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7,600 | Epicardial wavefronts arise from widely distributed transient sources during ventricular fibrillation in the isolated swine heart. | It has been proposed that VF waves emanate from stable localized sources, often called "mother rotors." However, evidence for the existence of these rotors is conflicting. Using a new panoramic optical mapping system that can image nearly the entire ventricular epicardium, we recently excluded epicardial mother rotors as the drivers of Wiggers' stage II VF in the isolated swine heart. Furthermore, we were unable to find evidence that VF requires sustained intramural sources. The present study was designed to test the following hypotheses: 1. VF is driven by a specific region, and 2. Rotors that are long-lived, though not necessarily permanent, are the primary generators of VF wavefronts. Using panoramic optical mapping, we mapped VF wavefronts from 6 isolated swine hearts. Wavefronts were tracked to characterize their activation pathways and to locate their originating sources. We found that the wavefronts that participate in epicardial reentry were not confined to a compact region; rather they activated the entire epicardial surface. New wavefronts feeding into the epicardial activation pattern were generated over the majority of the epicardium and almost all of them were associated with rotors or repetitive breakthrough patterns that lasted for less than 2 s. These findings indicate that epicardial wavefronts in this model are generated by many transitory epicardial sources distributed over the entire surface of the heart. |
7,601 | The influence of myocardial substrate on ventricular fibrillation waveform: a swine model of acute and postmyocardial infarction. | In cardiac arrest resulting from ventricular fibrillation, the ventricular fibrillation waveform may be a clue to its duration and predict the likelihood of shock success. However, ventricular fibrillation occurs in different myocardial substrates such as ischemia, heart failure, and structurally normal hearts. We hypothesized that ventricular fibrillation is altered by myocardial infarction and varies from the acute to postmyocardial infarction periods.</AbstractText>An animal intervention study was conducted with comparison to a control group.</AbstractText>This study took place in a university animal laboratory.</AbstractText>Study subjects included 37 swine.</AbstractText>Myocardial infarction was induced by occlusion of the midleft anterior descending artery. Ventricular fibrillation was induced in control swine, acute myocardial infarction swine, and in postmyocardial infarction swine after a 2-wk recovery period.</AbstractText>Ventricular fibrillation was recorded in 11 swine with acute myocardial infarction, ten postmyocardial infarction, and 16 controls. Frequency (mean, median, dominant, and bandwidth) and amplitude-related content (slope, slope-amp [slope divided by amplitude], and amplitude-spectrum area) were analyzed. Frequencies at 5 mins of ventricular fibrillation were altered in both acute myocardial infarction (p < .001 for all frequency characteristics) and postmyocardial infarction swine (p = .015 for mean, .002 for median, .002 for dominant frequency, and <.001 for bandwidth). At 5 mins, median frequency was highest in controls, 10.9 +/- .4 Hz; lowest in acute myocardial infarction, 8.4 +/- .5 Hz; and intermediate in postmyocardial infarction, 9.7 +/- .5 Hz (p < .001 for acute myocardial infarction and p = .002 for postmyocardial infarction compared with control). Slope and amplitude-spectrum area were similar among the three groups with a shallow decline after minute 2, whereas slope-amp remained significantly altered for acute myocardial infarction swine at 5 mins (p = .003).</AbstractText>Ventricular fibrillation frequencies depend on myocardial substrate and evolve from the acute through healing phases of myocardial infarction. Amplitude related measures, however, are similar among these groups. It is unknown how defibrillation may be affected by relying on the ventricular fibrillation waveform without considering myocardial substrate.</AbstractText> |
7,602 | Predictors of major postoperative cardiac complications in a surgical ICU. | Cardiovascular complications are associated with increased mortality and morbidity during the postoperative period, resulting in longer hospital stay and higher treatment costs.</AbstractText>The aim of this study was to identify predictors of major postoperative cardiac complications.</AbstractText>187 patients undergoing noncardiac surgery, admitted to a surgical intensive care unit (ICU) between November 2004 and April 2005. Variables recorded were age, gender, American Society of Anesthesiologists (ASA) physical status, type and magnitude of surgery, mortality, ICU and hospital length of stay (LOS), Simplified Acute Physiology Score II (SAPS II), cardiac troponin I (cTnI) at postoperative day 0, 1, 2 and 3, history of hypertension, hyperlipidemia, Revised Cardiac Risk Index (RCRI) score, major cardiac events (MCE): acute myocardial infarction (AMI), pulmonary edema (PE), ventricular fibrillation (VF) or primary cardiac arrest (PCA). Correlations between variables and MCE were made by univariate analysis by simple logistic regression with odds ratio (OR) and 95% confidence interval (95% CI).</AbstractText>Total of 14 MCE: 9 AMI, 1 VF, 4 PE. Significant risk factors for MCE were high-risk surgery (OR 8.26, 95% CI 1.76-38.85, p = 0.008), RCRI > or = 2 (OR 4.0, 95% CI 1.22-13.16, p = 0.022), admission cTnI (OR 1.46, 95% CI 1.07-1.99, p = 0.018); day 1 cTnI (OR 1.75, 95% CI 1.27-2.41, p = 0.001); day 2 cTnI (OR 2.23, 95% CI 1.24-3.98, p = 0.007), SAPS II (OR 1.08, 95% CI 1.04-1.12, p < 0.001). Patients with MCE had longer ICU LOS (19.1 +/- 19.3 days against 3.4 +/- 4.9) (OR 1.15, 95% CI 1.08-1.22, p < 0.001) and higher ICU mortality (21.4% versus 4.6%) (OR 5.63, 95% CI 1.31-24.23, p = 0.02) in the ICU.</AbstractText>High-risk surgery, RCRI > or = 2, cTnI levels and SAPS II were predictors of postoperative MCE. Patients with MCE had longer ICU stay and higher mortality rate.</AbstractText> |
7,603 | Fever-induced QTc prolongation and ventricular arrhythmias in individuals with type 2 congenital long QT syndrome. | Type 2 congenital long QT syndrome (LQT-2) is linked to mutations in the human ether a-go-go-related gene (HERG) and is characterized by rate-corrected QT interval (QTc) prolongation, ventricular arrhythmias, syncope, and sudden death. Recognized triggers of these cardiac events include emotional and acoustic stimuli. Here we investigated the repeated occurrence of fever-induced polymorphic ventricular tachycardia and ventricular fibrillation in 2 LQT-2 patients with A558P missense mutation in HERG. ECG analysis showed increased QTc with fever in both patients. WT, A558P, and WT+A558P HERG were expressed heterologously in HEK293 cells and were studied using biochemical and electrophysiological techniques. A558P proteins showed a trafficking-deficient phenotype. WT+A558P coexpression caused a dominant-negative effect, selectively accelerated the rate of channel inactivation, and reduced the temperature-dependent increase in the WT current. Thus, the WT+A558P current did not increase to the same extent as the WT current, leading to larger current density differences at higher temperatures. A similar temperature-dependent phenotype was seen for coexpression of the trafficking-deficient LQT-2 F640V mutation. We postulate that the weak increase in the HERG current density in WT-mutant coassembled channels contributes to the development of QTc prolongation and arrhythmias at febrile temperatures and suggest that fever is a potential trigger of life-threatening arrhythmias in LQT-2 patients. |
7,604 | Left atrial systolic force in hypertensive patients with left ventricular hypertrophy: the LIFE study. | In hypertensive patients without prevalent cardiovascular disease, enhanced left atrial systolic force is associated with left ventricular hypertrophy and increased preload. It also predicts cardiovascular events in a population with high prevalence of obesity. Relations between left atrial systolic force and left ventricular geometry and function have not been investigated in high-risk hypertrophic hypertensive patients. Participants in the Losartan Intervention For Endpoint reduction in hypertension echocardiography substudy without prevalent cardiovascular disease or atrial fibrillation (n = 567) underwent standard Doppler echocardiography. Left atrial systolic force was obtained from the mitral orifice area and Doppler mitral peak A velocity. Patients were divided into groups with normal or increased left atrial systolic force (>14.33 kdyn). Left atrial systolic force was high in 297 patients (52.3%), who were older and had higher body mass index and heart rate (all P < 0.01) but similar systolic and diastolic blood pressure, in comparison with patients with normal left atrial systolic force. After controlling for confounders, increased left atrial systolic force was associated with larger left ventricular diameter and higher left ventricular mass index (both P < 0.01). Prevalence of left ventricular hypertrophy was greater (84 vs. 64%; P < 0.001). Participants with increased left atrial systolic force exhibited normal ejection fraction; higher stroke volume, cardiac output, transmitral peak E velocities and peak A velocities; and lower E/A ratio (all P < 0.01). Enhanced left atrial systolic force identifies hypertensive patients with greater left ventricular mass and prevalence of left ventricular hypertrophy, but normal left ventricular chamber systolic function with increased transmitral flow gradient occurring during early filling, consistent with increased preload. |
7,605 | Circulating homocysteine levels in patients with radiofrequency catheter ablation for atrial fibrillation. | This study investigated the potential association between homocysteine levels and cardiovascular events or atrial fibrillation (AF) recurrence following radiofrequency catheter ablation (RFCA) in patients with AF.</AbstractText>Blood samples were obtained prior to the RFCA procedure. Levels of homocysteine and carboxy-terminal telopeptide of collagen type I (CITP), a collagen type I degradation marker, were measured in 96 patients receiving RFCA; 62 paroxysmal or persistent AF patients and 34 paroxysmal supra-ventricular tachycardia patients. Patients were followed up for 2.1 +/- 1.5 years. Plasma homocysteine levels were significantly higher in patients with persistent AF (P < 0.05) compared with levels in paroxysmal AF and control patients. Homocysteine levels also positively correlated with left atrial dimension (LAD) (P < 0.01) and CITP levels (P < 0.001). While no significant correlation was found between basal homocysteine levels and recurrent AF after RFCA in AF patients, patients in the high homocysteine group exhibited a significantly higher rate of cardiovascular events without AF recurrence compared with those in the low homocysteine group (P < 0.05).</AbstractText>High homocysteine levels are associated with the presence of persistent AF, which is accompanied by increased CITP levels and LAD. Also confirmed is the role of homocysteine as a risk factor for the pathogenesis of cardiovascular events after RFCA in AF patients. Measurement of homocysteine level may provide useful information for the managing cardiovascular risk in patients with AF.</AbstractText> |
