics, treatment, and outcome of patients hospitalized with AF with and without CKD in a large clinical registry. Data of patients hospitalized with AF between 1991 and 2012 in Qatar were analyzed. Of 5201 patients hospitalized for AF, 264 (5.1%) had CKD. Patients with AF and CKD were older with higher prevalence of other comorbidities and left ventricular dysfunction and were more likely to present with shortness of breath and chest pain compared with patients with AF alone who were more likely to present with palpitation. The crude in-hospital mortality was 3 times higher in patients with dual disease. On multivariable adjustments, CKD was an independent predictor of mortality (odds ratio: 2.84; 95% confidence interval: 1.33-6.08, P = .001). Further studies are warranted to try to reduce the increased mortality observed in this high-risk population. |
20,342 | Wolff-Parkinson-White Syndrome with Ventricular Hypertrophy in a Brazilian Family. | BACKGROUND PRKAG2 syndrome diagnosis is already well-defined as Wolff-Parkinson-White syndrome (WPW), ventricular hypertrophy (VH) due to glycogen accumulation, and conduction system disease (CSD). Because of its rarity, there is a lack of literature focused on the treatment. The present study aimed to describe appropriate strategies for the treatment of affected family members with PRKAG2 syndrome with a long follow-up period. CASE REPORT We studied 60 selected individuals from 84 family members (32 males, 53.3%) (mean age 27±16 years). Patients with WPW and/or VH were placed in a group of 18 individuals, in which 11 (61.1%) had VH and WPW, 6 (33.3%) had isolated WPW, and 1 (5.6%) had isolated VH. Palpitations occurred in 16 patients (88.9%), chest pain in 11 (61.1%), dizziness in 13 (72.2%), syncope in 15 (83.3%), and dyspnea in 13 (72%). Sudden cardiac death (SCD) occurred in 2 (11.1%), and 2 patients with cardiac arrest (CA) had asystole and pre-excited atrial flutter-fibrillation (AFL and AF) as the documented mechanism. Transient ischemic attack (TIA) and learning/language disabilities with delayed development were observed. Genetic analysis identified a new missense pathogenic variant (p.K290I) in the PRKAG2 gene. Cardiac histopathology demonstrated the predominance of vacuoles containing glycogen derivative and fibrosis. The treatment was based on hypertension and diabetes mellitus (DM) control, antiarrhythmic drugs (AD), anticoagulation, and radiofrequency catheter ablation (RCA). Six patients (33.3%) underwent pacemaker implantation (PM). CONCLUSIONS The present study describes the clinical treatment for a rare cardiac syndrome caused by a PRKAG2 mutation. |
20,343 | Value of cardiac magnetic resonance imaging and programmed ventricular stimulation in patients with frequent premature ventricular complexes undergoing radiofrequency ablation. | Frequent premature ventricular complexes (PVCs) have been associated with increased mortality. However, the optimal approach to the risk stratification of these patients is unclear.</AbstractText>The purpose of this study was to prospectively assess the use of cardiac magnetic resonance imaging (MRI) and programmed ventricular stimulation to identify patients with PVCs undergoing radiofrequency ablation at risk for adverse long-term outcomes.</AbstractText>A total of 321 consecutive patients (52 ± 15 years; 157 men [49%]; left ventricular ejection fraction 51% ± 12%) underwent PVC ablation between 2004 and 2015, preceded by cardiac MRI to assess for structural heart disease (SHD). Programmed stimulation was performed at the time of the ablation procedure. If ventricular tachycardia (VT) was induced in the presence of SHD, an implantable cardioverter-defibrillator (ICD) was implanted.</AbstractText>SHD was identified by MRI in 64 patients (20%), and sustained monomorphic VT was inducible in 15 patients (5%). Fourteen patients had both SHD and inducible VT, and received an ICD after the procedure. The primary endpoint of VT/ventricular fibrillation or death was met in 15 patients after a median 20 months of follow-up. The combination of SHD by MRI and VT inducibility conferred independently an increased risk of adverse outcome (multivariate hazard ratio 25.73, 95% confidence interval 6.74-98.20; P <.001).</AbstractText>Preablation cardiac MRI and programmed stimulation can be useful for risk stratification in patients with frequent PVCs. Patients with inducible VT in the setting of SHD may benefit from ICD implantation after ablation regardless of left ventricular ejection fraction.</AbstractText>Copyright © 2017 Heart Rhythm Society. All rights reserved.</CopyrightInformation> |
20,344 | Magnesium status and magnesium therapy in cardiac surgery: A systematic review and meta-analysis focusing on arrhythmia prevention. | To investigate magnesium as prophylaxis or treatment of postoperative arrhythmias in cardiac surgery (CS) patients. To assess impact on biochemical and patient-centered outcomes.</AbstractText>We searched MEDLINE, CENTRAL and EMBASE electronic databases from 1975 to October 2015 using terms related to magnesium and CS. English-Language RCTs were included involving adults undergoing CS with parenterally administered magnesium to treat or prevent arrhythmias, compared to control or standard antiarrythmics. We extracted incidence of postoperative arrhythmias, termination following magnesium administration and secondary outcomes (including mortality, length of stay, hemodynamic parameters, biochemistry).</AbstractText>Thirty-five studies were included, with significant methodological heterogeneity. Atrial fibrillation (AF) was most commonly reported, followed by ventricular, supraventricular and overall arrhythmia frequency. Magnesium appeared to reduce AF (RR 0.69, 95% confidence interval (95%CI) 0.56-0.86, p=0.002), particularly postoperatively (RR 0.51, 95%CI 0.34-0.77, p=0.003) for longer than 24h. Maximal benefit was seen with bolus doses up to 60mmol. Magnesium appeared to reduce ventricular arrhythmias (RR=0.46, 95%CI 0.24-0.89, p=0.004), with a trend to reduced overall arrhythmias (RR=0.80, 95%CI 0.57-1.12, p=0.191). We found no mortality effect or significant increase in adverse events.</AbstractText>Magnesium administration post-CS appears to reduce AF without significant adverse events. There is limited evidence to support magnesium administration for prevention of other arrhythmias.</AbstractText>Copyright © 2017 Elsevier Inc. All rights reserved.</CopyrightInformation> |
20,345 | Tachycardia-Induced J-Wave Changes in Patients With and Without Idiopathic Ventricular Fibrillation. | To know the underlying mechanisms of J waves, the response to atrial pacing was studied in patients with idiopathic ventricular fibrillation (IVF) and patients with non-IVF.</AbstractText>In 8 patients with IVF, the J-wave amplitude was measured before, during, and after atrial pacing. All patients had episodes of ventricular fibrillation without structural heart disease. The responses of J waves were compared with those of the 17 non-IVF control subjects who revealed J waves but no history of cardiac arrest and underwent electrophysiological study. The IVF patients were younger than the non-IVF patients (28±10 versus 52±14 years, respectively; P</i>=0.002) and had larger J waves with more extensive distribution. J waves decreased from 0.35±0.26 to 0.22±0.23 mV (P</i>=0.025) when the RR intervals were shortened from 782±88 to 573±162 ms (P</i>=0.001). A decrease (≥0.05 mV) in the J-wave amplitude was observed in 6 of the 8 patients. In addition, 1 patient showed a distinct reduction of J waves in the unipolar epicardial leads. In contrast, J waves were augmented in the 17 non-IVF subjects from 0.27±0.09 to 0.38±0.10 mV (P</i><0.001): augmented in 9 and unchanged in the 8 subjects. The different response patterns of J waves to rapid pacing suggest different mechanisms: early repolarization in IVF patients and conduction delay in non-IVF patients.</AbstractText>The response to atrial pacing was different between the IVF and non-IVF patients, which suggests the presence of different mechanisms for the genesis of J waves.</AbstractText>© 2017 American Heart Association, Inc.</CopyrightInformation> |
20,346 | Efficacy and safety of the subcutaneous implantable cardioverter defibrillator: a systematic review. | Subcutaneous implantable cardioverter defibrillators (S-ICDs) are considered an alternative to conventional transvenous ICDs (TV-ICDs) in patients not requiring pacing.</AbstractText>We searched MEDLINE and EMBASE for studies evaluating efficacy and safety outcomes in S-ICD patients. Outcomes were pooled across studies.</AbstractText>Sixteen studies were included with 5380 participants (mean age range 33-56 years). Short-term follow-up data were available for 1670 subjects. The most common complication was pocket infection, affecting 2.7%. Other complications included delayed wound healing (0.6%) and wound discomfort (0.8%). 3.8% of S-ICDs were explanted, most commonly for pocket infection. Mortality rates in hospital (0.4%) and during follow-up (3.4% from 12 studies reporting) were low. Incidence of ventricular arrhythmia varied from 0% to 12%. Overall shock efficacy exceeded 96%. Inappropriate shocks affected 4.3% and was most commonly caused by T-wave oversensing.</AbstractText>Although long-term randomised data are lacking, observational data suggest similar shock efficacy and short-term complication rates between the S-ICD and TV-ICD.</AbstractText>© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.</CopyrightInformation> |
20,347 | Device Therapy for Rate Control: Pacing, Resynchronisation and AV Node Ablation. | Atrioventricular node ablation (AVNA) is generally reserved for patients whose atrial fibrillation (AF) is refractory all other therapeutic options, since the recipients will often become pacemaker dependent. In such patients, this approach may prove particularly useful, especially if a tachycardia-induced cardiomyopathy is suspected. Historically, an "ablate and pace" approach has involved AVNA and right ventricular pacing, with or without an atrial lead. There is also an evolving role for atrioventricular node ablation in patients with AF who require cardiac resynchronisation therapy for treatment of systolic heart failure. A mortality benefit over pharmacotherapy has been demonstrated in observational studies and this concept is being further investigated in multi-centre randomised control trials. |
20,348 | Role of Global Longitudinal Strain in Predicting Outcomes in Hypertrophic Cardiomyopathy. | Global longitudinal strain (GLS) is a sensitive indicator of global left ventricular function particularly in those with normal ejection fraction. We examined the potential value of GLS in predicting outcomes in hypertrophic cardiomyopathy (HC). Conventional and strain echocardiography was performed in 400 patients with HC followed for a median 3.1 years (interquartile range 1.2 to 5.6). Peak systolic strain from 3 apical views was averaged to calculate GLS. Patients were divided based on a previously published cutoff value of -16%. Additionally, we identified 4 HC subgroups based on GLS: GLS ≤ -20%, -20% < GLS ≤ -16%, -16% < GLS ≤ -10%, and GLS > -10%. The primary end point was a composite of new-onset sustained ventricular tachycardia/fibrillation, heart failure, cardiac transplantation, and all-cause death. Patients with GLS > -16% had significantly more events (17% vs 7%, p = 0.002). In the 4-group analysis, event rates increased with worsening GLS (5%, 7%, 14%, and 33%, respectively, p = 0.001). Event-free survival was significantly superior in those with GLS ≤ -16% versus GLS > -16% (p = 0.004); similarly, GLS > -10% portended a significantly worse event-free survival compared with each of the other 3 groups (p <0.01 for all pairwise comparisons). By univariate and multivariate Cox regression analysis, GLS remained significantly associated with the composite end point. GLS > -10% had 4 times the risk of events compared with GLS ≤ -16% (p = 0.006). In conclusion, echo-based GLS is independently associated with outcomes in HC. Patients with GLS > -10% have significantly higher event rates. |
20,349 | The Role of Quinidine in the Pharmacological Therapy of Ventricular Arrhythmias 'Quinidine'. | Historically, quinidine was the first medicine used in the therapy of heart arrhythmias. Studies in the early 20th century identified quinidine, a diastereomer of the antimalarial quinine, as the most potent of the antiarrhythmic substances extracted from the cinchona plant. Quinidine is used by the 1920s, as an antiarrhythmic agent to maintain sinus rhythm after the conversion from atrial flutter or atrial fibrillation and to prevent recurrence of ventricular tachycardia or ventricular fibrillation. Its value in chronic prophylaxis of relapse of ventricular arrhythmia was brought under suspicion after publishing of meta analysis that showed that the application of quinidine increases mortality. Due to numerous proofs of increased risk for the appearance of ventricular arrhythmia and sudden death, as well as a number of other adverse effects and drug interactions, quinidine was withdrawn from use and in the recent years has become unavailable in many countries. On the other hand, recent studies have demonstrated that quinidine is the only oral medication that has consistently shown efficacy in preventing arrhythmias and terminating storms due to recurrent ventricular fibrillation, in patients with Brugada syndrome, idiopathic ventricular fibrillation and early repolarization syndrome. Quinidine is also the only antiarrhythmic drug that normalized the QT interval in patients with the congenital short QT syndrome. The aim of this review is to provide good insight into pro and contra arguments for quinidine use in ventricular arrhythmias evidence based on recently published literature. |