7,606 | Echocardiographic assessment of left ventricular diastolic function and filling pressure in atrial fibrillation. | Diastolic dysfunction has been linked to 2 epidemics: atrial fibrillation (AF) and heart failure. The presence and severity of diastolic dysfunction are associated with an increased risk for first AF and first heart failure in patients with sinus rhythm. Furthermore, the risk for heart failure is markedly increased once AF develops. The evaluation of diastolic function once AF has developed remains a clinical challenge. The conventional use of Doppler echocardiography for the assessment and grading of diastolic dysfunction relies heavily on evaluating the relation of ventricular and atrial flow characteristics. The mechanical impairment of the left atrium and the variable cycle lengths in AF render the evaluation of diastolic function difficult. A few Doppler echocardiographic methods have been proved clinically useful for the estimation of diastolic left ventricular filling pressures in AF, but these appear to be underutilized. Several innovative methods are emerging that promise to provide greater precision in diastolic function assessment, but their clinical utility in AF remains to be established. In conclusion, this review provides an up-to-date discussion of the evaluation of diastolic function assessment in AF and how it may be important in the clinical management of patients with AF. |
7,607 | Review article: Adenosine use in the emergency department. | To perform a review of the efficacy of adenosine, including its potential role as first-line treatment in unstable supraventricular tachycardia (SVT) and its use in wide complex tachycardias and diagnosing difficult arrhythmias. The dose and administration, nature and frequency of side-effects and relevant interactions and dosage adjustments are also discussed.</AbstractText>A search of the Medline database from 1950 to 2007 and the Embase Database from 1974 to 2007 was carried out. A manual search was performed of references of each article.</AbstractText>Adenosine is efficacious at treating stable SVT, but it is no more effective than cheaper alternatives. It has a possible role in the first-line treatment of unstable SVT and is generally safe and effective when used to treat and/or diagnose wide complex tachycardias. There is a small risk of inducing serious arrhythmias, such as prolonged atrioventricular blockade and ventricular fibrillation. There is evidence that recommended initial doses for infants might be too low, but initial doses for children and adults are adequate. There is evidence that central venous administration requires lower doses, but there are no studies addressing peripheral sites of administration and size of flush. Minor and self-limiting side-effects are common. The need for dosage adjustments in the presence of interacting medications is well documented, but no studies have addressed how to rationally effect these adjustments.</AbstractText>There is extensive evidence showing adenosine to be efficacious at treating SVT, but no more efficacious than cheaper alternatives. More studies are required to investigate other areas of adenosine use.</AbstractText> |
7,608 | The prognostic significance of serum glucose levels after the onset of ventricular arrhythmia on in-hospital mortality of patients with acute coronary syndrome. | Several studies have illustrated the role played by serum glucose levels in cardiovascular morbidity and mortality in general and, more particularly, after an acute coronary event.</AbstractText>The aim of this study was to evaluate the impact of serum potassium and glucose levels on in-hospital mortality in patients with ischemic heart disease, who exhibited severe ventricular arrhythmia.</AbstractText>We enrolled 162 consecutive patients who were referred to our institution for an acute coronary event and presented with sustained ventricular tachycardia or ventricular fibrillation during the first 24 hours of hospitalization. Serum potassium and glucose levels were measured in all patients at the onset of tachycardia and after 2, 4, 6, 12, 36, 48 hours.</AbstractText>During hospitalization, 23 out of 162 patients died (61% males). Serum glucose levels at the onset of the arrhythmia, as well as after 2, 12, 36 and 48 hours, were higher in the deceased (onset: 228.8 +/- 108 vs. 158 +/- 68 mg/dl, p = 0.0001, 2 h: 182 +/- 109 vs. 149 +/- 59 mg/dl, p = 0.03, 12 h: 155.5 +/- 72 vs. 128 +/- 48 mg/dl, p = 0.025, 36 h: 163.8 +/- 63 vs.116 +/- 42 mg/dl, p = 0.002, and 48 h: 138 +/- 64 vs. 122 +/- 42 mg/dl, p = 0.05, respectively), even after adjustment for age, sex, diabetes, left ventricular ejection fraction, type of acute coronary syndrome and site of infarction and medication intake. There was no difference in serum potassium levels between the deceased and survivors.</AbstractText>Serum glucose levels at the onset of arrhythmia and 2, 36 and 48 hours later seem to have prognostic significance for in-hospital mortality in patients hospitalized for an acute coronary event, who exhibit severe ventricular arrhythmia.</AbstractText> |
7,609 | Vernakalant: pharmacology electrophysiology, safety and efficacy. | The development of new antiarrhythmic agents for the treatment of atrial fibrillation is advancing simultaneously on several fronts. The molecular structure of existing agents such as amiodarone is being modified in an attempt to improve safety and reduce adverse effects. Similarly, atrial-selective antiarrhythmic drugs are being developed to minimize the occurrence of ventricular proarrhythmia. One of these atrial-selective compounds is vernakalant, which has demonstrated efficacy in terminating atrial fibrillation when given intravenously. In addition, preliminary data suggest that it could also suppress recurrences when used orally. This paper reviews the pharmacology, electrophysiology, efficacy and safety of intravenous and oral vernakalant. |
7,610 | [Electroanatomical mapping systems in catheter ablation of cardiac arrhythmias]. | Due to the recent technical development of the past years, most cardiac electrophysiological laboratories are equipped with computer-based electroanatomical mapping systems that precisely describe both the temporal and spatial characteristics of cardiac activation. This development has also been driven by the need for increased accuracy in arrhythmia localization as required for catheter ablation. Computer-based electroanatomical mapping systems are able to reconstruct cardiac anatomy and provide a straightforward representation of chamber activation. These systems capture and display details of intracardiac physiology and mark the site of interventions. Nowadays, several mapping technologies are available in the electrophysiological labs: CARTO XP, EnSite NavX and Array, Real-time Position Management. In this paper we aim to briefly present the principal technological and practical characteristics of these mapping systems regarding eligibility, ability and limitations. The development of computer-based mapping technologies is also discussed in detail, since future systems will be able to display any parametric process including vectors, strains, contraction patterns etc., a wide variety of physiologic parameters beyond activation times and voltage. Using electroanatomical mapping systems, the specific recording of both anatomy and physiology has contributed substantially to the expansion of ablation to atypical atrial flutters, ventricular tachycardia, congenital heart-disease-related arrhythmias and atrial fibrillation. While the technology is already facilitating, the obvious down-side to this technological explosion is cost. Subsequent studies will be needed, however, to show that this translates into improved outcomes and cost savings. |
7,611 | Automated external cardioversion defibrillation monitoring in cardiac arrest: a randomized trial. | In-hospital cardiac arrest has a poor prognosis despite active electrocardiography monitoring. The initial rhythm of approximately 25% of in-hospital cardiopulmonary resuscitation (CPR) events is pulseless ventricular tachycardia/ventricular fibrillation (VT/VF). Early defibrillation is an independent predictor of survival in CPR events caused by VT/VF. The automated external cardioverter defibrillator (AECD) is a device attached by pads to the chest wall that monitors, detects, and within seconds, automatically delivers electric countershock to an appropriate tachyarrhythmia.</AbstractText>To evaluate safety of AECD monitoring in hospitalized patients. To evaluate whether AECDs provide earlier defibrillation than hospital code teams.</AbstractText>The study is a prospective trial randomizing patients admitted to the telemetry ward to standard CPR (code team) or standard CPR plus AECD monitoring (PowerHeart CRM). The AECD is programmed to deliver one 150 J biphasic shock to patients in sustained VT/VF. Data is collected using the Utstein criteria for cardiac arrest. The primary endpoint is time-to-defibrillation; secondary outcomes include neurological status and survival to discharge, with 3-year follow-up.</AbstractText>To date, 192 patients have been recruited in the time period between 10/10/2006 to 7/20/2007. A total of 3,655 hours of telemetry data have been analyzed in the AECD arm. The AECD has monitored ambulatory telemetry patients in sinus rhythm, sinus tachycardia, supraventricular tachycardia, atrial flutter or fibrillation, with premature ventricular complexes and non-sustained VT without delivery of inappropriate shocks. One patient experienced sustained VT during AECD monitoring, who was successfully defibrillated (17 seconds after meeting programmed criteria). There are no events to report in the control arm. The patient survived the event without neurological complications. During the same time period, mean time to shock for VT/VF cardiac arrest occurring outside the telemetry ward was 230 +/- 50 seconds.</AbstractText>AECD monitoring is safe and likely results in earlier defibrillation than standard telemetry monitoring.</AbstractText>National Institutes of Health registration ID: NCT00382928.</AbstractText> |
7,612 | Impact of left atrial volume reduction concomitant with atrial fibrillation surgery on left atrial geometry and mechanical function. | Left atrial geometry and mechanical functions exert a profound effect on left ventricular filling and overall cardiovascular performance. We sought to investigate the perioperative factors that influence left atrial geometry and mechanical functions after the Maze procedure in patients with refractory atrial fibrillation and left atrial enlargement.</AbstractText>Seventy-four patients with atrial fibrillation and left atrial enlargement (diameter > or = 60 mm) underwent the Maze procedure in association with mitral valve surgery. The maximum left atrial volume and left atrial mechanical functions (booster pump, reservoir, and conduit function [%]) were calculated from the left atrial volume-cardiac cycle curves obtained by magnetic resonance imaging. A stepwise multiple regression analysis was performed to determine the independent variables that influenced the postoperative left atrial geometry and function.</AbstractText>The multivariate analysis showed that left atrial reduction surgery concomitant with the Maze procedure and the postoperative maintenance of sinus rhythm were predominant independent variables for postoperative left atrial geometry and mechanical functions. Among the 58 patients who recovered sinus rhythm, the postoperative left atrial geometry and function were compared between patients with (VR group) and without (control group) left atrial volume reduction. At a mean follow-up period of 13.8 months, sinus rhythm recovery rate was better (85% vs 68%, P < .05) in the VR group and maximum left atrial volume was less (116 +/- 25 mL vs 287 +/- 73 mL, P < .001) than in the control group. The maximum left atrial volume reduced with time only in the VR group (reverse remodeling). Postoperative booster pump and reservoir function in the VR group were better than in the control group (25% +/- 6% vs 11% +/- 4% and 34% +/- 7% vs 16% +/- 4%, respectively, P < .001), whereas the conduit function in the VR group was lower than in the control group, indicating that the improvement of the booster pump and reservoir function compensated for the conduit function to left ventricular filling.</AbstractText>Left atrial reduction concomitant with the Maze procedure helped restore both contraction (booster pump) and compliance (reservoir) of the left atrium and facilitated left atrial reverse remolding. Left atrial volume reduction and postoperative maintenance of sinus rhythm may be desirable in patients with refractory AF and left atrial enlargement.</AbstractText> |