20,350 | Comparison of posttransplant outcomes in patients with no, acute, or chronic amiodarone use before heart transplantation. | Major concerns about the safety of pretransplant amiodarone use have been raised. As a result of its long half-life, the cardiac allograft is exposed to amiodarone posing potential risks such as bradycardia, requirement for pacemaker implantation, or increased mortality after heart transplantation (HTX).</AbstractText>The aim of this study is to investigate the posttransplant outcomes of patients with no, acute, or chronic amiodarone use before HTX.</AbstractText>This retrospective single-center study included 530 adult patients who received HTX between 06/1989 and 12/2012. Patients were stratified by their amiodarone therapy before HTX: no continuous amiodarone use (≤90 days before HTX), acute amiodarone use (≤90 days before HTX), and chronic amiodarone use (>90 days before HTX). Differences between the 3 groups in demographics, posttransplant medication, echocardiographic features, heart rates including occurrences of bradycardia, permanent pacemaker implantation, atrial fibrillation (AF), and survival were analyzed.</AbstractText>A total of 412 patients (77.7%) were in the "no amiodarone" group, 23 patients (4.4%) in the "acute amiodarone" group, and 95 patients (17.9%) in the "chronic amiodarone" group. Left ventricular ejection fraction (P</i>=0.5819), heart rates including occurrence of bradycardia during posttransplant week 1 (P</i>=0.0979 and P</i>=0.2695), week 2 (P</i>=0.1214 and P</i>=0.8644), week 3 (P</i>=0.1033 and P</i>=0.8894), and week 4 (P</i>=0.2892 and P</i>=0.8644), permanent pacemaker implantation within 30-day (P</i>=0.8644), or overall follow-up after HTX (P</i>=0.8664) were not significant between groups. Patients with chronic pretransplant amiodarone therapy had the lowest rate of early posttransplant AF (P</i>=0.0065). There was no statistically significant difference between groups in 30-day (P</i>=0.8656), 1-year (P</i>=1.0000), 2-year (P</i>=0.8763), 5-year (P</i>=0.5174), or overall posttransplant follow-up mortality (P</i>=0.1936).</AbstractText>Administration of acute or chronic pretransplant amiodarone was not related to an increased occurrence of bradycardia, requirement for permanent pacemaker implantation, or mortality after HTX. Importantly, chronic amiodarone use effectively reduced early AF after HTX, whereas acute amiodarone use showed no such effect.</AbstractText> |
20,351 | Atrial Fibrillation and Heart Failure - Cause or Effect? | There are emerging epidemics of atrial fibrillation (AF) and heart failure in most developed countries, with a significant health burden. Due to many shared pathophysiological mechanisms, which facilitate the maintenance of each condition, AF and heart failure co-exist in up to 30% of patients. In the circumstance where known structural causes of heart failure (such as myocardial infarction) are absent, patients presenting with both conditions present a unique challenge, particularly as the temporal relationship of each condition can often remain elusive from the clinical history. The question of whether the AF is driving, or significantly contributing to the left ventricular (LV) dysfunction, rather than merely a consequence of heart failure, has become ever more pertinent, especially as catheter ablation now offers a significant advancement over existing rhythm control strategies. This paper will review the inter-related physiological drivers of AF and heart failure before considering the implications from the outcomes of recent clinical trials in patients with AF and heart failure. |
20,352 | Predictors of future arrhythmic events in patients with unexplained syncope. | The purpose of this study was to examine the usefulness of implantable loop recorders (ILRs) for symptom-rhythm correlation and to identify predictors of future arrhythmic events.</AbstractText>In our dual-centre study, we analysed ILR data of 189 patients (mean age 67.4 ± 15.2 years, 114 male) with unexplained syncope (single syncope 21 patients, recurrent 168 patients, traumatic injury 43 patients). Patients had severe comorbidities such as hypertension (n = 127), coronary artery disease (n = 31), diabetes mellitus (n = 33) and chronic renal insufficiency (n = 18). The median ILR usage was 29 months (M), with a range between 1 and 46 M.</AbstractText>Forty-nine (26%) patients experienced syncope during the study, with a median of 8 M to first recurrence of syncope. In 43 patients, pacemaker implantation was performed because of sinus node disease (n = 29), high-degree AV-block (n = 6) or atrial fibrillation with slow ventricular rate (n = 8). In five patients, an ICD was implanted because of documented ventricular tachycardia (n = 4) or left ventricular ejection fraction <35% (n = 1). One patient received ablation of the cavotricuspid isthmus because of documented atrial flutter. Concerning the clinical course, in five patients explantation of the ILR was necessary due to pocket infection. Three patients died due to non-cardiac causes. Logistic regression analysis revealed that older patients had a significantly higher risk for future arrhythmic events (OR 1.3, p = .039).</AbstractText>ILR monitoring is effective in indicating causes of unexplained syncope by providing symptom-rhythm associations. Only age was a predictor of future arrhythmic events. The mortality in patients with unexplained syncope was very low.</AbstractText> |
20,353 | Development of ventricular fibrillation after implantation of a biventricular implantable cardioverter defibrillator: what is the mechanism? | Syncopal spells in heart failure patient with cardiovascular implantable electronic devices (CIED) require multiple assessments. T-wave oversensing is a well-described phenomenon that remains significant in modern implantable cardioverter defibrillators (ICD) systems. It can lead to inappropriate therapies and loss of biventricular pacing in those with cardiac resynchronization devices. Strategies to overcome this problem are important. |
20,354 | Cardiac Ion Channel Regulation in Obesity and the Metabolic Syndrome: Relevance to Long QT Syndrome and Atrial Fibrillation.<Pagination><StartPage>431</StartPage><MedlinePgn>431</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">431</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3389/fphys.2017.00431</ELocationID><Abstract><AbstractText>Obesity and its associated metabolic dysregulation leading to metabolic syndrome is an epidemic that poses a significant public health problem. More than one-third of the world population is overweight or obese leading to enhanced risk of cardiovascular disease (CVD) incidence and mortality. Obesity predisposes to atrial fibrillation, ventricular, and supraventricular arrhythmias; conditions that are underlain by dysfunction in electrical activity of the heart. To date, current therapeutic options for cardiomyopathy of obesity are limited, suggesting that there is considerable room for development of therapeutic interventions with novel mechanisms of action that will help normalize rhythm in obese patients. Emerging candidates for modulation by obesity are cardiac ion channels and Ca handling proteins. However, the underlying molecular mechanisms of the impact of obesity on these channels/Ca handling proteins remain incompletely understood. Obesity is marked by accumulation of adipose tissue associated with a variety of adverse adaptations including dyslipidemia (or abnormal levels of serum free fatty acids), increased secretion of pro-inflammatory cytokines, fibrosis, hyperglycemia, and insulin resistance, that will cause electrical remodeling and thus predispose to arrhythmias. Further, adipose tissue is also associated with the accumulation of subcutaneous and visceral fat, which are marked by distinct signaling mechanisms. Thus, there may also be functional differences in the outcome of regional distribution of fat deposits on ion channel/Ca handling proteins expression. Evaluating alterations in their functional expression in obesity will lead to progress in the knowledge about the mechanisms responsible for obesity-related arrhythmias. These advances are likely to reveal new targets for pharmacological modulation. The objective of this article is to review cardiac ion channel/Ca handling proteins remodeling that predispose to arrhythmias. Understanding how obesity and related mechanisms lead to cardiac electrical remodeling is likely to have a significant medical and economic impact.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Aromolaran</LastName><ForeName>Ademuyiwa S</ForeName><Initials>AS</Initials><AffiliationInfo><Affiliation>Cardiovascular Research Program, VA New York Harbor Healthcare SystemBrooklyn, NY, United States.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Departments of Medicine, Cell Biology and Pharmacology, State University of New York Downstate Medical CenterBrooklyn, NY, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Boutjdir</LastName><ForeName>Mohamed</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Cardiovascular Research Program, VA New York Harbor Healthcare SystemBrooklyn, NY, United States.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Departments of Medicine, Cell Biology and Pharmacology, State University of New York Downstate Medical CenterBrooklyn, NY, United States.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medicine, New York University School of MedicineNew York, NY, United States.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>06</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Physiol</MedlineTA><NlmUniqueID>101549006</NlmUniqueID><ISSNLinking>1664-042X</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">atrial fibrillation</Keyword><Keyword MajorTopicYN="N">high-fat diet</Keyword><Keyword MajorTopicYN="N">ion channel remodeling</Keyword><Keyword MajorTopicYN="N">long QT syndrome</Keyword><Keyword MajorTopicYN="N">metabolic syndrome</Keyword><Keyword MajorTopicYN="N">obesity</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year><Month>4</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2017</Year><Month>6</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>7</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>7</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>7</Month><Day>7</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28680407</ArticleId><ArticleId IdType="pmc">PMC5479057</ArticleId><ArticleId IdType="doi">10.3389/fphys.2017.00431</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Abbott G. 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More than one-third of the world population is overweight or obese leading to enhanced risk of cardiovascular disease (CVD) incidence and mortality. Obesity predisposes to atrial fibrillation, ventricular, and supraventricular arrhythmias; conditions that are underlain by dysfunction in electrical activity of the heart. To date, current therapeutic options for cardiomyopathy of obesity are limited, suggesting that there is considerable room for development of therapeutic interventions with novel mechanisms of action that will help normalize rhythm in obese patients. Emerging candidates for modulation by obesity are cardiac ion channels and Ca handling proteins. However, the underlying molecular mechanisms of the impact of obesity on these channels/Ca handling proteins remain incompletely understood. Obesity is marked by accumulation of adipose tissue associated with a variety of adverse adaptations including dyslipidemia (or abnormal levels of serum free fatty acids), increased secretion of pro-inflammatory cytokines, fibrosis, hyperglycemia, and insulin resistance, that will cause electrical remodeling and thus predispose to arrhythmias. Further, adipose tissue is also associated with the accumulation of subcutaneous and visceral fat, which are marked by distinct signaling mechanisms. Thus, there may also be functional differences in the outcome of regional distribution of fat deposits on ion channel/Ca handling proteins expression. Evaluating alterations in their functional expression in obesity will lead to progress in the knowledge about the mechanisms responsible for obesity-related arrhythmias. These advances are likely to reveal new targets for pharmacological modulation. The objective of this article is to review cardiac ion channel/Ca handling proteins remodeling that predispose to arrhythmias. Understanding how obesity and related mechanisms lead to cardiac electrical remodeling is likely to have a significant medical and economic impact.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Aromolaran</LastName><ForeName>Ademuyiwa S</ForeName><Initials>AS</Initials><AffiliationInfo><Affiliation>Cardiovascular Research Program, VA New York Harbor Healthcare SystemBrooklyn, NY, United States.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Departments of Medicine, Cell Biology and Pharmacology, State University of New York Downstate Medical CenterBrooklyn, NY, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Boutjdir</LastName><ForeName>Mohamed</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Cardiovascular Research Program, VA New York Harbor Healthcare SystemBrooklyn, NY, United States.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Departments of Medicine, Cell Biology and Pharmacology, State University of New York Downstate Medical CenterBrooklyn, NY, United States.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medicine, New York University School of MedicineNew York, NY, United States.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>06</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Physiol</MedlineTA><NlmUniqueID>101549006</NlmUniqueID><ISSNLinking>1664-042X</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">atrial fibrillation</Keyword><Keyword MajorTopicYN="N">high-fat diet</Keyword><Keyword MajorTopicYN="N">ion channel remodeling</Keyword><Keyword MajorTopicYN="N">long QT syndrome</Keyword><Keyword MajorTopicYN="N">metabolic syndrome</Keyword><Keyword MajorTopicYN="N">obesity</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year><Month>4</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2017</Year><Month>6</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>7</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>7</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>7</Month><Day>7</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28680407</ArticleId><ArticleId IdType="pmc">PMC5479057</ArticleId><ArticleId IdType="doi">10.3389/fphys.2017.00431</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Abbott G. 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Disord. 16:1. 10.1186/s12872-015-0179-x</Citation><ArticleIdList><ArticleId IdType="doi">10.1186/s12872-015-0179-x</ArticleId><ArticleId IdType="pmc">PMC4700781</ArticleId><ArticleId IdType="pubmed">26728597</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="1">31643939</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK548627</ArticleId></ArticleIdList><Book><Publisher><PublisherName>National Institute of Diabetes and Digestive and Kidney Diseases</PublisherName><PublisherLocation>Bethesda (MD)</PublisherLocation></Publisher><BookTitle book="livertox">LiverTox: Clinical and Research Information on Drug-Induced Liver Injury</BookTitle><PubDate><Year>2012</Year></PubDate><BeginningDate><Year>2012</Year></BeginningDate><Medium>Internet</Medium></Book><ArticleTitle book="livertox" part="AntiarrhythmicAgents">Antiarrhythmic Agents</ArticleTitle><Language>eng</Language><PublicationType UI="D016454">Review</PublicationType><Abstract>The antiarrhythmics are a heterogeneous group of medications that act to decrease cardiac automaticity and slow conduction, and are used for either or both ventricular and atrial arrhythmias. The most common use of antiarrhythmics is in the treatment of atrial fibrillation or flutter, or prevention of their recurrence in patients after electrical or medical cardioversion. Use of antiarrhythmics for suppression of ventricular arrhythmias is controversial in that several studies have shown that suppression of ventricular premature contractions can be associated with a decrease rather than increase in survival. Thus, the antiarrhythmics are generally used only for clinically significant ventricular dysrrhythmias. The oral antiarrhythmics are often separated into classes based upon their major molecular target as either class I (sodium channel), II (beta adrenergic receptor), III (potassium channel), or IV (calcium channel). Many agents have multiple targets, but the classification is helpful particularly because of shared side effects. Oral antiarrhythmics available in the United States (and their year of approval) include quinidine (1950), procainamide (1950), disopyramide (1977), amiodarone (1985), flecainide (1985), mexiletine (1985), propafenone (1989) and dronedarone (2009). Agents used intravenously, usually for a short period only with severe arrhythmias, include adenosine (1989), ibutilide (1995), isoproterenol (1992) and dofetilide (2000). Agents used to slow atrial-ventricular conduction include cardiac glycosides (digoxin, digitoxin), calcium channel blockers (diltiazem, verapamil), and beta adrenergic blockers (esmolol, propranolol, and sotalol) which are discussed elsewhere. |
20,355 | Recovery of atrioventricular conduction in patients with heart block after transcatheter aortic valve replacement. | Recovery of conduction has been demonstrated in >50% of patients who receive pacemakers (PPMs) for high-degree atrioventricular block (HD-AVB) after transcatheter aortic valve replacement (TAVR). Little information is available about the time course of conduction recovery in these patients and if any features predict early recovery of conduction.</AbstractText>A retrospective review was performed of patients who underwent TAVR with balloon and self-expanding valves who required PPMs for HD-AVB. Serial PPM interrogations were analyzed to detect recovery of AV conduction. Analysis was performed to identify predictors and timing of conduction recovery.</AbstractText>Of a total population of 578 patients, 54 (9%) received PPMs for HD-AVB. In multivariate analysis, predictors of HD-AVB requiring a PPM included age (P = 0.014), right bundle branch block (OR 7.33 [3.64-14.8], P < 0.0001), atrial fibrillation (OR 2.16 [1.16-4.05], P = 0.016), and self-expanding valves (OR 4.19 [2.20-7.97], P < 0.0001). Of the 54 patients who received PPMs, 38 had follow-up sufficient to evaluate AV conduction recovery. Of these, 23 (61%) showed recovery of AV nodal conduction; 20 had already recovered by their first interrogation, a median of 22 days (IQR 14-31) post-PPM placement. There were no statistically significant predictors of AV nodal conduction recovery, including type of valve implanted.</AbstractText>A majority of patients who receive PPMs for HD-AVB after TAVR recover AV conduction during follow-up, and in most patients conduction recovery occurs within weeks. These findings imply that programming to minimize ventricular pacing may be beneficial in a majority of these patients.</AbstractText>© 2017 Wiley Periodicals, Inc.</CopyrightInformation> |
20,356 | Preclinical efficacy and safety of KCNH2-G628S gene therapy for postoperative atrial fibrillation. | Postoperative atrial fibrillation (POAF) is the most common complication occurring after cardiac surgery. Multiple studies have shown significantly increased risks of stroke, myocardial infarction, and death associated with POAF. Current prophylaxis strategies are inadequate to eliminate this problem. We examined the preclinical efficacy and safety of KCNH2-G628S gene transfer to prevent POAF.</AbstractText>Domestic pigs received AdKCNH2-G628S by epicardial atrial gene painting and atrial pacemaker implantation for continuous-burst pacing to induce atrial fibrillation. In an initial dose-ranging evaluation, 3 pigs received 5 × 1010</sup> to 5 × 1011</sup> virus particles. In the formal study, 16 pigs were randomized to 3 groups: 5 × 1011</sup> virus particles of AdKCNH2-G628S with 20% Pluronic P407 in saline, 20% Pluronic P407 in saline with no virus, and saline alone. Animals were followed with daily efficacy and safety evaluations through the period of peak adenovirus-mediated transgene expression. After 14 days, pacing was discontinued, and the animals were followed in sinus rhythm for an additional 14 days to assess any longer-term toxicity.</AbstractText>In the primary efficacy analysis, the G628S animals exhibited a significant increase in the average time in sinus rhythm compared with the Pluronic control group (59 ± 7% vs 14 ± 6%; P = .009). There was no significant difference between the Pluronic and saline controls (14 ± 6% vs 32 ± 12%; P = .16). Safety assessment showed improved left ventricular function in the G628S animals; otherwise there were no significant differences among the groups in any safety measure.</AbstractText>These data indicate that KCNH2-G628S gene therapy can successfully and safely reduce the risk of AF.</AbstractText>Published by Elsevier Inc.</CopyrightInformation> |
20,357 | Interlead heterogeneity of R- and T-wave morphology in standard 12-lead ECGs predicts sustained ventricular tachycardia/fibrillation and arrhythmic death in patients with cardiomyopathy. | Nonuniformities in depolarization and repolarization morphology are critical factors in ventricular arrhythmogenesis.</AbstractText>We assessed interlead R-wave heterogeneity (RWH) and T-wave heterogeneity (TWH) in standard 12-lead electrocardiograms (ECGs) using second central moment analysis. This technique quantifies variance about the mean morphology of beats in adjoining precordial leads, V4</sub> , V5</sub> , and V6</sub> in this study. The study was conducted in 120 consecutive patients without an apparent reversible trigger for ventricular tachycardia (VT), recent myocardial infarction, or active ischemia, who presented for electrophysiologic study, implantable cardioverter defibrillator (ICD) placement, or generator change at our institution from 2008 to 2011. Primary outcome was sustained VT/ventricular fibrillation (VF) or appropriate ICD therapies. Secondary outcome was arrhythmic death or resuscitated cardiac arrest. Cutpoints for elevated RWH (>160 μV) and TWH (>80 μV) identified 67% of primary outcome cases and 85% of secondary outcome cases. Cardiomyopathy patients who met the primary outcome (n = 42) had significantly higher TWH than those who did not (n = 28) (TWH: 95 ± 11 μV vs. 44 ± 9 μV, P < 0.002). Likewise, cardiomyopathy patients who met secondary outcome (N = 13) had VT/VF during follow-up and also had significantly higher TWH than survivors (N = 57) (TWH: 105 ± 24 μV vs. 67 ± 8 μV, P < 0.002). Kaplan-Meier analysis revealed significant differences in arrhythmia-free survival (P = 0.012) and total survival (P = 0.011) among cardiomyopathy patients with (n = 37) compared to without (n = 33) elevated RWH and/or TWH independent of age, sex, and left ventricular ejection fraction (LVEF).</AbstractText>Interlead RWH and TWH in 12-lead ECGs predict sustained ventricular arrhythmia, appropriate ICD therapies, and arrhythmic death or cardiac arrest in cardiomyopathy patients independent of LVEF and other standard variables.</AbstractText>© 2017 Wiley Periodicals, Inc.</CopyrightInformation> |
20,358 | Chronic total occlusion in an infarct-related coronary artery and the risk of appropriate ICD therapies. | Risk stratification for ventricular arrhythmias in patients with ischemic cardiomyopathy needs to be improved. Coronary chronic total occlusions in an infarct-related artery (IRA-CTOs) have been associated with an increased arrhythmic risk. This study aimed to evaluate the association between IRA-CTOs and appropriate implantable cardioverter-defibrillator (ICD) therapies.</AbstractText>Observational cohort study that included 342 patients with ischemic cardiomyopathy, an ICD implanted for primary or secondary prevention, and a coronary angiography performed shortly before ICD implantation. The ICD was implanted for primary prevention in 163 patients (48%). IRA-CTO was found in 161 patients (47%). During a median follow-up of 33 months, 41% of patients experienced at least one appropriate ICD therapy. Patients with IRA-CTO had higher proportions of appropriate ICD therapies (57% vs. 26%, P < 0.001) and appropriate ICD shocks (40% vs. 17%, P < 0.001). At multivariate Cox regression, IRA-CTO was the only variable that consistently resulted as independent predictor of appropriate ICD therapies and shocks both in the global population of the study (HR 2.3, P < 0.001 and HR 3, P < 0.001, respectively) and when analyzing separately patients with primary or secondary prevention ICD.</AbstractText>IRA-CTO is an independent predictor of appropriate ICD therapies, including appropriate ICD shocks. This association is consistent across all the subgroups analyzed. Patients with IRA-CTO have a very high risk of appropriate ICD therapies. These findings may help improving risk stratification as well as the management of ventricular arrhythmias in patients with ischemic cardiomyopathy.</AbstractText>© 2017 Wiley Periodicals, Inc.</CopyrightInformation> |
20,359 | Left atrial strain predicts recurrence of atrial arrhythmias after catheter ablation of persistent atrial fibrillation. | Success rates of catheter ablation (CA) of persistent atrial fibrillation (AF) are very variable. Identifying patients in whom sinus rhythm maintenance cannot be achieved after CA is a critical issue.</AbstractText>2D speckle-tracking echocardiography was performed before the first CA procedure in consecutive patients with persistent AF. Left atrial (LA) strain was correlated with recurrence of atrial arrhythmias during the follow-up period of 15 months after one CA procedure with or without antiarrhythmic drugs (primary endpoint). In a secondary analysis, recurrences after two CA procedures were analysed.</AbstractText>102 patients were included. Patients with recurrence of atrial arrhythmias after one CA procedure (n=55) had significantly lower LA strain than those without recurrence (LA strain 9.7±2.4% vs 16.2±3.0%; p<0.001). Recurrence rate was significantly higher in patients with LA strain <10% than in those with LA strain between 10% and 14.5% and >14.5% (97.7%, 42.1% and 10.3%, respectively; p<0.001). In Cox regression analysis including age, comorbidities, left ventricular dysfunction and LA enlargement, low LA strain (<10%) was the strongest factor associated with recurrence of AF (HR 6.4 (2.4-16.9), p<0.001). Even after inclusion of a second CA procedure, LA strain <10% maintained a high predictive value for recurrence of atrial arrhythmias (86.4% (95% CI 73.3% to 93.6%)).</AbstractText>In patients with persistent AF, LA strain imaging could be very useful to select those patients who have a high risk of not benefiting from CA.</AbstractText> |
20,360 | Outcomes and Prognostic Impact of Prophylactic Oral Anticoagulation in Anterior ST-Segment Elevation Myocardial Infarction Patients With Left Ventricular Dysfunction. | The contemporary role of prophylactic anticoagulation following extensive anterior wall ST-segment myocardial infarction (STEMI) is unclear.</AbstractText>We evaluated anterior STEMI patients with left ventricle dysfunction (left ventricular ejection fraction ≤40%) ("high risk"), categorized by prophylactic warfarin use, within a regional STEMI. Patients with pre-existing atrial fibrillation were excluded. The primary outcome was an adjusted (for Global Registry of Acute Coronary Events risk score) 1-year composite of recurrent ischemia, stroke/transient ischemic attack/systemic embolism, or all-cause death. Of the 2032 STEMI admissions, 436 (21.5%) were high risk. After excluding 19 (4.4%) patients with definite left ventricle thrombus and 21 (4.8%) in-hospital deaths (2 had left ventricle thrombus), prophylactic warfarin was utilized in 236/398 (59.3%) high-risk survivors. Prescriptions were comparable across sex, but recipients were on average younger (58.5 years versus 64.0 years, P</i><0.001) and lower risk (Global Registry of Acute Coronary Events risk: 163 versus 181, P</i><0.001). No association on the adjusted ischemic composite (23.3% versus 25.3%, odds ratio 0.96, 95% CI 0.60-1.55) or thromboembolic events (2.1% versus 1.2%, odds ratio 1.99, 95% CI 0.38-10.51) was observed, but reduced 1-year all-cause mortality was noted (2.5% versus 8.6%, odds ratio 0.30, 95% CI 0.11-0.81); numerically higher major bleeding was observed at 1 year (2.5% versus 1.2%, odds ratio 2.17, 95% CI 0.43-10.96).</AbstractText>A high utilization of prophylactic warfarin occurs in anterior STEMI patients with left ventricle dysfunction, yet appears to provide no additional benefit on the ischemic composite. The association with lower all-cause mortality, but higher bleeding, calls for an improved understanding of its role in high-risk STEMI.</AbstractText>© 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.</CopyrightInformation> |