7,613 | [Cell therapy and arrhythmias: state of the art]. | Cell therapy is an adjunctive treatment to improve left ventricular function after myocardial injury. Multiple cell types have been tested experimentally in animal models of myocardial disease, with functional improvement as the primary endpoint. Regarding safety, the major concern has been that cell transplantation could generate an arrhythmogenic substrate as reported in clinical studies using myoblasts. The mechanism of these transplantation-related arrhythmias remains elusive but the cellular heterogeneity, resulting from differences in electrical membrane properties between recipient/donor cells, could provide a substrate for reentry circuits. The knowledge achieved from experimental studies on the substrate of arrhythmias in cell therapy gives useful information that could be translated into the development of a biological pacemaker or a non-pharmacological approach to atrial fibrillation. Limitations of current pharmacological and catheter ablation options to achieve rate control in patients with atrial fibrillation have motivated new strategies of cell therapy for non-pharmacological rate control without producing high-degree atrioventricular block. Although several issues remain to be addressed, some aspects of cell therapy are likely to be translated into clinical practice. |
7,614 | Does cardiac resynchronisation therapy improve survival and quality of life in patients with end-stage heart failure? | A best evidence topic in cardiac surgery was written according to a structured protocol. The question addressed was whether bi-ventricular pacing, also referred to as cardiac resynchronisation therapy (CRT), improves survival and quality of life in patients with severe (NYHA III/IV) symptomatic heart failure. Cardiac pacing can be achieved by stimulation of the right ventricle, left ventricle (LV) or by bi-ventricular pacing. This best evidence topic considers only bi-ventricular pacing. This involves placement of pacing leads in the right ventricle, epicardially on the LV with a lead typically placed in a branch of the coronary sinus and, unless the patient is in permanent atrial fibrillation, in the right atrium. Bi-ventricular pacing allows the optimisation of atrio-ventricular timing and resynchronisation of septal and postero-lateral left ventricular contraction. Symptomatic heart failure has a high morbidity and a poor prognosis. Patients with dyspnoea at rest or on minimal exertion (NYHA III/IV) are at high risk of death due to progressive heart failure, while those with less severe symptoms are more likely to experience sudden cardiac death. Up to 50% of patients with NYHA class III/IV symptoms have a prolonged QRS duration (>120 ms) on 12-lead ECG (usually in a LBBB pattern). This intra-ventricular conduction delay is a surrogate marker of mechanical dyssynchrony (an uncoordinated regional contraction-relaxation pattern) and is associated with reduced cardiac output and increased mortality. Bi-ventricular pacing can reduce the delay in activation of the LV free wall found in many patients with LV systolic dysfunction, thereby improving mechanical synchrony and cardiac output. It may also reduce pre-systolic mitral regurgitation. Three hundred and fifty-six papers were identified using the search method outlined, nine randomised controlled trials and a meta-analysis in addition to published guidelines presented the best evidence to answer the clinical question. Current best available evidence suggests that in patients with left ventricular systolic dysfunction (LVEF </=35%), prolonged QRS duration (QRS >or=120 ms), and NYHA class III or IV symptoms despite optimal pharmacological therapy, bi-ventricular pacing significantly reduces the number of hospitalisations from heart failure, improves functional status (NYHA class, peak oxygen uptake and exercise tolerance) and improves health related quality of life. The CARE-HF study also demonstrated a reduction in mortality from progressive heart failure and all-cause mortality. |
7,615 | Heart-brain interactions in cardiac arrhythmias: role of the autonomic nervous system. | The autonomic nervous system plays an important role in the genesis of ventricular arrhythmias and sudden cardiac death. Evidence is substantial for a neural component in sudden cardiac death. Sympathetic nerve sprouting and regional myocardial hyperinnervation following myocardial injury promote cardiac arrhythmia and sudden cardiac death through several potential mechanisms. Modulating autonomic tone is a potential method to reduce the risk of ventricular arrhythmias. Thoracic spinal cord stimulation is showing promise as a treatment for refractory angina. In addition, spinal cord stimulation has protected against ventricular tachycardia/ventricular fibrillation in animal models of postinfarction heart failure. |
7,616 | Significance of morphological and electrophysiological left ventricular restoration in idiopathic dilated cardiomyopathy. | Treatment of non-ischemic dilated cardiomyopathy (NIDCM) remains a challenge. Morphological left ventricular (LV) restoration such as septal anterior ventricular exclusion (SAVE) can be effective in treating NIDCM; however, residual electrophysiological disorders such as atrioventricular and intraventricular conduction disturbances become apparent in the form of atrial fibrillation (AF) and LV dyssynchrony, which deteriorate postoperative LV function. Thus, the combination of morphological and electrophysiological LV restoration may further improve LV function. Here, we report the case of a patient with end-stage NIDCM complicated with AF and LV dyssynchrony, who was successfully treated with the combined use of SAVE, undersized mitral annuloplasty, left atrial (LA) Maze procedure with cryoablation, and postoperative biventricular pacing. This combination treatment was beneficial in restoring the sinus rhythm and LA and LV functions with improved and synergic wall motion by excluding the dyskinetic/akinetic area, downsizing the LV, resolving mitral regurgitation, and optimizing conduction and rhythm abnormalities. Notably, biventricular pacing was shown to be effective in resolving residual dyssynchrony between the septum and lateral wall after SAVE, wherein a firm, non-compliant Dacron patch was sutured to the septum. |
7,617 | A comprehensive approach to management of ventricular arrhythmias. | This review presents five cases that highlight the complexity of taking care of patients with ventricular arrhythmias. Three of the cases discuss management of patients with nonsustained ventricular tachycardia in the setting of structural heart disease: dilated cardiomyopathy, hypertrophic cardiomyopathy, and after myocardial infarction. A fourth case asks whether data from implantable cardioverter defibrillator (ICD) trials can be extrapolated to older patients, and the fifth case discusses management of recurrent ventricular arrhythmias in a patient with an ICD. |
7,618 | Role of ablation therapy in ventricular arrhythmias. | Catheter ablation is an effective therapy for symptomatic ventricular arrhythmia (VA) in patients with and without structural heart disease. It is the treatment of choice to cure or reduce recurrent VA in patients who have an implantable cardioverter defibrillator and can be a life-saving procedure in patients who have electrical storm. Catheter ablation for VAs remains a challenging procedure and requires a precise understanding of cardiac electrophysiology, the arrhythmia mechanisms, and mapping techniques. Various mapping techniques such as pace mapping, activation mapping, entrainment mapping, and substrate mapping are used. These techniques complement each other in localizing the critical isthmus of a reentrant VT or the source of origin of a focal VT. Most VAs can be ablated endocardially. Epicardial ablation is needed for VAs with an epicardial circuit or a focal source. |
7,619 | Problems with implantable cardiac device therapy. | Implantable cardioverter-defibrillators (ICDs) improve survival in patients who have left ventricular dysfunction; however, they are associated with numerous problems at implant and during follow-up. The diagnosis and management of these problems is usually straightforward, but more difficult problems may include the management of patients who have elevated energy requirements to terminate ventricular fibrillation or of those who have postoperative device infections. Long-term issues in ICD patients include the occurrence of inappropriate or frequent appropriate shocks. ICD generators and leads are more prone to failures than are pacing systems alone; management of patients potentially dependent on "recalled" devices to deliver life-saving therapy is a particularly complex issue. The purpose of this article is to review the diagnosis and management of these more troublesome ICD problems. |
7,620 | Use of traditional and biventricular implantable cardiac devices for primary and secondary prevention of sudden death. | Sudden cardiac death is the leading cause of cardiac mortality, particularly among high-risk populations with known left ventricular systolic dysfunction. Multiple randomized clinical trials demonstrated a significant mortality benefit of the implantable cardioverter defibrillator (ICD) compared with antiarrhythmic drug therapy or standard medical care. Initial ICD trials showed a mortality improvement for patients who previously had experienced aborted sudden cardiac death or sustained ventricular tachycardia (secondary prevention). Primary prevention trials in selected high-risk patients who had both ischemic and nonischemic cardiomyopathy also demonstrated a mortality benefit associated with ICD treatment. More recently, cardiac resynchronization therapy with or without defibrillator capability has been shown to reduce morbidity and mortality among advanced heart failure patients with a prolonged QRS duration. |
7,621 | Role of drug therapy for sustained ventricular tachyarrhythmias. | Antiarrhythmic drug therapy, broadly defined, is the mainstay of treatment and prevention of ventricular tachycardia (VT)/ventricular fibrillation (VF), which can lead to sudden death. This article evaluates the evidence for and appropriate use of class I antiarrhythmic drugs, class III antiarrhythmic drugs, beta-blockers, nondihydropyridine calcium-channel blockers, statins, angiotensin enzyme inhibitors, angiotensin receptor blockers, aldosterone blockers, and digoxin for antiarrhythmic benefits in patients who have a propensity for VT/VF and therefore are at risk of sudden death. |
7,622 | Dose-dependent influence of two-week administration of simvastatin and metoprolol injection on the blood pressure in normocholesterolemic rats. | Beta-blockers are widely used in clinical practice. It is connected with their multiple cardiac effects: slowing heart rate, decrease of myocardial contractility and lowering of systemic blood pressure. Early use of beta-blocker in acute myocardial infarction reduces the risks of reinfarction and ventricular fibrillation. However, the above effects may be associated with the risk of cardiogenic shock. Many patients with cardiovascular diseases receiving beta-blockers are recommended to statin therapy, as well. There are several reports indicating that statins have beneficial cardiovascular effects through their broad spectrum of cholesterol-independent action. It has been revealed that statins could decrease blood pressure, as well. The aim of the study was to evaluate the influence of simvastatin in different doses and metoprolol injection on the blood pressure in normocholesterolemic rats. The experiments were performed on Wistar rats, outbred males. Simvastatin at 1, 10 and 20 mg/kg or vehicle (0.2% methylcellulose) were given intragastrically during two-week period. After two week simvastatin administration, rats were injected intraperitoneally with metoprolol at 5 mg/kg b. w. The arterial blood pressure signals were provided by Isotec pressure transducer connected to a direct current bridge amplifier and catheter was implanted into the right carotid artery.</AbstractText>Two week administration of simvastatin in different doses to normocholesterolaemic rats does not modify metoprolol impact on the blood pressure.</AbstractText> |