20,361 | Effect of Percutaneous Edge-to-Edge Repair on Mitral Valve Area and Its Association With Pulmonary Hypertension and Outcomes. | Percutaneous edge-to-edge repair using the MitraClip system causes reduction in mitral valve area (MVA). However, its clinical impact is not fully elucidated. This study assessed the impact of postprocedural MVA reduction on pulmonary hypertension and outcomes. A total of 92 patients with grades 3 to 4 + mitral regurgitation (MR) who underwent MitraClip therapy were retrospectively reviewed. Using intraprocedural, 3-dimensional transesophageal echocardiography, postprocedural MVA was obtained by 2 optimized planes through the medial and lateral orifices of the repaired valve. MVA was reduced by 60.1% immediately after MitraClip procedure (p <0.001). Postprocedural MVA correlated moderately with mean transmitral pressure gradient (TMPG) in the majority of patients (r = -0.56, p <0.001), but discordance of MVA and TMPG was observed in 40% of patients. In multivariable linear regression analysis, postprocedural MVA ≤1.94 cm<sup>2</sup> was independently associated with a blunted decrease in systolic pulmonary artery pressure at 1-month follow-up (β-estimate -4.63, 95% confidence interval -9.71 to -0.15, p = 0.042). Postprocedural MVA ≤1.94 cm<sup>2</sup> was an independent predictor of all-cause mortality and heart failure hospitalization after MitraClip (hazard ratio 4.28, 95% confidence interval 1.56 to 11.7, p = 0.005) even after adjustment for age, gender, atrial fibrillation, cause of MR, left ventricular systolic function, pre-existing pulmonary hypertension, and residual MR. After further adjustment for TMPG ≥5 mm Hg, postprocedural MVA ≤1.94 cm<sup>2</sup> remained predictive for adverse outcomes (p = 0.048). In conclusion, the intraprocedural assessment of MVA by 3-dimensional transesophageal echocardiography can predict hemodynamic response and postprocedural prognosis after MitraClip therapy. |
20,362 | Valvular Heart Disease in Adults: Management of Native Valve Disease. | Patients with valvular heart disease (VHD) should be treated for diabetes, hypertension, and hyperlipidemia. They also should receive therapy for left ventricular dysfunction, undergo interval echocardiography, and participate in aerobic exercise. Valve replacement should be considered for patients with aortic stenosis (AS) and syncope, presyncope, heart failure, angina, or severe AS with left ventricular dysfunction. Valve replacement is performed with open or transcatheter procedures; the latter are preferred for patients with high surgical risk. Patients with chronic aortic regurgitation (AR) should undergo open surgical replacement if they are symptomatic or are asymptomatic but have severe regurgitation and left ventricular dysfunction. No transcatheter procedures currently are approved for AR. Patients with mitral stenosis (MS) should receive drugs for heart rate control and anticoagulation if they have atrial fibrillation. Invasive treatment involves valve replacement or percutaneous commissurotomy. Management of severe chronic mitral regurgitation consists of valve replacement or, for patients with high surgical risk, a percutaneous transcatheter procedure that clips the mitral leaflets together. When severe, tricuspid regurgitation can be managed with valve replacement. Pregnant patients with VHD require special management. Women with severe AS or MS should avoid becoming pregnant until VHD is managed definitively. |
20,363 | Rotors exhibit greater surface ECG variation during ventricular fibrillation than focal sources due to wavebreak, secondary rotors, and meander. | Ventricular fibrillation is a common life-threatening arrhythmia. The ECG of VF appears chaotic but may allow identification of sustaining mechanisms to guide therapy.</AbstractText>We hypothesized that rotors and focal sources manifest distinct features on the ECG, and computational modeling may identify mechanisms of such features.</AbstractText>VF induction was attempted in 31 patients referred for ventricular arrhythmia ablation. Simultaneous surface ECG and intracardiac electrograms were recorded using biventricular basket catheters. Endocardial phase maps were used to mechanistically classify each VF cycle as rotor or focally driven. ECGs were analyzed from patients demonstrating both mechanisms in the primary analysis and from all patients with induced VF in the secondary analysis. The ECG voltage variation during each mechanism was compared. Biventricular computer simulations of VF driven by focal sources or rotors were created and resulting ECGs of each VF mechanism were compared.</AbstractText>Rotor-based VF exhibited greater voltage variation than focal source-based VF in both the primary analysis (n = 8, 110 ± 24% vs. 55 ± 32%, P = 0.02) and the secondary analysis (n = 18, 103 ± 30% vs. 67 ± 34%, P = 0.009). Computational VF simulations also revealed greater voltage variation in rotors compared to focal sources (110 ± 19% vs. 33 ± 16%, P = 0.001), and demonstrated that this variation was due to wavebreak, secondary rotor initiation, and rotor meander.</AbstractText>Clinical and computational studies reveal that quantitative criteria of ECG voltage variation differ significantly between VF-sustaining rotors and focal sources, and provide insight into the mechanisms of such variation. Future studies should prospectively evaluate if these criteria can separate clinical VF mechanisms and guide therapy.</AbstractText>© 2017 Wiley Periodicals, Inc.</CopyrightInformation> |
20,364 | Myocardial Protective Effect of Antegrade Cardioplegic Cardiac Arrest Versus Ventricular Fibrillation During Cardiopulmonary Bypass on Immediate Postoperative and Mid-Term Left Ventricular Function in Right Ventricular Outflow Tract Surgery. | The objective of this study is to examine the myocardial protective effect of antegrade cardioplegic cardiac arrest (ACC) versus ventricular fibrillation (VF) on short-term and mid-term left ventricular (LV) function in right ventricular outflow tract (RVOT) surgery. RVOT operations conducted from January 2006 to December 2015 were reviewed. The numbers of cases using ACC and VF were 71 and 49, respectively. Postoperative mortality and morbidity were compared between the two groups. Before and after propensity score matching, left ventricular ejection fraction (LVEF) and left ventricular end-systolic/end-diastolic diameter (LVESD/LVEDD) in echocardiography were measured immediately after operation and at mid-term follow-up between postoperative 6 and 24 months. There was no perioperative mortality or cerebrovascular accident. There was no statistically significant difference in the incidence of ventricular and atrial arrhythmia. In the overall patient group, LVESD was significantly decreased in the ACC group compared to the VF group immediately after operation (-0.65 ± 3.55 mm vs. 2.99 ± 4.98 mm, P = 0.001). Mid-term follow-up data demonstrated that LVEF at midterm was higher in the ACC group than in the VF group (64.80% ± 7.40% vs. 60.24% ± 7.93%, P = 0.022). However, the increased amount compared to preoperative value was not statistically significant (1.94% ± 12.65% vs. -2.94% ± 9.41%, P = 0.059). After propensity score matching, the LVEF was significantly improved in the ACC group compared to the VF group at the mid-term follow-up (6.16% ± 6.77% vs. -5.41% ± 9.05%, P = 0.001). Multiple linear regression model demonstrated that lower preoperative LVEF, ACC rather than VF, and exclusion of RVOT reconstruction procedure were positive prognostic factors for the improvement of LVEF at mid-term follow up. The results of this study suggest that myocardial protection using ACC is safe and may be more beneficial in LV function recovery up to the mid-term follow-up after pulmonary valve replacement and other RVOT procedures. |
20,365 | Digoxin Use and Subsequent Clinical Outcomes in Patients With Atrial Fibrillation With or Without Heart Failure in the ENGAGE AF-TIMI 48 Trial. | Digoxin is widely used in patients with atrial fibrillation despite the lack of randomized controlled trials. Observational studies report conflicting results regarding its association with mortality, perhaps because of residual confounding by the presence of heart failure (HF).</AbstractText>In the ENGAGE AF-TIMI 48 (Effective Anticoagulation With Factor Xa Next Generation in Atrial Fibrillation-Thrombolysis in Myocardial Infarction 48) trial, clinical outcomes of patients with atrial fibrillation with and without HF were examined by baseline digoxin use during a median follow-up of 2.8 years. HF was defined at baseline as prior or current clinical stage C or D HF. Of 21 105 patients enrolled, 6327 (30%) were treated with digoxin at baseline. Among patients without HF (n=8981), digoxin use (20%) was independently associated with sudden cardiac death (adjusted hazard ratio, 1.51; 95% CI, 1.10-2.08), with no significant interaction by age, sex, left ventricular ejection fraction, renal function, or concomitant medications (P</i>>0.05 for each). Consistent results were observed using propensity matching (adjusted hazard ratio for sudden cardiac death, 1.90; 95% CI, 1.36-2.65). Among patients with HF (n=12 124), digoxin use (37%) was associated with an increase in all-cause death, cardiovascular death, sudden cardiac death, and death caused by HF/cardiogenic shock (P</i><0.01 for each), but not with noncardiovascular death, stroke/systemic embolism, or myocardial infarction.</AbstractText>In this observational analysis of patients with atrial fibrillation without investigator-reported HF, digoxin use was significantly associated with sudden cardiac death. While residual confounding cannot be excluded, the association between digoxin use and worse clinical outcomes highlights the need to examine digoxin use, particularly when prescribed to control heart rate in patients with atrial fibrillation in a randomized trial.</AbstractText>URL: http://www.clinicaltrials.gov. Unique identifier: NCT00781391.</AbstractText>© 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.</CopyrightInformation> |
20,366 | Alternans in atria: Mechanisms and clinical relevance. | Atrial fibrillation is the most common sustained arrhythmia and its prevalence is rapidly rising with the aging of the population. Cardiac alternans, defined as cyclic beat-to-beat alternations in contraction force, action potential (AP) duration and intracellular Ca<sup>2+</sup> release at constant stimulation rate, has been associated with the development of ventricular arrhythmias. Recent clinical data also provide strong evidence that alternans plays a central role in arrhythmogenesis in atria. The aim of this article is to review the mechanisms that are responsible for repolarization alternans and contribute to the transition from spatially concordant alternans to the more arrhythmogenic spatially discordant alternans in atria. |
20,367 | Right ventricular and tricuspid valve function in patients chronically implanted with leadless pacemakers. | Leadless cardiac pacing has recently been proposed as alternative to conventional right ventricular (RV) pacing. With this approach, devices are directly screwed or fixed with tines in the RV wall, but the possible consequences on RV and tricuspid valve (TV) structure and function remain unknown. We thus conducted a study to evaluate this potential impact in chronically implanted patients.</AbstractText>Repeated echocardiographic studies were performed prior to implantation, at discharge, and 2 months thereafter on all consecutive patients implanted with a leadless pacemaker at our centre between October 2014 and end-December 2015. Whenever possible, patients were evaluated in non-paced rhythm. Anatomical and functional parameters of RV, TV, and left cardiac structures were assessed. Overall, 23 patients (12 females, aged 85.2 ± 6.3 years) were included, with 14 implanted using Nanostim™ (Saint Jude Medical) and 9 with Micra™ (Medtronic). Indications for pacing were paroxysmal atrio-ventricular block in 12 patients, intermittent sinus bradycardia in 5, unexplained syncope in 3, and atrial fibrillation with slow ventricular rate in the remaining 3. The pacing percentage was 34 ± 42% at the last visit. Most devices were implanted in the septo-apical or mid-septal region. There were no significant changes in echocardiographic parameters observed. One patient developed significantly increased TV regurgitation, without abnormal leaflet motion or TV annulus size changes, suggesting it to be due to RV pressure changes.</AbstractText>In patients chronically implanted with leadless pacemakers, there were no significant changes in heart structure and function observed, especially concerning the RV and TV.</AbstractText> |
20,368 | Left atrial strain predicts hemodynamic parameters in cardiovascular patients. | We aimed to evaluate the predictive value of left atrial (LA) reservoir, conduit, and contractile function parameters as assessed by speckle tracking echocardiography (STE) for invasively measured hemodynamic parameters in a patient cohort with myocardial and valvular diseases.</AbstractText>Sixty-nine patients undergoing invasive hemodynamic assessment were enrolled into the study. Invasive hemodynamic parameters were obtained by left and right heart catheterization. Transthoracic echocardiography assessment of LA reservoir, conduit, and contractile function was performed by STE.</AbstractText>Forty-nine patients had sinus rhythm (SR) and 20 patients had permanent atrial fibrillation (AF). AF patients had significantly reduced LA reservoir function compared to SR patients. In patients with SR, LA reservoir, conduit, and contractile function inversely correlated with pulmonary capillary wedge pressure (PCWP), left ventricular end-diastolic pressure, and mean pulmonary artery pressure (PAP), and showed a moderate association with cardiac index. In AF patients, there were no significant correlations between LA reservoir function and invasively obtained hemodynamic parameters. In SR patients, LA contractile function with a cutoff value of 16.0% had the highest diagnostic accuracy (area under the curve, AUC: 0.895) to predict PCWP ≥18 mm Hg compared to the weaker diagnostic accuracy of average E/E' ratio with an AUC of 0.786 at a cutoff value of 14.3. In multivariate analysis, LA contractile function remained significantly associated with PCWP ≥18 mm Hg.</AbstractText>In a cohort of patients with a broad spectrum of cardiovascular diseases LA strain shows a valuable prediction of hemodynamic parameters, specifically LV filling pressures, in the presence of SR.</AbstractText>© 2017, Wiley Periodicals, Inc.</CopyrightInformation> |
20,369 | Usefulness of left ventricular speckle tracking echocardiography and novel measures of left atrial structure and function in diagnosing paroxysmal atrial fibrillation in ischemic stroke and transient ischemic attack patients. | Asymptomatic paroxysmal atrial fibrillation (PAF) is often assumed to be the cause of cryptogenic ischemic strokes (IS) and transient ischemic attacks (TIA). We examined the usefulness of measures obtained by 2D speckle tracking echocardiography and novel left atrial measurements, in the diagnosis of PAF in patients with IS and TIA. We retrospectively included 205 patients who after acute IS or TIA underwent an echocardiogram in sinus rhythm. Patients were designated as PAF-patients if they had one or more reported incidents of AF before or after their echocardiographic examination. None of the conventional echocardiographic parameters were significantly associated with PAF. Of the speckle tracking measurements, only early diastolic strain rate (0.7±0.2 s<sup>-1</sup> vs. 0.8±0.3 s<sup>-1</sup>, p = 0.048) and global longitudinal displacement (GLD) (3.15 ± 1.40 mm vs. 3.87 ± 1.56 mm, p = 0.007) proved significantly different. Of the left atrial parameters both minimal and maximal left atrium volume divided by left ventricular length (min LAV/LVL and max LAV/LVL, respectively) were significantly impaired (min LAV/LVL: 3.7 ± 2.1 cm<sup>2</sup> vs. 2.8 ± 1.11 cm<sup>2</sup>, p = 0.012; max LAV/LVL: 6.6 ± 3.1 cm<sup>2</sup> vs. 5.6 ± 1.7 cm<sup>2</sup>, p = 0.012). GLD, min max LAV/LVL proved significant after adjustment for age, gender, CHA<sub>2</sub>DS<sub>2</sub>-VASc and NIHSS. By combining information regarding age, GLD, min and max LAV/LVL the diagnostic accuracy of PAF improved, resulting in a significantly increased area under the curve (p = 0.037). In patients with IS and TIA GLD, min and max LAV/LVL were independently associated with the presence of PAF. |
20,370 | The impact of serum potassium-influencing antihypertensive drugs on the risk of out-of-hospital cardiac arrest: A case-control study. | Sudden cardiac arrest (SCA) is a complex multifactorial event and most commonly caused by ventricular tachycardia/ fibrillation (VT/ VF). Some antihypertensive drugs could induce hypokalaemia or hyperkalaemia, which may increase susceptibility to VT/VF and SCA.</AbstractText>To assess the association between different classes of antihypertensive drugs classified according to their potential impact on serum potassium levels and the occurrence of out-of-hospital cardiac arrest (OHCA) based on VT/VF.</AbstractText>A case-control study was performed among current users of antihypertensive drugs. Cases were OHCA victims with electrocardiogram documented VT/VF drawn from the AmsteRdam REsuscitation STudies (ARREST) registry, and controls were non-OHCA individuals from the PHARMO database. Antihypertensive drugs were classified into: (i) antihypertensives with neutral effect on serum potassium levels; (ii) hypokalaemia-inducing antihypertensives; (iii) hyperkalaemia-inducing antihypertensives; (iv) combination of antihypertensives with hypo- and hyperkalaemic effects.</AbstractText>We included 1345 cases and 4145 controls. The risk of OHCA was significantly increased among users of hypokalaemia-inducing antihypertensives [adjusted odds ratio (OR) 1.39; 95% confidence interval (CI) 1.10-1.76] and among users of a combination of antihypertensives with hypo- and hyperkalaemic effects (adjusted OR 1.42; 95%CI 1.17-1.72) vs. users of antihypertensives with neutral effect. There was no difference in OHCA risk between users of hyperkalaemia-inducing antihypertensives vs. users of antihypertensive drugs with neutral effect (adjusted OR 1.15; 95%CI 0.95-1.40).</AbstractText>The risk of OHCA is significantly increased in patients who were current users of hypokalaemia-inducing antihypertensives and patients using a combination of antihypertensives with hypo- and hyperkalaemic effects.</AbstractText>© 2017 The British Pharmacological Society.</CopyrightInformation> |
20,371 | The association of QT interval components with atrial fibrillation. | Although abnormalities of the QT interval are associated with atrial fibrillation (AF), it is unclear whether ventricular depolarization (QRS duration) or repolarization (JT interval) is a more important marker of AF risk.</AbstractText>This analysis included 4,181 (95% white; 59% women) participants from the Cardiovascular Health Study (CHS) who were free of baseline AF and major intraventricular delay. A linear scale was used to compute heart rate adjusted QT (QTa), QRS (QRSa</sub> ), and JT (JTa</sub> ) intervals. Prolonged QTa</sub> , QRSa</sub> , and JTa</sub> were defined by values greater than the sex-specific 95th percentile for each measurement. AF events were ascertained during the annual study electrocardiograms and from hospitalization discharge data. Cox regression was used to compute hazard ratios (HR) and 95% confidence intervals (CI) for the associations of prolonged QTa</sub> , QRSa</sub> , and JTa</sub> with AF, separately.</AbstractText>Over a mean follow-up of 12.1 years, a total of 1,236 (30%) AF events were detected. An increased risk of AF (HR = 1.50. 95% CI = 1.20, 1.88) was observed with prolonged QTa</sub> . When we examined the association between individual components of the QTa</sub> interval and AF, the risk of AF was limited to prolonged JTa</sub> (HR = 1.31, 95% CI = 1.04, 1.65) and not prolonged QRSa</sub> (HR = 1.00, 95% CI = 0.77, 1.30). Similar results were obtained per 1-SD increase in QTa</sub> (HR = 1.07, 95% CI = 1.01, 1.13), QRSa</sub> (HR = 0.99, 95% CI = 0.94, 1.06), and JTa</sub> (HR = 1.07, 95% CI = 1.01, 1.13).</AbstractText>The JT interval is a more important marker of AF risk in the QT interval among persons who do not have ventricular conduction delays.</AbstractText>© 2017 Wiley Periodicals, Inc.</CopyrightInformation> |
20,372 | A review of the atrial upper rate algorithms of St. Jude Medical (Abbott) cardiac implantable electronic devices : Incidence of repetitive nonreentrant ventriculoatrial synchrony (RNRVAS). | This review focuses on the manifestations of the three triggered atrial upper rate functions of St Jude Medical cardiac implantable electronic devices. The occurrence of repetitive nonreentrant ventriculoatrial synchrony (RNRVAS) is also evaluated as a basis for the development of automatic mode switching (AMS) and as a trigger for atrial tachycardia/atrial fibrillation (AT/AF) event recordings. RNRVAS is a common trigger for AMS because all the atrial events or intervals are used to calculate the filtered atrial rate interval (FARI). Once AMS is initiated, it will also effectively stop RNRVAS because entry into AMS also shortens the postventricular atrial refractory period (PVARP). Recent design developments to eliminate or minimize unusual upper rare responses include the following: (1) P waves in the PVARP are no longer counted towards the FARI if they are followed by an atrial paced event. (2) In new devices the AT/AF detection algorithm substitutes the Moving Average Interval (a relatively complex calculation) with the new FARI average. (3) Improved design of the rate-responsive PVARP with a far more aggressive response than in the past (enhanced atrial protection interval). |
20,373 | The Feasibility and Safety of Surgery in Patients Receiving Immune Checkpoint Inhibitors: A Retrospective Study. | Immune checkpoint inhibitors (ICI) are revolutionizing care for cancer patients. The list of malignancies for which the Food and Drug Administration is granting approval is rapidly increasing. Furthermore, there is a concomitant increase in clinical trials incorporating ICI. However, the safety of ICI in patients undergoing surgery remains unclear. Herein, we assessed the safety of ICI in the perioperative setting at a single center. We conducted a retrospective review of patients who underwent planned surgery while receiving ICI in the perioperative setting from 2012 to 2016. We collected 30-day postoperative morbidity and mortality utilizing the Clavien-Dindo classification system. We identified 17 patients who received perioperative ICI in 22 operations. Patients were diagnosed with melanoma (<i>n</i> = 14), renal cell carcinoma (<i>n</i> = 2), and urothelial carcinoma (<i>n</i> = 1). Therapies included pembrolizumab (<i>n</i> = 10), ipilimumab (<i>n</i> = 5), atezolizumab (<i>n</i> = 5), and ipilimumab/nivolumab (<i>n</i> = 2). Procedures included cutaneous/subcutaneous resection (<i>n</i> = 6), lymph node resection (<i>n</i> = 5), small bowel resection (<i>n</i> = 5), abdominal wall resection (<i>n</i> = 3), other abdominal surgery (<i>n</i> = 3), orthopedic surgery (<i>n</i> = 1), hepatic resection (<i>n</i> = 1), and neurosurgery (<i>n</i> = 2). There were no Grade III-IV Clavien-Dindo complications. There was one death secondary to ventricular fibrillation in the setting of coronary artery disease. ICI appear safe in the perioperative setting, involving multiple different types of surgery, and likely do not need to be stopped in the perioperative setting. Further studies are warranted to confirm these findings. |
20,374 | Nonalcoholic Fatty Liver Disease (NAFLD) and Risk of Cardiac Arrhythmias: A New Aspect of the Liver-heart Axis. | Nonalcoholic fatty liver disease (NAFLD) is a pathologic condition frequently observed in clinical practice. To date, the prevalence of NAFLD is approximately 25-30% among adults of the general population in Western countries but increases to approximately 70-75% among patients with type 2 diabetes mellitus. In the last decade, accumulating evidence has clearly demonstrated that patients with NAFLD have not only an increased liver-related morbidity and mortality but also an increased risk of fatal and non-fatal cardiovascular events. In particular, several studies have documented the existence of an independent association among NAFLD and cardiac changes in structure and function in both non-diabetic and diabetic patients. In addition, mounting evidence also suggests that there is a strong relationship between NAFLD and cardiac arrhythmias, such as atrial fibrillation, QTc prolongation and ventricular arrhythmias. This is of clinical interest, as it could explain, at least in part, the increased risk of death for cardiovascular disease in patients with NAFLD. Therefore, seeing that cardiovascular disease complications are the leading cause of disability and death in NAFLD patients, the recent European clinical practice guidelines advised to check the cardiovascular system in all patients with NAFLD. This clinical mini review will briefly describe the increasing body of evidence regarding the association between NAFLD and cardiac arrhythmias, and discuss the potential biological mechanisms underlying this association. |
20,375 | ECG markers associated with ischemic stroke at young age - a case-control study. | Certain electrocardiographic (ECG) abnormalities are associated with ischemic stroke (IS), especially cardioembolic subtype. Besides atrial fibrillation, markers of left ventricular hypertrophy (LVH) or atrial pathology also reflect elevated risk. We studied the association of ECG markers with IS in young adults.</AbstractText>We performed a case-control study including 567 consecutive IS patients aged 15-49 years (inclusion period: 1994-2007) and one or two age- and sex-matched control subjects enrolled during 1978-1980 (n = 1033), and investigated also the stroke aetiologic subgroups. We studied ECGs of all participants for markers of atrial abnormality, i.e. P-terminal force (PTF) on lead V1, interatrial blocks (IAB; P-wave duration ≥110 ms), and LVH. Conditional logistic regression analyses were used.</AbstractText>IAB (hazard ratio [HR]: 1.57, 95% confidence interval [CI]: 1.16-2.13) and PTF combined with LVH (HR: 6.83, 95% CI: 1.65-28.31), were independently associated with IS. LVH, abnormal P-wave (HR: 6.87, 95% CI: 1.97-135.29), PTF, IAB, and combinations of these P-wave abnormalities with LVH - were associated with cardioembolic subtype. Abnormal P-wave and IAB were associated with cryptogenic stroke subtype. In unadjusted analysis, LVH was associated with small-vessel disease subtype.</AbstractText>P-wave abnormalities on ECG were associated with cardioembolic but also with a cryptogenic subtype of IS. Key messages ECG patterns associated with atrial pathology are markers of increased risk of ischemic stroke in young adults. The ECG markers reflecting atrial pathology were seen in patients with cardioembolic and cryptogenic subtypes of ischemic stroke.</AbstractText> |
20,376 | Incidence and outcome of in-hospital cardiac arrest in Italy: a multicentre observational study in the Piedmont Region. | to report the incidence, characteristics, and outcome of in-hospital cardiac arrest (IHCA) in a large Italian region.</AbstractText>all hospitals participating in the IHCA Registry Initiative of Piedmont.</AbstractText>observational cohort study in adult (>18year old) inpatients resuscitated from IHCA during three consecutive years (2012-2014). The main outcome measures were IHCA incidence and survival to hospital discharge.</AbstractText>A total of1539 arrests in adult inpatients were recorded in the study period, yielding an overall incidence of 1.51 arrests/1000 admissions. The incidence was highest at day 1 after hospital admission and in the morning hours, with a peak at 9.00 a.m. Median age was 77 (interquartile range 68-83) years. The presenting rhythm was ventricular fibrillation/pulseless ventricular tachycardia in 291/1539 (18.9%) cases. A total of 549/1539 (35.7%) patients achieved recovery of spontaneous circulation (ROSC) and 228/1539(14.8%) survived hospital discharge, with 207 (90.8%) of the latter having good neurological outcome (Cerebral Performance Categories [CPC] 1 or 2).After adjustment for major confounders, a pre-arrest CPC=1, a cardiac cause of arrest, a shockable presenting rhythm, and a shorter duration of resuscitation were independently associated with a higher likelihood of survival to discharge.</AbstractText>in this Italian registry the incidence of IHCA and its circadian distribution were comparable to those in the NCAA registry in the UK. Patients were older and had a lower ROSC rate than these observed in other large IHCA registries, but post-ROSC survival rate and factors affecting survival to discharge were similar.</AbstractText>Copyright © 2017. Published by Elsevier B.V.</CopyrightInformation> |