7,623 | Atrial and ventricular fibrosis induced by atrial fibrillation: evidence to support early rhythm control. | Atrial fibrillation (AF) with poorly controlled ventricular response is known to be detrimental to ventricular function, conversely, heart failure (HF) increases susceptibility to AF.</AbstractText>This study sought to examine the electropathological effects of 3 months of atrial fibrillation (AF) in dogs with and without concomitant ventricular dysfunction.</AbstractText>Three groups of dogs were studied: dogs with chronic AF induced by rapid pacing and concomitant ventricular dysfunction induced by rapid ventricular response with intact atrioventricular node (AVN), dogs with ablated AVN and AF while the ventricle was paced at 80 beats/min, and normal sham dogs. After 3 months of AF, the first 2 groups underwent direct current cardioversion (DCCV) to normal sinus rhythm and were monitored for 3 months, followed by retesting of AF susceptibility. Tissue fibrosis was assessed at various sites by trichrome staining and quantitative immunohistochemistry.</AbstractText>AF was induced within 12 +/- 4 days and 30 +/- 13 days, respectively, in the intact and ablated AVN groups (P <.01). After 3 months of AF, left ventricular ejection fraction was 30.4% +/- 10.1% and 55% +/- 5% in the intact and ablated AVN groups (P <.01), respectively. After 3 months of normal sinus rhythm, AF was reinduced after 4 +/- 2 and 7.2 +/- 2 days, respectively (P = NS). There were no regional differences and an abundance of fibrosis within atria. Atrial fibrosis was significantly increased in intact AVN versus ablated AVN and sham groups, and also was greater in AVN-ablated versus sham dogs. Ventricular fibrosis was increased in intact AVN versus ablated AVN and sham groups and was not significantly different in ablated AVN and sham groups.</AbstractText>AF without ventricular dysfunction results in atrial fibrosis and increased susceptibility to AF, suggesting that AF alone causes atrial fibrosis. AF with rapid ventricular response further increases atrial and ventricular fibrosis. Conversion to normal sinus rhythm should be done as early as possible to avoid atrial and ventricular fibrosis and increased susceptibility to AF.</AbstractText> |
7,624 | Common beta-adrenergic receptor polymorphisms are not associated with risk of sudden cardiac death in patients with coronary artery disease. | Previous studies suggest that beta-adrenergic receptor (betaAR) single nucleotide polymorphisms (SNPs) are associated with out-of-hospital sudden cardiac death (SCD) and overall mortality, but did not specifically examine risk of ventricular arrhythmias (VA).</AbstractText>This study examined the effects of functional SNPs of beta1AR and beta2AR on the risk of VA and SCD in patients with coronary artery disease (CAD).</AbstractText>beta1AR (Ser49Gly, Arg389Gly) and beta2AR (Gly16Arg, Gln27Glu) SNPs were genotyped in a case-control study comparing 107 patients with CAD and aborted SCD due to VA with 287 CAD control subjects and 101 healthy control subjects. These variants were also examined in the Heart and Estrogen Replacement Study (HERS) cohort of women with CAD followed for SCD (n = 66) and nonfatal VA (NFVA) (n = 33) over 6.8 years.</AbstractText>In the case-control study, no statistically significant association was observed for the odds of SCD with any of the SNPs or haplotypes tested. Similarly, HERS revealed null effects for these SNPs and haplotypes in relation to risk of SCD, SCD + NFVA, and all-cause mortality. Point estimates and confidence intervals for risk of SCD associated with beta2AR27 were similar in both populations (Glu27 carriers vs Gln27 homozygotes: adjusted odds ratio 1.23 [95% confidence interval 0.75 to 2.03, P = .41] in the case-control study, and adjusted relative risk (RR) 1.18 [95% confidence interval 0.69 to 2.00, P = .55] in HERS). These null findings trend in the opposite direction and differ from previous published estimates (P = .01 and .07, respectively).</AbstractText>We did not find an increase in risk of SCD associated with any of these common betaAR polymorphisms.</AbstractText> |
7,625 | Association of prolonged QRS duration with ventricular tachyarrhythmias and sudden cardiac death in the Multicenter Automatic Defibrillator Implantation Trial II (MADIT-II). | There is conflicting literature on the relationship between prolonged QRS duration (QRSd) and arrhythmic events, including sudden cardiac death (SCD), in heart failure patients with or without implantable cardioverter-defibrillators (ICDs).</AbstractText>The purpose of this study was to evaluate the prognostic significance of prolonged QRSd relative to arrhythmic outcomes in medically and ICD-treated patients enrolled in the Multicenter Automatic Defibrillator Implantation Trial (MADIT) II.</AbstractText>Using a Cox proportional hazards model adjusting for ejection fraction, heart failure class, and blood urea nitrogen, we estimated the association of prolonged QRSd >/=140 ms with SCD in the medically treated arm and SCD or first appropriate ICD therapy for rapid ventricular tachycardia/fibrillation (VT/VF; cycle length </=260 ms) in the ICD-treated arm.</AbstractText>In the medically treated arm, prolonged QRSd was a significant independent predictor of SCD (hazard ratio 2.12; 95% confidence interval 1.20-3.76; P = .01). However, in the ICD-treated arm, prolonged QRSd did not predict SCD or rapid VT/VF (hazard ratio 0.77; 95% CI 0.47-1.24; P = .28). The difference in the prognostic effect of prolonged QRSd in these two groups was significant (P<.01). These results were not affected by varying the cycle length that defines rapid VT/VF or the duration that defines QRSd prolongation.</AbstractText>In patients with prior myocardial infarction and EF </=30%, prolonged QRSd does not predict SCD/VT/VF in ICD-treated patients but does predict SCD in medically treated patients. This underscores the nonequivalence of VT/VF and SCD and the need for caution in inferring risk of SCD when using nonrandomized databases that include only patients with ICDs.</AbstractText> |
7,626 | The prohibition on shocking apparent asystole: a history and critique of the argument. | A recommendation against shocking asystole has been part of the American Heart Association's Emergency Cardiovascular Care (ECC) Guidelines since 1992. The principal rationale offered then for the prohibition on shocking apparent asystole (PSAA) has since been refuted and has gradually been dropped, but the recommendation itself remains in the 2005 Guidelines. The PSAA now rests mainly on the lack of solid evidence of a survival benefit--a curious criterion given the lack of such evidence for most ECC treatment recommendations. "Occult" ventricular fibrillation and problems with distinguishing between fine ventricular fibrillation and asystole may lead to delays and omissions of potentially lifesaving shocks. No studies on the subject have been conducted since the PSAA first appeared. Removal of the PSAA from the ECC Guidelines is warranted to reopen research on this topic and support the goal of early defibrillation. |
7,627 | Atenolol in combination with epinephrine improves the initial outcome of cardiopulmonary resuscitation in a swine model of ventricular fibrillation. | The aim of the present study was to assess whether a beta-adrenergic blocking agent such as atenolol, administered during cardiopulmonary resuscitation, would improve initial resuscitation success.</AbstractText>Ventricular fibrillation was induced in 20 Landrace/Large White piglets, which were left untreated for 8 minutes before attempted resuscitation with precordial compression, mechanical ventilation, and electrical defibrillation. Animals were randomized into 2 groups (10 animals each) to receive saline as placebo (20 mL dilution, bolus) + epinephrine (0.02 mg/kg) (group A) or atenolol (0.05 mg/kg per 20 mL dilution, bolus) + epinephrine (0.02 mg/kg) (group B) during cardiopulmonary resuscitation. Electrical defibrillation was attempted after 10 minutes of ventricular fibrillation.</AbstractText>Nine animals in group B restored spontaneous circulation in comparison to only 4 in group A. Aortic systolic and diastolic pressures as well as coronary perfusion pressure were significantly increased during cardiopulmonary resuscitation in group B. Furthermore, postresuscitation heart rate of the atenolol-treated group was significantly decreased.</AbstractText>A beta-adrenergic blocking agent, when administered during cardiopulmonary resuscitation, significantly improves initial resuscitation success and increases blood and coronary perfusion pressures during cardiopulmonary resuscitation.</AbstractText> |
7,628 | Combination pharmacological cardioversion of permanent atrial fibrillation in post-prosthetic mitral valve replacement outpatients: a novel approach for the treatment of atrial fibrillation. | This study explored the efficacy and safety of combination pharmacological cardioversion of permanent atrial fibrillation in outpatients following prosthetic mitral valve replacement. The study group comprised 99 outpatients who were randomly divided into two groups. In group 1 (n = 50), only ventricular heart rate was controlled. In group 2 (n = 49), combination pharmacological cardioversion therapy with low-dose oral amiodarone (2 mg/kg), captopril (0.25 mg/kg) and simvastatin (0.3 mg/kg) was administered daily. During 12 months of serial pharmacological treatment, the cardioversion rate was 6% for group 1 and 39% for group 2; the likelihood of cardioversion differed significantly between the two groups. In group 2, one patient developed severe pruritus that necessitated withdrawal from the study and six patients ceased captopril treatment after contracting a persistent cough. In summary, combination pharmacological cardioversion was found to be effective and safe in outpatients who had undergone prosthetic mitral valve replacement. |
7,629 | New antiarrhythmic drugs for atrial fibrillation: focus on dronedarone and vernakalant. | The prevalence of atrial fibrillation (AF) is forecast to rise to 2-5% of the general population by 2050. Of the two fundamental treatment strategies for AF management, rhythm control is the approach which is generally preferred for active, symptomatic, and/or younger patients, whereas rate control is all that is found necessary in the more elderly, sedentary, asymptomatic individual. In many cases, at neither extreme, there remains a genuine choice of therapy, and for those patients, antiarrhythmic strategies would be preferred if effective and safe antiarrhythmic medications were available. Many new antiarrhythmic agents exploiting new mechanisms of action or novel combinations of established antiarrhythmic activity are currently being investigated. Agents which selectively inhibit ion channels specifically involved in atrial repolarization, so-called atrial repolarization delaying agents, are widely acknowledged as potentially ideal antiarrhythmic treatments, as they will probably be both effective and safe, at the very least (free of pro-arrhythmic effects at the ventricular level). Modified analogues of traditional antiarrhythmic drugs with different combinations of ion channel and receptor blocking effects, novel mechanisms of action, and less complicated metabolic profiles are also under development. Completely innovative antiarrhythmic agents with new antiarrhythmic mechanisms, such as stretch receptor antagonism, sodium calcium exchanger blockade, late sodium channel inhibition, and gap junction modulation are also being explored. In addition, there is increasing evidence in support of the antiarrhythmic action of non-antiarrhythmic drugs. Treatments with statins, omega-3 fatty acids, angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, and aldosterone antagonists are all potentially valuable, over and above any effect related to the treatment of underlying heart disease. |