20,377 | Electrophysiological Characteristics and Radiofrequency Catheter Ablation Treatment of Idiopathic Ventricular Arrhythmias Successfully Ablated From the Ostium of the Coronary Sinus. | Idiopathic ventricular arrhythmias (VAs) rarely arise from the epicardium at the crux of the heart. However, the electrophysiological characteristics of VAs successfully ablated from the ostium of the coronary sinus (CSO) have not yet been documented.Methods and Results:Electrocardiographic and electrophysiological data were analyzed in patients with idiopathic VAs successfully ablated from the CSO.Among 309 patients with idiopathic VAs treated with radiofrequency catheter ablation (RFCA), 6 (1.94%; 3 men; age: 66.3±9.7 years) had VAs successfully ablated from the CSO. Only 1 patient had sustained ventricular tachycardia. The morphology of the QRS showed a left superior axis and QS pattern in leads III and aVF. Furthermore, the precordial maximum deflection index was >0.55 in all patients and a right bundle branch block pattern was recorded in 5 of 6 patients. All VAs were successfully eliminated by RFCA within the CSO. Intracardiac ECGs at sites where VAs were eliminated by RFCA showed clear atrial and ventricular potentials (atrial amplitude: 0.21±0.11 mV; ventricular amplitude: 0.43±0.24 mV), except in 1 case of atrial fibrillation. No patients had recurrence during the 3.4±1.8-year follow-up period.</AbstractText>The idiopathic VAs in our study were eliminated by RFCA within the CS, where a clear atrial amplitude was recorded.</AbstractText> |
20,378 | Alpha Klotho and Fibroblast Growth Factor-23 Among Alcoholics. | Alcoholism may be a cardiovascular risk factor. Osteocyte derived molecules such as fibroblast growth factor 23 (FGF-23) and soluble α Klotho have recently been associated with cardiovascular disease, but their role in alcoholics is unknown. We here analyze the behavior of FGF23 and α Klotho in alcoholics.</AbstractText>Ninety-seven alcoholic patients were assessed for liver function, presence of hypertension, diabetes, atrial fibrillation, left ventricular hypertrophy (LVH), vascular calcifications (assessed by chest X-ray) and nutritional status (lean and fat mass measured by densitometry). We measured plasma levels of FGF-23 and serum soluble α Klotho, using ELISA in 97 patients and 20 age- and sex-matched controls.</AbstractText>FGF-23 levels were higher in patients than in controls (Z = 3.50; P < 0.001). FGF-23 (Z = 5.03; P < 0.001) and soluble α Klotho (Z = 5.61; P < 0.001) were higher in cirrhotics, and both were related to liver function, independently of serum creatinine FGF-23 levels were higher among alcoholics with diabetes (Z = 2.55; P = 0.011) or hypertension (Z = 2.56; P = 0.01), and increased body fat (ρ = 0.28; P = 0.022 for trunk fat), whereas α Klotho levels were higher in patients with LVH (Z = 2.17; P = 0.03) or atrial fibrillation (Z = 2.34; P = 0.019).</AbstractText>FGF-23 was higher in alcoholics than in controls, especially among cirrhotics, and soluble α Klotho levels were also higher among cirrhotics. Both were related to liver function impairment, independently of serum creatinine levels, and also showed significant associations with vascular risk factors, such as hypertension, diabetes or trunk fat amount in the case of FGF-23, or LVH or atrial fibrillation in the case of α Klotho.</AbstractText>We report increased values of fibroblast growth factor 23 (FGF-23) and soluble α Klotho in cirrhotic alcoholics. Both molecules are associated with liver function impairment, and with some cardiovascular risk factors such as diabetes, hypertension, increased body fat, left ventricular hypertrophy and atrial fibrillation independently of serum creatinine.</AbstractText>© The Author 2017. Medical Council on Alcohol and Oxford University Press. All rights reserved.</CopyrightInformation> |
20,379 | Evaluation of Plasma Thrombomodulin in Patients with Coronary Slow Flow. | It has been reported that coronary slow flow (CSF) is associated with acute myocardial infarction, ventricular tachycardia, ventricular fibrillation, and even sudden cardiac death. Although studies concerning the etiopathogenesis of CSF are scarce, diffuse atherosclerosis and endothelial dysfunction are thought to play important roles. It has been suggested that a high plasma thrombomodulin (TM) level seems to play an important role in the pathogenesis of atherosclerosis and endothelial dysfunction.</AbstractText>We hypothesized that a high plasma TM level might be associated with CSF and aimed to research the relationship between plasma TM level and CSF.</AbstractText>Fifty-two CSF patients with angiographically proven CSF and 44 cases with normal coronary flow were included in this study. Coronary flow velocity was determined by the thrombolysis in myocardial infarction (TIMI) frame count method. Plasma TM levels were measured in all the study subjects.</AbstractText>Plasma TM levels were significantly higher in the CSF group compared to the control group (3.9 ± 0.5 vs. 3.6 ± 0.3 ng/mL, p = 0.01). There was a positive relationship (r = 0.31, p = 0.002) between plasma TM level and mean TIMI frame count (TFC). Factors associated with mean TFC were plasma TM level (β = 0.206, p = 0.038) and red cell distribution width (β = 0.088, p = 0.009) in multiple linear regression analysis.</AbstractText>Patients with CSF have a higher plasma TM level, and this may play an important role in the pathogenesis of CSF. An elevated plasma TM level may be a predictor of CSF. Future studies are needed to confirm these results.</AbstractText>© 2017 S. Karger AG, Basel.</CopyrightInformation> |
20,380 | Acute Hemodynamic and Tissue Effects of Cryoballoon Ablation on Pulmonary Vessels: The IVUS-Cryo Study. | Cryoballoon-based pulmonary vein isolation (CB-PVI) has been widely used for the treatment of atrial fibrillation. Although generally safe and effective, the procedure may be associated with pulmonary vein (PV) stenosis and bronchial or esophageal injury. The mechanisms leading to these complications have not been studied in detail. Our aim was to examine acute effects of cryoballoon on the pulmonary vessel and right heart pressures as well as PV wall morphology.</AbstractText>In 8 patients (5 men, mean age 55±14 years) undergoing CB-PVI, pressure in each PV was measured by catheter located inside the PV directly before and after CB-PVI. The right atrial, right ventricular, and pulmonary artery pressures as well as pulmonary arterial wedge capillary pressure in the pulmonary artery branch corresponding to target PV were also measured. Morphological changes in PVs were assessed using intravascular ultrasonography.There were no significant differences in PV pressures before and after ablation. The pulmonary arterial wedge capillary pressure significantly increased during cryoapplication (left superior: 20±10 versus 29±8.5 mm Hg, P</i>=0.004; left inferior: 24±10 versus 32±6 mm Hg, P</i>=0.012; right superior: 25±9 versus 35±10 mm Hg, P</i>=0.002; right inferior: 24±10 versus 37±12 mm Hg, P</i>=0.0036). The right atrial and pulmonary artery pressures increased significantly after CB-PVI (9±6 versus 13±8 mm Hg, P</i>=0.004, and 20±9 versus 24±10 mm Hg, P</i>=0.048, respectively). Intravascular ultrasonography showed acute edema and dissection-like changes causing relative lumen narrowing in 90% of PVs.</AbstractText>CB-PVI causes significant rise in pulmonary artery and right atrial pressures as well as PV wall damage. The clinical significance of these findings warrants further investigations.</AbstractText>© 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.</CopyrightInformation> |
20,381 | Simultaneous recordings of intrinsic cardiac nerve activity and skin sympathetic nerve activity from human patients during the postoperative period. | Intrinsic cardiac nerve activity (ICNA) and skin nerve activity (SKNA) are both associated with cardiac arrhythmias in dogs.</AbstractText>The purpose of this study was to test the hypothesis that ICNA and SKNA correlate with postoperative cardiac arrhythmias in humans.</AbstractText>Eleven patients (mean age 60 ± 13 years; 4 women) were enrolled in this study. Electrical signals were simultaneously recorded from electrocardiogram (ECG) patch electrodes on the chest wall and from 2 temporary pacing wires placed during open heart surgery on the left atrial epicardial fat pad. The signals were filtered to display SKNA and ICNA. Premature atrial contractions (PACs) and premature ventricular contractions were determined manually. The SKNA and ICNA of the first 300 minutes of each patient were calculated minute by minute to determine baseline average amplitudes of nerve activities and to determine their correlation with arrhythmia burden.</AbstractText>We processed 1365 ± 973 minutes of recording per patient. Low-amplitude SKNA and ICNA were present at all time, while the burst discharges were observed much less frequently. Both SKNA and burst ICNA were significantly associated with the onset of PACs and premature ventricular contractions. Baseline average ICNA (aICNA), but not average SKNA, had a significant association with PAC burden. The correlation coefficient (r) between aICNA and PAC burden was 0.78 (P < .01). A patient with the greatest aICNA developed postoperative atrial fibrillation.</AbstractText>ICNA and SKNA can be recorded from human patients in the postoperative period. The baseline magnitude of ICNA correlates with PAC burden and development of postoperative atrial fibrillation.</AbstractText>Copyright © 2017 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
20,382 | Mechanosensitivity of microdomain calcium signalling in the heart. | In cardiac myocytes, calcium (Ca<sup>2+</sup>) signalling is tightly controlled in dedicated microdomains. At the dyad, i.e. the narrow cleft between t-tubules and junctional sarcoplasmic reticulum (SR), many signalling pathways combine to control Ca<sup>2+</sup>-induced Ca<sup>2+</sup> release during contraction. Local Ca<sup>2+</sup> gradients also exist in regions where SR and mitochondria are in close contact to regulate energetic demands. Loss of microdomain structures, or dysregulation of local Ca<sup>2+</sup> fluxes in cardiac disease, is often associated with oxidative stress, contractile dysfunction and arrhythmias. Ca<sup>2+</sup> signalling at these microdomains is highly mechanosensitive. Recent work has demonstrated that increasing mechanical load triggers rapid local Ca<sup>2+</sup> releases that are not reflected by changes in global Ca<sup>2+</sup>. Key mechanisms involve rapid mechanotransduction with reactive oxygen species or nitric oxide as primary signalling molecules targeting SR or mitochondria microdomains depending on the nature of the mechanical stimulus. This review summarizes the most recent insights in rapid Ca<sup>2+</sup> microdomain mechanosensitivity and re-evaluates its (patho)physiological significance in the context of historical data on the macroscopic role of Ca<sup>2+</sup> in acute force adaptation and mechanically-induced arrhythmias. We distinguish between preload and afterload mediated effects on local Ca<sup>2+</sup> release, and highlight differences between atrial and ventricular myocytes. Finally, we provide an outlook for further investigation in chronic models of abnormal mechanics (eg post-myocardial infarction, atrial fibrillation), to identify the clinical significance of disturbed Ca<sup>2+</sup> mechanosensitivity for arrhythmogenesis. |
20,383 | Management of Refractory Ventricular Fibrillation: Extracorporeal Membrane Oxygenation or Epinephrine? | [Figure: see text] |
20,384 | Brugada syndrome: A general cardiologist's perspective. | Brugada syndrome (BrS) is one of the commonest inherited primary arrhythmia syndromes typically presenting with arrhythmic syncope or sudden cardiac death (SCD) due to polymorphic ventricular tachycardia and ventricular fibrillation precipitated by vagotonia or fever in apparently healthy adults, less frequently in children. The prevalence of the syndrome (0.01%-0.3%) varies among regions and ethnicities, being the highest in Southeast Asia. BrS is diagnosed by the "coved type" ST-segment elevation≥2mm followed by a negative T-wave in ≥1 of the right precordial leads V<sub>1</sub>-V<sub>2</sub>. The typical electrocardiogram in BrS is often concealed by fluctuations between normal, non-diagnostic and diagnostic ST-segment pattern in the same patient, thus hindering the diagnosis. Presently, the majority of BrS patients is incidentally diagnosed, and may remain asymptomatic for their lifetime. However, BrS is responsible for 4-12% of all SCDs and for ~20% of SCDs in patients with structurally normal hearts. Arrhythmic risk is the highest in SCD survivors and in patients with spontaneous BrS electrocardiogram and arrhythmic syncope, but risk stratification for SCD in asymptomatic subjects has not yet been fully defined. Recent achievements have expanded our understanding of the genetics and electrophysiological mechanisms underlying BrS, while radiofrequency catheter ablation may be an effective new approach to treat ventricular tachyarrhythmias in BrS patients with arrhythmic storms. The present review summarizes our contemporary understanding and recent advances in the inheritance, pathophysiology, clinical assessment and treatment of BrS patients. |
20,385 | Selective inhibition of FLT3 by gilteritinib in relapsed or refractory acute myeloid leukaemia: a multicentre, first-in-human, open-label, phase 1-2 study. | Internal tandem duplication mutations in FLT3 are common in acute myeloid leukaemia and are associated with rapid relapse and short overall survival. The clinical benefit of FLT3 inhibitors in patients with acute myeloid leukaemia has been limited by rapid generation of resistance mutations, particularly in codon Asp835 (D835). We aimed to assess the highly selective oral FLT3 inhibitor gilteritinib in patients with relapsed or refractory acute myeloid leukaemia.</AbstractText>In this phase 1-2 trial, we enrolled patients aged 18 years or older with acute myeloid leukaemia who either were refractory to induction therapy or had relapsed after achieving remission with previous treatment. Patients were enrolled into one of seven dose-escalation or dose-expansion cohorts assigned to receive once-daily doses of oral gilteritinib (20 mg, 40 mg, 80 mg, 120 mg, 200 mg, 300 mg, or 450 mg). Cohort expansion was based on safety and tolerability, FLT3 inhibition in correlative assays, and antileukaemic activity. Although the presence of an FLT3 mutation was not an inclusion criterion, we required ten or more patients with locally confirmed FLT3 mutations (FLT3mut+</sup>) to be enrolled in expansion cohorts at each dose level. On the basis of emerging findings, we further expanded the 120 mg and 200 mg dose cohorts to include FLT3mut+</sup> patients only. The primary endpoints were the safety, tolerability, and pharmacokinetics of gilteritinib. Safety and tolerability were assessed in the safety analysis set (all patients who received at least one dose of gilteritinib). Responses were assessed in the full analysis set (all patients who received at least one dose of study drug and who had at least one datapoint post-treatment). Pharmacokinetics were assessed in a subset of the safety analysis set for which sufficient data for concentrations of gilteritinib in plasma were available to enable derivation of one or more pharmacokinetic variables. This study is registered with ClinicalTrials.gov, number NCT02014558, and is ongoing.</AbstractText>Between Oct 15, 2013, and Aug 27, 2015, 252 adults with relapsed or refractory acute myeloid leukaemia received oral gilteritinib once daily in one of seven dose-escalation (n=23) or dose-expansion (n=229) cohorts. Gilteritinib was well tolerated; the maximum tolerated dose was established as 300 mg/day when two of three patients enrolled in the 450 mg dose-escalation cohort had two dose-limiting toxicities (grade 3 diarrhoea and grade 3 elevated aspartate aminotransferase). The most common grade 3-4 adverse events irrespective of relation to treatment were febrile neutropenia (97 [39%] of 252), anaemia (61 [24%]), thrombocytopenia (33 [13%]), sepsis (28 [11%]), and pneumonia (27 [11%]). Commonly reported treatment-related adverse events were diarrhoea (92 [37%] of 252]), anaemia (86 [34%]), fatigue (83 [33%]), elevated aspartate aminotransferase (65 [26%]), and increased alanine aminotransferase (47 [19%]). Serious adverse events occurring in 5% or more of patients were febrile neutropenia (98 [39%] of 252; five related to treatment), progressive disease (43 [17%]), sepsis (36 [14%]; two related to treatment), pneumonia (27 [11%]), acute renal failure (25 [10%]; five related to treatment), pyrexia (21 [8%]; three related to treatment), bacteraemia (14 [6%]; one related to treatment), and respiratory failure (14 [6%]). 95 people died in the safety analysis set, of which seven deaths were judged possibly or probably related to treatment (pulmonary embolism [200 mg/day], respiratory failure [120 mg/day], haemoptysis [80 mg/day], intracranial haemorrhage [20 mg/day], ventricular fibrillation [120 mg/day], septic shock [80 mg/day], and neutropenia [120 mg/day]). An exposure-related increase in inhibition of FLT3 phosphorylation was noted with increasing concentrations in plasma of gilteritinib. In-vivo inhibition of FLT3 phosphorylation occurred at all dose levels. At least 90% of FLT3 phosphorylation inhibition was seen by day 8 in most patients receiving a daily dose of 80 mg or higher. 100 (40%) of 249 patients in the full analysis set achieved a response, with 19 (8%) achieving complete remission, ten (4%) complete remission with incomplete platelet recovery, 46 (18%) complete remission with incomplete haematological recovery, and 25 (10%) partial remission INTERPRETATION: Gilteritinib had a favourable safety profile and showed consistent FLT3 inhibition in patients with relapsed or refractory acute myeloid leukaemia. These findings confirm that FLT3 is a high-value target for treatment of relapsed or refractory acute myeloid leukaemia; based on activity data, gilteritinib at 120 mg/day is being tested in phase 3 trials.</AbstractText>Astellas Pharma, National Cancer Institute (Leukemia Specialized Program of Research Excellence grant), Associazione Italiana Ricerca sul Cancro.</AbstractText>Copyright © 2017 Elsevier Ltd. All rights reserved.</CopyrightInformation> |
20,386 | Atrial Fibrillation: Current Therapies. | A rate control, or a rhythm control, strategy can be applied to the management of atrial fibrillation. Rate control of atrial fibrillation consists of decreasing the ventricular response rate by limiting the number of supraventricular impulses that can travel through the atrioventricular node. The goal of decreasing heart rate in dogs with atrial fibrillation is usually achieved with a combination of the calcium channel blocker diltiazem and digoxin. Rhythm control of atrial fibrillation encompasses pharmacologic and nonpharmacologic methods to terminate the arrhythmia and restore sinus rhythm. Transthoracic synchronized electrical cardioversion is commonly used to stop atrial fibrillation. |
20,387 | Current state of the art for cardiac arrhythmia gene therapy. | Cardiac arrhythmias are a leading cause of morbidity and mortality. Currently available therapeutic options lack sufficient efficacy and safety. Gene therapy has been proposed for treatment of cardiac arrhythmias. This review will discuss the current state of development for arrhythmia gene therapy. So far, all published studies are short-term, proof-of-concept animal studies. Potential replacement of cardiac pacemakers has been shown for combination gene therapy using the HCN2 gene and either the gene for adenylate cyclase, the skeletal muscle isoform of the sodium channel, or a dominant negative mutant of the potassium channel responsible for resting membrane potential. Atrial fibrillation has been prevented by gene transfer of either a dominant negative mutant of a repolarizing potassium channel, a gap junction, or an siRNA directed against caspase 3. Inherited arrhythmia syndromes have been corrected by replacement of the causative genes. Post-infarct ventricular tachycardia has been reduced by gene therapy with the skeletal muscle sodium channel and connexins and eliminated with the dominant negative mutant of the potassium channel responsible for resting membrane potential. These ideas show considerable promise. Long-term efficacy and safety studies are required to see if they can become viable therapies. |
20,388 | Myocardial scar location as detected by cardiac magnetic resonance is associated with the outcome in heart failure patients undergoing surgical ventricular reconstruction. | Post-infarction myocardial scar causes adverse left ventricular remodelling and negatively affects the prognosis. We sought to investigate whether scar extent and location obtained by cardiac magnetic resonance may affect the reverse remodelling and survival of heart failure patients undergoing surgical ventricular reconstruction.</AbstractText>From January 2011 to December 2015, 151 consecutive patients with previous myocardial infarction and left ventricular remodelling underwent surgical ventricular reconstruction at our Institution, of which 88 (58%) patients had a preoperative protocol-standardized late gadolinium enhancement (LGE)-cardiac magnetic resonance examination during the week before surgery. We excluded 40 patients with devices (26%), 15 patients with irregular heart rhythm (permanent atrial fibrillation, 10% not included in the device group) or mixed contraindications (severe claustrophobia or presence of material magnetic resonance not compatible). Among the 145 survivors, 11 patients received an implantable cardioverter defibrillator after surgery (mostly for persistent low ejection fraction) and were excluded as well, yielding a total of 59 patients (48 men, aged 65 ± 9 years) who repeated a protocol-standardized LGE-cardiac magnetic resonance examination even 6 months postoperatively and therefore represent the study population. Patients were grouped according to the presence of LGE in the antero-basal left ventricular segments (Group A) or the absence of LGE in the same segments (Group B). The postoperative left ventricular end-systolic volume index was considered the primary end-point.</AbstractText>After surgery, left ventricular end-systolic volume index and end-diastolic volume index significantly decreased (P < 0.001, for both), while diastolic sphericity index and ejection fraction significantly increased (P = 0.015 and P < 0.001, respectively). The presence of LGE in the antero-basal left ventricular segments (10 patients, Group A) was the only independent predictor of outcome (P = 0.02) at multivariate analysis, being the postoperative left ventricular end-systolic volume index significantly higher compared to that of patients of Group B (49 patients) (78 ± 26 ml/m2 vs 55 ± 20 ml/m2, P = 0.003). Furthermore, patients with a postoperative left ventricular end-systolic volume index >60 ml/m2 showed a higher risk of cardiac events (hazard ratio = 3.67, P = 0.02).</AbstractText>In patients undergoing surgical ventricular reconstruction, LGE scar location affects the left ventricular reverse remodelling, which in turn might limit the survival benefit.</AbstractText>© The Author 2017. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.</CopyrightInformation> |
20,389 | Single-lead f-wave extraction using diffusion geometry. | A novel single-lead f-wave extraction algorithm based on the modern diffusion geometry data analysis framework is proposed.</AbstractText>The algorithm is essentially an averaged beat subtraction algorithm, where the ventricular activity template is estimated by combining a newly designed metric, the 'diffusion distance', and the non-local Euclidean median based on the non-linear manifold setup. We coined the algorithm [Formula: see text].</AbstractText>Two simulation schemes are considered, and the new algorithm [Formula: see text] outperforms traditional algorithms, including the average beat subtraction, principal component analysis, and adaptive singular value cancellation, in different evaluation metrics with statistical significance.</AbstractText>The clinical potential is shown in the real Holter signal, and we introduce a new score to evaluate the performance of the algorithm.</AbstractText> |
20,390 | Aldosterone and renin in cardiac patients referred for catheterization. | Little is known regarding alterations of the renin-angiotensin system in patients referred for cardiac catheterization. Here, we measured plasma levels of active renin and aldosterone in patients referred for cardiac catheterization in order to determine the prevalence of elevated renin, aldosterone, and the aldosterone-renin ratio.A chemiluminescence assay was used to measure plasma aldosterone concentration (PAC) and active renin levels in 833 consecutive patients, after an overnight fasting and without any medication for least 12 hours. We evaluated associations of the hormonal elevations in relation to hypertension, atrial fibrillation (AF), hypertensive cardiomyopathy, coronary artery disease (CAD), valvular disease, impaired left ventricular ejection fraction (LVEF < 35%), and pulmonary hypertension (arterial pulmonary mean pressure >25 mm Hg).Hyperaldosteronism occurred in around one-third of all examined patients, without significant differences between patients with or without the named cardiac diseases. In a comparison between patients with or without any given cardiac disease condition, renin was significantly elevated in patients with either hypertension (36.4% vs 15.9%), CAD (33.9% vs 22.1%), or impaired LVEF (47.3% vs 24.8%). The angiotensin-renin ratio was elevated in AF patients and in patients with hypertensive cardiomyopathy. Patients with AF and coexisting hypertension had elevated renin more frequently than AF patients without coexisting hypertension (35.3% vs 16.5%; P  =  .005). Patients with persistent/permanent AF more frequently had elevated renin than patients with paroxysmal AF (34.1% vs 15.8%; P  =  .007).This prospective study of consecutive cardiac disease patients referred for cardiac catheterization has revealed distinct cardiac disease condition-associated differences in the frequencies of elevations in plasma renin, PAC, and the aldosterone-renin ratio. |
20,391 | Comet assay in evaluating deoxyribonucleic acid damage after out-of-hospital cardiac arrest. | This study aimed to investigate whether out-of-hospital cardiac arrest (OHCA) may induce severe DNA damage measured using comet assay in successfully resuscitated humans and to evaluate a short-term prognostic role.</AbstractText>In this prospective, controlled, blinded study (1/2013-1/2014), 41 patients (age, 63±14 years) successfully resuscitated from non traumatic OHCA and 10 healthy controls (age, 53±17 years) were enrolled. DNA damage [double-strand breaks (DSBs) and single-strand breaks (SSBs)] was measured using comet assay in peripheral lymphocytes sampled at admission. Clinical data were recorded (according to Utstein style). A good short-term prognosis was defined as survival for 30 days.</AbstractText>Among the patients, there were 71% (29/41) short-term survivors. After OHCA, DNA damage (DSBs and SSBs) was higher (11.0±7.6% and 0.79±2.41% in tail) among patients than among controls (1.96±1.63% and 0.02±0.03% in tail), and it was more apparent for DSBs (p<0.001 and p=0.085). There was no difference in the DNA damage between patients with cardiac and non-cardiac etiology, or between survivors and nonsurvivors. Among Utstein style parameters, ventricular fibrillation, asystole, and early electrical defibrillation influenced DSBs; none of the factors influenced SSBs. Factors influencing survival were SSBs, ventricular fibrillation, length of cardiopulmonary resuscitation by professionals ≤15 min, cardiogenic shock, and postanoxic encephalopathy. In contrast to DSBs [area under the curve (AUC)=0.520], SSBs seem to have a potential in prognostication (AUC=0.639).</AbstractText>This study for the first time demonstrates revelation of DNA damage using comet assay in patients successfully resuscitated from OHCA. Whether DNA damage measured using comet assay may be a prognostic marker remains unknown, although our data may encourage some suggestions.</AbstractText> |