7,630 | Recommendations for performing acetylcholine tests safely: STOP dangerous complications induced by acetylcholine tests (STOP DCIAT). | We examined some recommendations for performing acetylcholine (ACh) tests safely.</AbstractText>We performed 1000 ACh tests from 1991 to December 2004. ACh was injected in incremental doses of 20/50/80 microg into the RCA and of 20/50/100 microg into the LCA. During these periods, we encountered various major/minor complications; 12 ventricular tachycardia (1.2%) necessary one dc, one ventricular fibrillation (0.1%) necessary dc, 3 shock like the left main stem spasm (0.3%), one cardiac tamponade necessary surgical drainage (0.1%), and 164 Paf (164/959:17.1%) necessary administration of antiarrhythmic agents to sinus rhythm in about one third patients (31.7%). We did not experience irreversible severe complications, such as acute myocardial infarction or death.</AbstractText>(1) Stand by direct current with pasting, (2) Thump version when ventricular tachycardia or fibrillation occurred, (3) Over infusion to avoid hypovolemia, (4) Perform angiography before complete spasm provocation if a severe spasm, (5) Drainage if cardiac tamponade occurred, (6) Cibenzoline or disopyramid administration when ACh induced paroxysmal atrial fibrillation, (7) Incremental ACh dose up should be performed, (8) Administer small amount of noradrenaline if shock observed and (9) Test shot should be performed before 1-min angiography.</AbstractText>We recommend STOP DCIAT for performing ACh tests safely.</AbstractText> |
7,631 | Terminal stage cardiac findings in patients with cardiac Fabry disease: an electrocardiographic, echocardiographic, and autopsy study. | Fabry disease is caused by deficiency of alpha-galactosidase A, and typically causes multi-organ dysfunction. Patients with manifestations limited to the heart, mainly left ventricular hypertrophy (LVH), have been reported as a disease variation. We have reported a 3% prevalence of this cardiac variant in men with LVH, which we designated 'cardiac Fabry disease'. The purposes of this study were to evaluate the terminal stage cardiac manifestations and autopsy findings in patients with cardiac Fabry disease.</AbstractText>We examined seven terminal stage patients with cardiac Fabry disease. During hospitalization, standard 12-lead electrocardiograms, Holter electrocardiograms, and echocardiograms were obtained. Autopsies were performed and macroscopic along with microscopic findings were evaluated.</AbstractText>Six patients died of heart failure and one of ventricular fibrillation. Electrocardiograms revealed the presence of conduction abnormalities and nonsustained ventricular tachycardia. Echocardiograms and autopsy findings revealed LVH in all patients. Localized basal posterior wall thinning of the left ventricle was detected in the six patients who died of heart failure. All patients had severe left ventricular dysfunction. Histologically, myocardial cells, but not cardiac vascular endothelial cells, showed glycosphingolipid accumulation. No accumulation was observed in other organs or in systemic vascular endothelial cells.</AbstractText>Severe left ventricular dysfunction with associated conduction disturbances and ventricular arrhythmias occur in patients with terminal stage cardiac Fabry disease. Furthermore, LVH is present and associated with thinning of the base of the left ventricular posterior wall. In contrast to typical Fabry disease, accumulation of glycosphingolipids was observed in myocardial cells but not in other organs.</AbstractText> |
7,632 | Coronary artery spasm--clinical features, diagnosis, pathogenesis, and treatment. | Coronary (artery) spasm plays an important role in the pathogenesis of ischemic heart disease, including stable angina, unstable angina, myocardial infarction, and sudden death. The prevalence of coronary spasm differs among populations, is higher in Japan and Korea than in the Western countries probably due to genetic as well as environmental factors. Coronary spasm occurs most often from midnight to early morning and is usually not induced by exercise in the daytime. The attacks of coronary spasm are associated with either ST segment elevation or depression, or negative U wave on ECG. Patients with multi-vessel coronary spasm may suffer from lethal arrhythmia, including advanced AV block, ventricular tachycardia or fibrillation, or even sudden death, and they are often resistant to conventional medical therapy including Ca-channel blockers (CCBs). Endothelial nitric oxide (NO) activity is reduced and markers of oxidative stress are elevated in patients with coronary spasm. Thrombogenesis is enhanced and plasma levels of hsCRP and P-selection are elevated in patients with coronary spasm. Thus, patients with coronary spasm have endothelial dysfunction and are suffering from a low-grade chronic inflammation. Polymorphisms of endothelial NO synthase, smoking, and low-grade inflammation are the most important risk factors for coronary spasm. Coronary spasm is a hyper-contraction of coronary smooth muscle triggered by an increase of intracellular Ca2+ in the presence of an increased Ca2+ sensitivity. It has been shown that RhoA/ROCK pathway is involved in Ca2+ sensitivity and that the reduced endothelial NO activity results in increased Ca2+ sensitivity through enhanced RhoA/ROCK pathway. Accordingly, it is possible that in addition to CCBs, RhoA/ROCK pathway blockers may prove to be useful for the treatment of coronary spasm. |
7,633 | Cardiomyopathy induced by pulmonary vein tachycardia cured by catheter ablation. | A 51-year-old male was referred for consideration for heart transplantation because of recently diagnosed congestive heart failure refractory to medical therapy. Previous echocardiography demonstrated a left ventricular ejection fraction of approximately 15% with global hypokinesia. Coronary angiography did not reveal any clinically significant obstructive coronary artery disease and an electrocardiogram documented atrial fibrillation with a rapid ventricular rate of 130 beats/min. Other laboratory tests including thyroid function test were unremarkable. The patient's main complaints were dyspnea on exertion, and orthopnea with minimal palpitations.</AbstractText>Physical examination, laboratory testing, electrocardiography, Holter monitoring, chest radiography, transthoracic echocardiography, transesophageal echocardiography, coronary angiogram, and electrophysiologic study with catheter ablation.</AbstractText>Cardiomyopathy resulting from pulmonary vein tachycardia.</AbstractText>Catheter-based radiofrequency ablation of the focus of pulmonary vein tachycardia.</AbstractText> |
7,634 | Remodelling of gap junctions and connexin expression in diseased myocardium. | Gap junctions form the cell-to-cell pathways for propagation of the precisely orchestrated patterns of current flow that govern the regular rhythm of the healthy heart. As in most tissues and organs, multiple connexin types are expressed in the heart: connexin43 (Cx43), Cx40 and Cx45 are found in distinctive combinations and relative quantities in different, functionally-specialized subsets of cardiac myocyte. Mutations in genes that encode connexins have only rarely been identified as being a cause of human cardiac disease, but remodelling of connexin expression and gap junction organization are well documented in acquired adult heart disease, notably ischaemic heart disease and heart failure. Remodelling may take the form of alterations in (i) the distribution of gap junctions and (ii) the amount and type of connexins expressed. Heterogeneous reduction in Cx43 expression and disordering in gap junction distribution feature in human ventricular disease and correlate with electrophysiologically identified arrhythmic changes and contractile dysfunction in animal models. Disease-related alterations in Cx45 and Cx40 expression have also been reported, and some of the functional implications of these are beginning to emerge. Apart from ventricular disease, various features of gap junction organization and connexin expression have been implicated in the initiation and persistence of the most common form of atrial arrhythmia, atrial fibrillation, though the disparate findings in this area remain to be clarified. Other major tasks ahead focus on the Purkinje/working ventricular myocyte interface and its role in normal and abnormal impulse propagation, connexin-interacting proteins and their regulatory functions, and on defining the precise functional properties conferred by the distinctive connexin co-expression patterns of different myocyte types in health and disease. |
7,635 | Prevalence of sleep disordered breathing in paroxysmal and persistent atrial fibrillation patients with normal left ventricular function. | Recent studies have suggested an emerging link between sleep apnoea and atrial fibrillation (AF). These studies included patients with reduced left ventricular (LV) function which may cause both AF and sleep disordered breathing (SDB). We examined the prevalence of SDB in a population of patients with AF and normal LV function.</AbstractText>Ninety patients with paroxysmal or persistent AF and 45 controls were prospectively enrolled and matched 2:1 for age (AF 56 +/- 12 years; controls 54 +/- 11years) and sex. All patients had normal LV function. SDB was diagnosed using all-night portable polysomnography. Apnoea-hypopnoea index (AHI) in AF patients was higher than in controls (23.19 +/- 19.26 vs. 14.66 +/- 12.43, P = 0.01). The proportion with significant SDB (AHI > 15) was also greater in AF patients (62 vs. 38%, P = 0.01). After adjustment for relevant covariates, the odds ratio for the association between AF and SDB (AHI > 15) was 3.04 (95% CI 1.24-7.46, P = 0.02). The paroxysmal AF group was classified as either 'low-frequency AF' (< or =6) or 'high-frequency AF' (>6) episodes in the past year. High-frequency AF was associated with a higher prevalence (75 vs. 43%, P = 0.012) and severity (mean AHI 28.08 +/- 22.94 vs. 16.69 +/- 15.06, P = 0.028) of SDB when compared with those with low-frequency AF.</AbstractText>A high prevalence of SDB is found in relatively young patients with both paroxysmal and persistent AF with normal LV function. This AF population warrants careful consideration for the presence of SDB.</AbstractText> |
7,636 | Patient-tailored implantable cardioverter defibrillator testing using the upper limit of vulnerability: the TULIP protocol. | We evaluated the feasibility of the TULIP (Threshold test using Upper Limit during ImPlantation) protocol, which was designed to provide a confirmed, low defibrillation energy value during implantable cardioverter defibrillator (ICD) implantation with only two induced ventricular fibrillation (VF) episodes.</AbstractText>Ninety-eight patients (62 +/- 12 years, 86 male) from 13 clinical centres underwent an active can ICD implantation. A single coupling interval derived from electrocardiogram lead II during ventricular pacing was used for VF induction shocks at 13, 11, 9, and 6 J in a step-down manner until the upper limit of VF induction (ULVI) was determined. If ULVI >or=9 J, a defibrillation energy of ULVI + 4 J was tested. For ULVI <9 J, the defibrillation test energy was 9 J. In 79/98 patients (80.6%), two induced VF episodes were sufficient to obtain confirmed defibrillation energy of 11.1 +/- 3.3 J. The mean strength of the successful VF induction shock was 6.8 +/- 4.3 J, the coupling interval was 303 +/- 35 ms, and the number of delivered induction shocks until the first VF induction was 3.9 +/- 1.6.</AbstractText>TULIP is a safe and simple device testing procedure allowing the determination of confirmed, low defibrillation energy in most patients with two VF episodes induced at a single coupling interval.</AbstractText> |
7,637 | Anti-arrhythmic drug therapy for atrial fibrillation: current anti-arrhythmic drugs, investigational agents, and innovative approaches. | By 2050, atrial fibrillation (AF) will be present in 2% of the general population and in a far higher proportion of elderly patients. Currently, we are content with rate control and anticoagulation in elderly asymptomatic patients, whereas in younger patients with symptomatic recurrent AF, pulmonary vein isolation is the treatment of choice. However, in a large number of patients, there remains a genuine choice between anti-arrhythmic therapy to suppress the arrhythmia and rate control to control the ventricular rate. This review provides a contemporary evidence-based insight into the buoyant development of new anti-arrhythmic agents, exploring new mechanisms of action or novel combinations of established anti-arrhythmic activity. An attractive prospect for AF therapy is the introduction of agents with selective affinity to ion channels specifically involved in atrial repolarization, so-called atrial repolarization-delaying agents. Presently, there are several potential anti-arrhythmic drugs with this mode of action, which are currently in pre-clinical and clinical development. Vernakalant is in the most advanced phase of investigation and its intravenous formulation has recently been recommended for approval for pharmacological cardioversion of AF. However, although this agent has some electrophysiological effects which are specific to the atria, it has others which affect both the atria and the ventricles. Other drugs, such as XEND0101, block a single atrial-specific membrane current. The success of such agents depends critically on their atrial electrophysiological selectivity, freedom from cardiac adverse effects, and general safety. Other possibilities include modified analogues of traditional anti-arrhythmic drugs with additional novel mechanisms of action and less complex metabolic profiles. Dronedarone is an investigational agent with multiple electrophysiological effects, which is devoid of iodine substituents and is believed to have a better side effect profile than its predecessor amiodarone. The development portfolio of dronedarone is practically complete and approval for several indications in AF may soon be assessed. Innovative anti-arrhythmic agents with unconventional anti-arrhythmic mechanisms, such as stretch receptor antagonism, sodium-calcium exchanger blockade, late sodium channel inhibition, and gap junction modulation, have not yet reached clinical studies in AF. Gene- and cell-based therapies, which can selectively target individual currents, could provide ideal one-time only curative therapy for arrhythmias, and the first proof-of-concept studies have been reported. There is accumulating evidence in support of the anti-arrhythmic effects of non-anti-arrhythmic drugs. Treatments with angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, statins, and omega-3 fatty acids all seem promising, over and above any effect related to the treatment of underlying heart disease. However, despite exciting results from animal experiments and promising outcomes from retrospective analyses, there is no robust evidence of specific effects of these drugs to transform current clinical practice. |
7,638 | Fortuitous therapeutic effect of Taser shock for a patient in atrial fibrillation. | Neuromuscular incapacitating devices are used by law enforcement and military forces worldwide. The most frequently used of these devices are from Taser International. Although they are regarded as a less than lethal alternative, there have been several case reports aimed at linking the potential causal relationship of a shock from a neuromuscular incapacitating device and sudden cardiac death caused by induced ventricular tachycardia or ventricular fibrillation. In this report, we describe the first known account in which a neuromuscular incapacitating device had a temporal relationship to a more positive therapeutic outcome for a patient. |
7,639 | Impact of valve prosthesis-patient mismatch estimated by echocardiographic-determined effective orifice area on long-term outcome after aortic valve replacement. | The impact of valve prosthesis-patient mismatch on long-term outcome after aortic valve replacement estimated by various variables such as projected indexed effective orifice area and internal geometric orifice area obtained from in vivo or in vitro published data is still controversial.</AbstractText>The effective orifice area was measured by echocardiography in 533 patients. The mean age of the patients was 71 +/- 9 years; mean follow-up time was 4.7 +/- 2.2 years. The impact of severe (indexed effective orifice area <or=0.6 cm(2)/m(2)) and moderate mismatch (0.6 cm(2)/m(2) < indexed effective orifice area <or=0.85 cm(2)/m(2)) on survival was evaluated by Cox regression.</AbstractText>Severe mismatch (hazard ratio: 1.9 [1.08-3.21]) was a significant predictor of survival time after adjustment for age, left ventricular ejection fraction, atrial fibrillation, New York Heart Association class, serum creatinine, and hemoglobin level. The 5- and 7-year survival rates were 71% +/- 4% and 54% +/- 8% for patients with severe mismatch and 83% +/- 4% and 80% +/- 8% for patients with mild mismatch, respectively. The correlation between projected and measured indexed effective orifice area was of medium strength (r = 0.49), and the frequency of observed mismatch depended linearly on the projected indexed effective orifice area. Although projected indexed effective orifice area and indexed internal geometric orifice area were significant predictors of severe mismatch, the sensitivity and specificity for severe prosthesis-patient mismatch were only 75% and 52%, using an optimal threshold of projected indexed effective orifice area defined by the Youden index.</AbstractText>Severe prosthesis-patient mismatch estimated by effective orifice area measured within 10 days was an independent risk factor of survival time. Projected indexed effective orifice area determined at surgery does not sufficiently predict mismatch.</AbstractText> |
7,640 | Three-dimensional ultrasound for image-guided mapping and intervention: methods, quantitative validation, and clinical feasibility of a novel multimodality image mapping system. | Multiple factors create discrepancies between electroanatomic maps and merged, preacquired computed tomographic images used in guiding atrial fibrillation ablation. Therefore, a Carto-based 3D ultrasound image system (Biosense Webster Inc) was validated in an animal model and tested in 15 atrial fibrillation patients.</AbstractText>Twelve dogs underwent evaluation using a newly developed Carto-based 3D ultrasound system. After fiducial clip markers were percutaneously implanted at critical locations in each cardiac chamber, 3D ultrasound geometries, derived from a family of 2D intracardiac echocardiographic images, were constructed. Point-source error of 3D ultrasound-derived geometries, assessed by actual real-time 2D intracardiac echocardiographic clip sites, was 2.1+/-1.1 mm for atrial and 2.4+/-1.2 mm for ventricular sites. These errors were significantly less than the variance on CartoMerge computed tomographic images (atria: 3.3+/-1.6 mm; ventricles: 4.8+/-2.0 mm; P<0.001 for both). Target ablation at each clip, guided only by 3D ultrasound-derived geometry, resulted in lesions within 1.1+/-1.1 mm of the actual clips. Pulmonary vein ablation guided by 3D ultrasound-derived geometry resulted in circumferential ablative lesions. Mapping in 15 patients produced modestly smaller 3D ultrasound versus electroanatomic map left atrial volumes (98+/-24 cm(3) versus 109+/-25 cm(3), P<0.05). Three-dimensional ultrasound-guided pulmonary vein isolation and linear ablation in these patients were successfully performed with confirmation of pulmonary vein entrance/exit block.</AbstractText>These data demonstrate that 3D ultrasound images seamlessly yield anatomically accurate chamber geometries. Image volumes from the ultrasound system are more accurate than possible with CartoMerge computed tomographic imaging. This clinical study also demonstrates the initial feasibility of this guidance system for ablation in patients with atrial fibrillation.</AbstractText> |
7,641 | Calcium-handling abnormalities underlying atrial arrhythmogenesis and contractile dysfunction in dogs with congestive heart failure. | Congestive heart failure (CHF) is a common cause of atrial fibrillation. Focal sources of unknown mechanism have been described in CHF-related atrial fibrillation. The authors hypothesized that abnormal calcium (Ca(2+)) handling contributes to the CHF-related atrial arrhythmogenic substrate.</AbstractText>CHF was induced in dogs by ventricular tachypacing (240 bpm x2 weeks). Cellular Ca(2+)-handling properties and expression/phosphorylation status of key Ca(2+) handling and myofilament proteins were assessed in control and CHF atria. CHF decreased cell shortening but increased left atrial diastolic intracellular Ca(2+) concentration ([Ca(2+)](i)), [Ca(2+)](i) transient amplitude, and sarcoplasmic reticulum (SR) Ca(2+) load (caffeine-induced [Ca(2+)](i) release). SR Ca(2+) overload was associated with spontaneous Ca(2+) transient events and triggered ectopic activity, which was suppressed by the inhibition of SR Ca(2+) release (ryanodine) or Na(+)/Ca(2+) exchange. Mechanisms underlying abnormal SR Ca(2+) handling were then studied. CHF increased atrial action potential duration and action potential voltage clamp showed that CHF-like action potentials enhance Ca(2+)(i) loading. CHF increased calmodulin-dependent protein kinase II phosphorylation of phospholamban by 120%, potentially enhancing SR Ca(2+) uptake by reducing phospholamban inhibition of SR Ca(2+) ATPase, but it did not affect phosphorylation of SR Ca(2+)-release channels (RyR2). Total RyR2 and calsequestrin (main SR Ca(2+)-binding protein) expression were significantly reduced, by 65% and 15%, potentially contributing to SR dysfunction. CHF decreased expression of total and protein kinase A-phosphorylated myosin-binding protein C (a key contractile filament regulator) by 27% and 74%, potentially accounting for decreased contractility despite increased Ca(2+) transients. Complex phosphorylation changes were explained by enhanced calmodulin-dependent protein kinase IIdelta expression and function and type-1 protein-phosphatase activity but downregulated regulatory protein kinase A subunits.</AbstractText>CHF causes profound changes in Ca(2+)-handling and -regulatory proteins that produce atrial fibrillation-promoting atrial cardiomyocyte Ca(2+)-handling abnormalities, arrhythmogenic triggered activity, and contractile dysfunction.</AbstractText> |
7,642 | Precipitation of ventricular fibrillation by intravenous diltiazem and metoprolol in a young patient with occult Wolff-Parkinson-White syndrome. | We report the case of a young man who presented with a rapid, narrow-complex atrial fibrillation. A few hours after being administered intravenous metoprolol and diltiazem for rate control, he developed intermittent ventricular preexcitation on the electrocardiogram (ECG) and experienced ventricular fibrillation, from which he was successfully defibrillated. A subsequent electrocardiogram in sinus rhythm demonstrated previously unknown Wolff-Parkinson-White pattern. A left lateral accessory pathway was successfully ablated. Wolff-Parkinson-White syndrome should be included in the differential diagnosis when a young patient presents with atrial fibrillation, even if the ventricular complexes on the ECG are not preexcited. |