20,392 | Right atrial myocardial deformation by two-dimensional speckle tracking echocardiography predicts recurrence in paroxysmal atrial fibrillation. | Atrial fibrillation (AF) is a bi-atrial disease yet little attention has been given to right heart function in AF. We propose that the assessment of right atrial (RA) and right ventricular function (RV) using two-dimensional speckle tracking echocardiography (2D-STE) could be valuable in predicting AF recurrence in patients with paroxysmal AF (PAF).</AbstractText>Thirty patients with PAF were prospectively recruited from a dedicated AF clinic. Right atrial size, volume, and area and RV dimensions were analyzed along with RA and RV strain derived from 2D-STE at baseline and at 3 and 12 months.</AbstractText>Higher RA booster strain independently predicted sinus rhythm (SR) maintenance for up to 1 year (P = 0.001). RV strain was impaired in patients with recurrent AF compared to those in SR (P < 0.05) but did not predict AF recurrence. Two-dimensional STE for RA and RV function was simple to perform with excellent reproducibility (adjusted R 2</sup> 0.92-0.99).</AbstractText>Two-dimensional STE is useful and highly reproducible in assessing right heart function in AF patients. RA booster strain function was predictive of sinus rhythm maintenance for up to 1 year.</AbstractText> |
20,393 | The crucial role of activin A/ALK4 pathway in the pathogenesis of Ang-II-induced atrial fibrosis and vulnerability to atrial fibrillation. | Atrial fibrosis, the hallmark of structural remodeling associated with atrial fibrillation (AF), is characterized by abnormal proliferation of atrial fibroblasts and excessive deposition of extracellular matrix. Transforming growth factor-β1 (TGF-β1)/activin receptor-like kinase 5 (ALK5)/Smad2/3/4 pathway has been reported to be involved in the process. Recent studies have implicated both activin A and its specific downstream component activin receptor-like kinase 4 (ALK4) in stimulating fibrosis in non-cardiac organs. We recently reported that ALK4 haplodeficiency attenuated the pressure overload- and myocardial infarction-induced ventricular fibrosis. However, the role of activin A/ALK4 in the pathogenesis of atrial fibrosis and vulnerability to AF remains unknown. Our study provided experimental and clinical evidence for the involvement of activin A and ALK4 in the pathophysiology of atrial fibrosis and AF. Patients with AF had higher activin A and ALK4 expression in atriums as compared to individuals devoid of AF. After angiotensin-II (Ang-II) stimulation which mimicked atrial fibrosis progression, ALK4-deficient mice showed lower expression of ALK4 in atriums, reduced activation of atrial fibroblasts, blunted atrial enlargement and atrial fibrosis, and further reduced AF vulnerability upon right atrial electrophysiological studies as compared to wild-type littermates. Moreover, we found that apart from the well-known TGF-β1/ALK5 pathway, the activation of activin A/ALK4/smad2/3 pathway played an important role in the pathogenesis of Ang-II-mediated atrial fibrosis and inducibility of AF, suggesting that targeting ALK4 might be a potential therapy for atrial fibrosis and AF. |
20,394 | Danon disease for the cardiologist: case report and review of the literature. | Danon disease is a rare, X-linked dominant genetic disorder that is caused by defects in the lysosome-associated membrane protein 2 (LAMP2) gene. It manifests predominantly in young males with a classic triad of cardiomyopathy, skeletal myopathy, and intellectual disability. Death from cardiac disease is the ultimate cause of demise in many patients if left untreated. Given the rarity of the condition, the natural history is poorly understood. Here, we present a case report on a 14-year-old Hispanic boy with Danon disease, highlighting major clinical events and diagnostic study findings over a six-year period from age of symptom onset to age of death. He had significant hypertrophic cardiomyopathy (ventricular septal thickness 65 mm) and experienced various arrhythmias during his clinical course including Wolf-Parkinson-White syndrome, non-sustained ventricular tachycardia, and pre-excited atrial fibrillation with a fasciculoventricular anomalous accessory pathway. He had sudden cardiac death from ventricular fibrillation at age 14 and his heart had a weight of 1425 grams at autopsy. We also provide a review of the cardiac Danon disease literature related to diagnostic and management approaches to aid cardiologists in evaluating and treating cardiac manifestations in Danon disease patients. |
20,395 | Risk stratification of patients with left atrial appendage thrombus prior to catheter ablation of atrial fibrillation: An approach towards an individualized use of transesophageal echocardiography. | The need for transesophageal echocardiography (TEE) before catheter ablation of atrial fibrillation (CA-AF) is still being questioned. The aim of this study is to analyze patients' (patients) risk factors of left atrial appendage thrombus (LAAT) prior to CA-AF in daily clinical practice, according to oral anticoagulation (OAC) strategies recommended by current guidelines.</AbstractText>All patients scheduled for CA-AF from 01/2015 to 12/2016 in our center were included and either treated with NOACs (novel-OAC; paused 24-hours preablation) or continuous vitamin K antagonists (INR 2.0-3.0). All patients received a preprocedural TEE at the day of ablation. Two groups were defined: (1) patients without LAAT, (2) patients with LAAT. The incidence of LAAT was 0.78% (13 of 1,658 patients). No LAAT was detected in patients with a CHA2</sub> DS2</sub> -VASc score of ≤1 (n = 640 patients) irrespective of the underlying AF type. Independent predictors for LAAT are: higher CHA2</sub> DS2</sub> -VASc scores (odds ratio [OR] 1.54, 95%-confidence interval [CI]: 1.07-2.23, P = 0.0019), a history of nonparoxysmal AF (OR 7.96, 95%-CI: 1.52-146.64, P = 0.049), hypertrophic cardiomyopathy (HCM; OR 9.63, 95% CI: 1.36-43.05, P = 0.007), and a left ventricular ejection fraction (LVEF) < 30% (OR 8.32, 95% CI: 1.18-36.29, P = 0.011). The type of OAC was not predictive (P = 0.70).</AbstractText>The incidence of LAAT in patients scheduled for CA-AF is low. Therefore, periprocedural OAC strategies recommended by current guidelines seem feasible. Preprocedural TEE may be dispensed in patients with a CHA2</sub> DS2</sub> -VASc score ≤1. However, a CHA2</sub> DS2</sub> -VASc score ≥2, reduced LVEF, HCM, or history of nonparoxysmal AF are independently associated with an increased risk for LAAT.</AbstractText>© 2017 Wiley Periodicals, Inc.</CopyrightInformation> |
20,396 | Relaxin reduces susceptibility to post-infarct atrial fibrillation in mice due to anti-fibrotic and anti-inflammatory properties. | Relaxin-2 (RLX) is a peptide hormone that exerts beneficial anti-fibrotic and anti-inflammatory effects in diverse models of cardiovascular disease. The goal of this study was to determine the effects of RLX treatment on the susceptibility to atrial fibrillation (AF) after myocardial infarction (MI).</AbstractText>Mice with cryoinfarction of the left anterior ventricular wall were treated for two weeks with either RLX (75 μg/kg/d) or vehicle (sodium acetate) delivered via subcutaneously implanted osmotic minipumps.</AbstractText>RLX treatment significantly attenuated the increase in AF-inducibility following cryoinfarction and reduced the mean duration of AF episodes. Furthermore, epicardial mapping of both atria revealed an increase in conduction velocity. In addition to an attenuation of atrial hypertrophy, chronic application of RLX reduced atrial fibrosis, which was linked to a significant reduction in atrial mRNA expression of connective tissue growth factor. Transcript levels of the pro-inflammatory cytokines interleukin-6 and interleukin-1β were reduced in RLX treated mice, but macrophage infiltration into atrial myocardium was similar in the vehicle and RLX treated groups.</AbstractText>Treatment with RLX in mice after MI reduces susceptibility to AF due to anti-inflammatory and anti-fibrotic properties. Because to these favorable actions, RLX may become a new therapeutic option in the treatment of AF, even when complicating MI.</AbstractText>Copyright © 2017 Elsevier Inc. All rights reserved.</CopyrightInformation> |
20,397 | The influence of sex and age on ventricular arrhythmia in a population-based registry. | Post-hoc analyses of clinical trials and population-based studies have shown no difference in mortality between men and women, but often show that men are more likely to receive appropriate ICD therapy. We utilized a population-based registry to investigate the interaction of sex and age and the occurrence of ventricular arrhythmia in an ICD population.</AbstractText>A total of 776 consecutive patients receiving an ICD for primary or secondary prevention in a provincial ICD registry were studied. No significant mortality difference was found between men and women (27.5% versus 23.7%, p=0.39). Overall, men were more likely to receive appropriate ICD therapy compared to women (39.3% versus 26.7%, p=0.006). The hazard ratio for appropriate therapy in men vs. women <60years of age was 3.22, CI 95% (1.56-6.65), p=0.002, and the same comparison in men vs. women over the age of 60 showed no significant difference (HR 1.11, CI 95% [0.74-1.65], p=0.61). This interaction between age and sex remained significant when adjusted for New York Heart Associated Class, ejection fraction, coronary artery disease and indication for ICD (p=0.02).</AbstractText>This study demonstrates that the risk of appropriate ICD therapy increases as women are older, reaching similar risk as men in that age group. Further study of the mechanism of the interaction of age and sex as they modulate the occurrence of ventricular arrhythmia may be warranted.</AbstractText>Copyright © 2017 Elsevier B.V. All rights reserved.</CopyrightInformation> |
20,398 | Lifelong arrhythmic risk stratification in arrhythmogenic right ventricular cardiomyopathy: distribution of events and impact of periodical reassessment. | The arrhythmic risk stratification of arrhythmogenic right ventricular cardiomyopathy (ARVC) remains controversial. We evaluated the long-term distribution of life-threatening arrhythmic events assessing the impact of periodical risk reassessment.</AbstractText>Ninety-eight ARVC patients with no previous major ventricular arrhythmias were retrospectively analysed. Patients were assessed at baseline, at 22 [inter-quartile range (IQR) 16-26], 49 (IQR 41-55) and 97 months (IQR 90-108). The primary endpoint was a composite of sudden cardiac death, ventricular fibrillation, sustained ventricular tachycardia or appropriate implanted cardioverter-defibrillator intervention. During a median follow-up of 91 months (IQR 34-222) 28 patients (29%) experienced the composite endpoint. The median time for the primary event was 35 months (IQR 18-86 months), and 39% of events occurred beyond 49 months of follow-up. History of syncope (HR 4.034; 95% CI, 1.488 to 10.932; P-value = 0.006), non-sustained ventricular tachycardia (NSVT; HR 3.534; 95% CI 1.265-9.877; P-value = 0.016), premature ventricular contractions (PVC) >1000/24h (HR 2.761; 95% CI 1.120-6.807; P-value = 0.027), and right ventricular fractional area change (RVFAC; HR 0.945; 95% CI 0.906-0.985; P-value = 0.008) were found as independent predictors at baseline multivariate analysis. Nevertheless, when the prognostic impact of each variable was reassessed overtime only NSVT (HR 3.282; 95% CI, 1.122 to 9.598, P-value = 0.023) and RVFAC (HR 0.351, 95% CI, 0.157 to 0.780; P-value = 0.010) remained independent predictors throughout the whole follow-up.</AbstractText>In our cohort of ARVC patients only NSVT and RVFAC maintained their independent prognostic impact in predicting arrhythmic events during the long-term follow-up. Periodical re-assessment of risk in these patients is strongly recommended.</AbstractText> |
20,399 | Noninvasive evaluation of reverse atrial remodeling after catheter ablation of atrial fibrillation by P wave dispersion. | Atrial fibrillation (AF) itself creates structural and electrophysiological changes such as atrial enlargement, shortening of refractory period and decrease in conduction velocity, called "atrial remodeling", promoting its persistence. Although the remodeling process is considered to be reversible, it has not been elucidated in detail. The aim of this study was to assess the feasibility of P wave dispersion in the assessment of reverse atrial remodeling following catheter ablation of AF. Consecutive 126 patients (88 males, age 63.0 ± 10.4 years) who underwent catheter ablation for paroxysmal AF were investigated. P wave dispersion was calculated from the 12 lead ECG before, 1 day, 1 month, 3 months and 6 months after the procedure. Left atrial diameter (LAD), left atrial volume index (LAVI), left ventricular ejection fraction (LVEF), transmitral flow velocity waveform (E/A), and tissue Doppler (E/e') on echocardiography, plasma B-type natriuretic peptide (BNP) concentrations, serum creatinine, and estimated glomerular filtration rate (eGFR) were also measured. Of all patients, 103 subjects remained free of AF for 1 year follow-up. In these patients, P wave dispersion was not changed 1 day and 1 month after the procedure. However, it was significantly decreased at 3 and 6 months (50.1 ± 14.8 to 45.4 ± 14.4 ms, p < 0.05, 45.2 ± 9.9 ms, p < 0.05, respectively). Plasma BNP concentrations, LAD and LAVI were decreased (81.1 ± 103.8 to 44.8 ± 38.3 pg/mL, p < 0.05, 38.2 ± 5.7 to 35.9 ± 5.6 mm, p < 0.05, 33.3 ± 14.2 to 29.3 ± 12.3 mL/m<sup>2</sup>, p < 0.05) at 6 months after the procedure. There were no significant changes in LVEF, E/A, E/e', serum creatinine, and eGFR during the follow up period. P wave dispersion was decreased at 3 and 6 months after catheter ablation in patients without recurrence of AF. P wave dispersion is useful for assessment of reverse remodeling after catheter ablation of AF. |
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