7,643 | Automatic determination of timing intervals for upper limit of vulnerability using ICD electrograms. | Implantable cardioverter defibrillator (ICD) implant testing based on the upper limit of vulnerability, or vulnerability testing, permits assessment of defibrillation safety margins without inducing ventricular fibrillation (VF) in most patients. Vulnerability testing requires that T-wave shocks be timed at the most vulnerable intervals of the cardiac cycle, defined as intervals at which the strongest shock induces VF. Our goal was to develop and test an automated method to select these timing intervals using ICD intracardiac electrograms (EGMs).</AbstractText>At ICD implant in 22 patients, we determined the range of the most vulnerable intervals by scanning the T wave with shocks. Simultaneously, EGMs were recorded for 351 pacing sequences used for measurement of timing intervals or T-wave shocks. EGMs were analyzed off-line using a novel automated method to identify a stable point near the maximum slope of the T wave in the far-field (shock) EGM. Fiducial timing points based both on the EGM and on the electrocardiogram (ECG) were used to predict the most vulnerable intervals. We compared the predicted most vulnerable to the measured most vulnerable intervals determined by T-shock scans.</AbstractText>Automatically determined timing points from EGMs and operator-determined timing points from the surface ECG had comparable accuracy in identifying the measured most vulnerable intervals (91% EGM vs 86% ECG, P = NS).</AbstractText>An automated method based on ICD EGMs identifies the most vulnerable intervals with accuracy comparable to the operator-performed, clinical method based on the surface ECG. This EGM method can be implemented efficiently in an ICD to automate vulnerability testing.</AbstractText> |
7,644 | Organized incessant atrial arrhythmias in the setting of severe, isolated biatrial scarring. | Diffuse transmural fibrosis and scarring limited to the area without atrial dilation or significant structural heart or other systemic disease has not been reported. We present three cases of a syndrome characterized by refractory organized atrial arrhythmias, diffuse atrial scarring with electrical silence, and mechanical paralysis in the absence of atrial dilation or any systemic or neurodegenerative disorders.</AbstractText>Patients referred for electrophysiology study of atrial arrhythmias were included. Electroanatomic mapping with the Carto system (Biosense Webster, Diamond Bar, CA, USA) and magnetic resonance imaging (MRI) with scar sequencing were performed.</AbstractText>There was no family or personal history of cardiac, muscular, or developmental diseases. All patients had organized atrial arrhythmias. Echocardiograms showed atrial standstill with normal atrial and ventricular dimensions. No other structural abnormalities were noted. Carto mapping revealed severe biatrial diffuse scarring. The left atrial (LA) was less affected than the right atrial (RA). MRI findings confirmed biatrial scarring. During tachycardia, islands of dissociated electrical activity could be seen in the right atria. Entrainment mapping was not performed in the atria as high-output pacing could not capture the atria. Coronary sinus entrainment demonstrated the coronary sinus(CS) not to be critical to the tachycardia. Ablation was targeted toward channels of low voltage but was not successful in any cases. All required atrioventricular (AV) nodal ablation with pacing.</AbstractText>An association between biatrial cardiomyopathy and scarring with normal atrial dimensions has been described. Since severe scarring has not been reported with organized arrhythmias this may represent a new syndrome.</AbstractText> |
7,645 | Effects of the location of myocardial infarction on the spectral characteristics of ventricular fibrillation. | The location of the myocardial infarction (MI) might modify the spectral characteristics of ventricular fibrillation (VF) in humans.</AbstractText>To evaluate the effect of the location of the infarcted area on the spectral parameters of VF.</AbstractText>Patients with chronic MI (29 anterior, 32 inferior) and induced VF during cardioverter defibrillator implant were retrospectively studied. Dominant frequency (f(d)), organization index (OI), and power of the harmonic peaks were calculated in the device-stored electrograms (EGM) during sinus rhythm (SR) and VF.</AbstractText>The f(d) of the VF was not affected by the left ventricular ejection fraction (LVEF) or the MI location (anterior: 4.54 +/- 0.74 Hz, inferior: 4.77 +/- 0.48 Hz, n.s.). The OI was also similar in both groups. However, in patients with inferior MIs, normalized peak power at f(d) was higher (118.3 +/- 18.5 vs 100.6 +/- 28.2, P < 0.01) and the normalized peak power of the harmonics was lower than in the anterior MI group. The analysis of EGM during SR showed similar results. The size of the necrotic area and its distance to the recording electrode might partially explain these results.</AbstractText>In our series, the spectral characteristics of the EGMs during VF showed significant differences depending on the MI localization. A higher fraction of energy (in the low-frequency region) was seen in inferior MIs, whereas the peak power at the harmonics increased in anterior MIs. A similar effect was seen during SR and VF, suggesting that it is caused by local electrophysiology abnormalities induced by the MI rather than by different intrinsic characteristics of the VF.</AbstractText> |
7,646 | CDP-choline prevents cardiac arrhythmias and lethality induced by short-term myocardial ischemia-reperfusion injury in the rat: involvement of central muscarinic cholinergic mechanisms. | In the present study, we aimed to determine whether cytidine-5'-diphosphatecholine (CDP-choline or citicoline) can improve the outcome of short-term myocardial ischemia-reperfusion injury in rats. Ischemia was produced in anesthetized rats by ligature of the left anterior descending coronary artery for 7 min followed by a reperfusion period of 7 min. Reperfusion-induced ventricular tachycardia (VT), ventricular fibrillation (VF), survival rate, and changes in arterial pressure were evaluated. Saline (1 ml/kg), CDP-choline (100, 250,and 500 mg/kg), or lidocaine (5 mg/kg) was intravenously injected in the middle of the ischemic period. Intracerebroventricular (i.c.v.) mecamylamine (50 microg) or atropine sulfate (10 microg) pretreatments were made 10 min before the coronary occlusion period. Pretreatment with intravenous (i.v.) atropine methylnitrate (2 and 5 mg/kg; i.v.) or bilateral vagotomy was performed 5 min before the induction of ischemia. An in vivo microdialysis study was performed in the nucleus ambiguus area (NA); choline and acetylcholine levels were measured in extracellular fluids. In control rats, VT, VF, and lethality were observed in 85%, 60% and 50% of the animals, respectively. Intravenous CDP-choline produced a short-term increase in blood pressure and reduced the incidence of VT, VF, and lethality dose-dependently when injected in the middle of the ischemic period. CDP-choline at doses of 250 and 500 mg/kg completely prevented death. Intracerebroventricular atropine sulfate pretreatment completely abolished the protective effect of CDP-choline, while mecamylamine pretreatment had no effect on the drug. CDP-choline increased the levels of extracellular choline and acetylcholine in the NA area. Bilateral vagotomy completely abolished the protective effect of CDP-choline in the reperfusion period. Moreover, the intravenous pretreatment with atropine methylnitrate produced dose-dependent blockade in the reduction of VT, VF, and mortality rates induced by CDP-choline. Neither of these pretreatments except mecamylamine affected the pressor effect of CDP-choline. Intracerebroventricular mecamylamine attenuated the increase in blood pressure induced by CDP-choline. In conclusion, intravenously injected CDP-choline prevents cardiac arrhythmias and death induced by short-term myocardial ischemia-reperfusion injury. Activation of central muscarinic receptors and vagal pathways mediates the protective effect of CDP-choline. The protective effect of CDP-choline is not related to its pressor effect. |
7,647 | Does continuous insulin therapy reduce postoperative supraventricular tachycardia incidence after coronary artery bypass operations in diabetic patients? | To compare continuous insulin infusion (CII) and intermittent subcutaneous insulin therapy for preventing supraventricular tachycardia. The authors propose that continuous insulin therapy is more effective to reduce supraventricular tachycardias.</AbstractText>A prospective randomized study.</AbstractText>This study was performed in 2 different centers between April 2005 and February 2007: Gülhane Military Medical Academy and University of Süleyman Demirel.</AbstractText>Two hundred diabetic patients were included in this prospective randomized study. Patients were divided into 2 groups according to their insulin therapy in 2 different centers.</AbstractText>Group 1 included 100 diabetes mellitus (DM) patients, and CIIs were administrated. These patients received a CII infusion titrated per protocol in the perioperative period (Portland protocol). Group 2 also included 100 DM patients, and subcutaneous insulin was injected every 4 hours in a directed attempt to maintain blood glucose levels below 200 mg/dL. Sliding scale dosage of insulin was titrated to each patient's glycemic response during the prior 4 hours.</AbstractText>There were 5 hospital mortalities in the intermittent insulin group. The causes of death were pump failure in 3 patients and ventricular fibrillation in 2 patients. There were 2 hospital mortalities in the CII group (p = 0.044). Thirty-six patients in the intermittent insulin group and 21 patients in the CII group required positive inotropic drugs after cardiopulmonary bypass (p = 0.028). Low cardiac output developed in 28 and 16 patients in the intermittent and CII groups, respectively (p = 0.045). Univariate analysis identified positive inotropic drug requirement (p = 0.011, odds ratio [OR] = 3.41), ejection fraction (EF) (p = 0.001, OR = 0.92), cross-clamp time (p = 0.046, OR = 0.97), left internal mammary artery (p = 0.023, OR = 0.49), chronic obstructive pulmonary disease (COPD) (forced expiratory volume in 1 second <75% of predicted value (p = 0.009, OR = 2.02), intra-aortic balloon pump (p = 0.045, OR = 1.23), body mass index (p = 0.035 OR = 5.60), and CII (p < 0.001, OR = 0.36) as predictors of SVT. Stepwise multivariate analysis confirmed the significance of some of the previously mentioned variables as predictors of SVT. The value of -2 log likelihood of multivariate analyses was 421.504. These were EF (p < 0.001, OR = 0.91), positive inotropic drug requirement (p < 0.001, OR = 3.94), COPD (p = 0.036, OR = 2.11), and CII (p < 0.001, OR = 0.19).</AbstractText>Continuous insulin therapy in the perioperative period reduces infectious complications, such as sternal wound infection and mediastinitis, cardiac mortality caused by pump failure, and the risk of development of supraventricular tachycardias.</AbstractText> |
7,648 | Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) presenting with ventricular fibrillation in an adult: a case report. | Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) is a rare congenital anomaly. The usual clinical course is severe left sided heart failure and mitral valve insufficiency presenting during the first months of life. However, in some cases collateral blood supply from the right coronary artery is sufficient and symptoms may be subtle or even absent. Arrhythmias or sudden cardiac death in adult life may be the first clinical presentation in patients with ALCAPA. We report a case, where a 39-year old woman presented with ventricular fibrillation during phycial exertion. Coronary angiography and CT-angiography revealed an anomalous origin of the left coronary artery, and an aortic reimplantation of the left coronary artery was performed followed by ICD implantation. A review of the literature on ALCAPA is presented along with CT images before and after surgery. |
7,649 | Beyond the implantable cardioverter-defibrillator: are we making progress? | Sudden cardiac death due to ventricular fibrillation occurs when a dynamic interaction between triggers and substrate leads to the development of reentry, initiation of ventricular tachycardia, and its degeneration to fibrillation. To move beyond the implantable cardioverter-defibrillator as the only effective therapy for aborting sudden cardiac death, an improved understanding of trigger-substrate interaction is essential. This brief review summarizes some of the recent progress in this direction. |
7,650 | Successful radiofrequency catheter ablation for electrical storm of ventricular fibrillation in a patient with Brugada syndrome. | The case of a 41-year-old man with Brugada syndrome (BS) who suffered electrical storms (ES) of ventricular fibrillation (VF) is presented. Although intravenous infusion of isoproterenol (ISP) suppressed the VF occurrence, he consistently experienced recurrence of VF following discontinuation of ISP infusion. Quinidine and cilostazol were ineffective. An analysis of VF episodes on electrocardiogram monitoring revealed that the QRS morphology of the first beat of all VF episodes was identical to that of premature ventricular complexes (PVCs) with a left bundle branch-block morphology and inferior axis, which occurred repetitively before the episodes of VF and were recorded throughout the day. In addition, stored electrograms from the implantable cardioverter defibrillator showed that the first beat of all VF episodes had the same morphology. On electrophysiological study, the VF-triggering PVC was found to originate from the posterior portion of the right ventricular outflow tract area and their elimination, which was achieved with radiofrequency catheter ablation (RFCA), resulted in the suppression of ES. Although several other PVCs were still observed, the patient has been free of VF during the 29-month follow-up period. This case indicates that RFCA of VF-triggering PVCs may be useful in the treatment of drug-resistant ES in patients with BS. |
7,651 | Comparison of electropharmacological effects of bepridil and sotalol in halothane-anesthetized dogs. | Bepridil is known to have a multiple ion channel-blocking property in the heart, which has been applied for the treatment of atrial fibrillation and drug-refractory ventricular tachyarrhythmias. In this study, the electro-pharmacological effects of bepridil were compared with those of dl-sotalol, a representative class III antiarrhythmic drug, using the halothane-anesthetized canine model.</AbstractText>Cardiovascular and electrophysiological variables were measured under the halothane anesthesia. Intravenous administration of bepridil (0.3 mg/kg, n=4) delayed the intraventricular conduction and prolonged the ventricular effective refractory period, whereas dl-sotalol (0.3 mg/kg, iv, n=4) inhibited atrioventricular conduction and prolonged the atrial and ventricular effective refractory period. The additional administration of 10 times the higher dose of bepridil or dl-sotalol (ie, 3 mg/kg, iv, n=4 for each group) decreased blood pressure, suppressed ventricular contraction and sinus automaticity, and prolonged the atrial and ventricular effective refractory period and monophasic action potential duration, in addition to the effects of the low dose.</AbstractText>The electropharmacological effects of bepridil and dl-sotalol were similar, although their potency for each cardiovascular variable varied significantly. These findings can be useful when selecting these drugs according to the pathophysiological condition of a patient.</AbstractText> |
7,652 | Clinical trials update from the American College of Cardiology 2008: CARISMA, TRENDS, meta-analysis of Cox-2 studies, HAT, ON-TARGET, HYVET, ACCOMPLISH, MOMENTUM, PROTECT, HORIZON-HF and REVERSE. | This article provides information and a commentary on trials relevant to the pathophysiology, prevention and treatment of heart failure, presented at the American College of Cardiology. Unpublished reports should be considered as preliminary data, as analyses may change in the final publication. CARISMA investigated the use of implantable loop recorders for detecting life-threatening arrhythmias in patients with LVSD after MI and found that brady- and ventricular tachy-arrhythmias predicted an adverse prognosis. The TRENDS study showed that the burden of atrial fibrillation detected by pacemakers or defibrillators predicted the risk of embolic events but not with sufficient precision to justify changes in anti-thrombotic management. A meta-analysis of six trials reported an increased cardiovascular risk associated with celecoxib, particularly for heart failure, which was related to dose and baseline cardiovascular risk. The HAT study failed to show a benefit of providing post-MI patients with a home defibrillator. MOMENTUM, a study of a device designed to augment aortic blood flow, was stopped early due to increased bleeding risk. Results from PROTECT support the use of rolofylline 30 mg/day in acute heart failure, a definitive study is now underway. Istaroxime, an agent that appears to have both inotropic and lusitropic effects, improved haemodynamics when added to standard therapy in patients stabilised after admission with heart failure in HORIZON-HF. The REVERSE study suggested that CRT improves ventricular function and reduces morbidity even in patients with few or no symptoms of heart failure and may delay or prevent worsening heart failure. |
7,653 | Influence of the skeletal muscle activity on time and frequency domain properties of the body surface ECG during evolving ventricular fibrillation in the pig. | To evaluate influence of the skeletal muscle activity (SMA) on time and frequency domain properties of ECG during VF.</AbstractText>We studied the first 9min of electrically induced VF (N=7). We recorded Lead II ECG, 247 unipolar epicardial ventricular electrograms (UEGs) and 3 bipolar skeletal electromyograms (EMGs) near the positions of the ECG electrodes (sampling rate, 500Hz). We reconstructed ECG (RECG) from UEGs using forward-solution transformation matrix. Spectral properties of ECG, RECG, UEGs and MEGs were assessed in the range 2-250Hz by the median frequency (MF) and the upper limit of frequency range containing 99% of spectral energy (Flim(99)). Scaling exponent of ECG, RECG and EMGs was calculated in the ranges of 1-8 and 5-20 sampling intervals (ScE1-8 and ScE5-20, respectively).</AbstractText>We observed non-monotonic increases in MF and Flim(99) of the ECG, but not UEGs and RECG, at 1-5min of VF. Maximum values of MF and Flim(99) in ECG, UEGs and RECG were (in Hz): 32+/-29 and 166+/-67; 11+/-2 and 36+/-7; 10+/-2 and 32+/-6, respectively. The transient increases in the high-frequency content of the ECG were correlated with enhanced activity in EMGs, characterized by an almost uniform spectrum in the range 2-250Hz (MF=92+/-29; Flim(99)=245+/-4Hz). Peak values of ScE(1-8) were the highest in EMGs (1.95+/-0.04), intermediate in the ECG (1.59+/-0.26), and the lowest in RECG (1.088+/-0.007).</AbstractText>SMA significantly contributes to ECG during VF and can bias metrics used for assessment of VF organization.</AbstractText> |
7,654 | A survey of labour ward clinicians' knowledge of maternal cardiac arrest and resuscitation. | Guidelines for the management of cardiac arrest during pregnancy exist but they are based on little research. The study hypothesis was that experienced medical clinicians who specialise in obstetric care would not follow current International Liaison Committee on Resuscitation/American Heart Association recommendations in this situation.</AbstractText>Following waiver of informed consent by the institutional review board, an anonymous structured scenario questionnaire survey was conducted among relevant hospital clinicians. Demographic details included field of expertise and resuscitation experience. A single case vignette of maternal cardiac arrest was presented, followed by nine questions to examine knowledge of existing recommendations for maternal cardiopulmonary resuscitation. Statistical analyses were performed using SPSS version 12 software (SPSS Inc, Chicago, IL).</AbstractText>The overall response rate was 67% (30/45 questionnaires). Specialist obstetricians, midwives and anaesthetists from 17 hospitals participated. Forty-three percent (n=13) claimed broad experience, 50% (n=15) claimed some experience and 6.7% (n=2) claimed no experience in adult resuscitation. Participants were divided in their opinions regarding every choice of action: positioning, need to administer cricoid pressure during mask ventilation, timing of intubation, location of external chest compression, location of paddle placement for delivery of shock during ventricular fibrillation, the timing of defibrillation versus fetal delivery, medication doses and the need to rupture the membranes at an early phase of the resuscitation.</AbstractText>Specialist clinicians who treat pregnant women in hospital on a daily basis possess a limited knowledge of the recommendations for treating maternal cardiac arrest.</AbstractText> |
7,655 | Tissue Doppler index, E/E', and ischemic stroke in patients with atrial fibrillation and preserved left ventricular ejection fraction. | Although several risk factors for stroke have been reported in patients with atrial fibrillation (AF), the relation of LV diastolic dysfunction to stroke is still uncertain in these patients. We evaluated the relationship between tissue Doppler-derived index, E/E', as well as other clinical and echocardiographic parameters and ischemic stroke by this cross-sectional study.</AbstractText>Three hundred thirty patients with persistent AF who had preserved LV ejection fraction were included from 6 centers. Clinical data were obtained and standard transthoracic echocardiography was performed. Patients without a history of ischemic stroke (n=280) were compared with patients with this complication (n=50). Potential determinants of ischemic stroke were identified by logistic regression analyses.</AbstractText>In univariate analyses, age, history of hypertension, diabetes mellitus, hyperlipidemia and symptomatic heart failure, plasma brain natriuretic peptide (BNP) level, early mitral inflow velocity (E), diastolic mitral annular velocity (E'), and E/E' ratio were significantly correlated to ischemic stroke. Multivariate regression analyses identified two significant variables that were independently associated with ischemic stroke: hypertension (odds ratio=6.03, p=0.008), and E/E' (odds ratio=1.21, p=0.002).</AbstractText>These findings may have clinical implications that LV diastolic dysfunction, reflected by E/E', is a significant determinant of ischemic stroke in AF. A larger prospective data is needed to confirm the value of E/E' in risk stratification for ischemic stroke in this population.</AbstractText> |
7,656 | Facilitated PCI in patients with ST-elevation myocardial infarction. | We hypothesized that percutaneous coronary intervention (PCI) preceded by early treatment with abciximab plus half-dose reteplase (combination-facilitated PCI) or with abciximab alone (abciximab-facilitated PCI) would improve outcomes in patients with acute ST-segment elevation myocardial infarction, as compared with abciximab administered immediately before the procedure (primary PCI).</AbstractText>In this international, double-blind, placebo-controlled study, we randomly assigned patients with ST-segment elevation myocardial infarction who presented 6 hours or less after the onset of symptoms to receive combination-facilitated PCI, abciximab-facilitated PCI, or primary PCI. All patients received unfractionated heparin or enoxaparin before PCI and a 12-hour infusion of abciximab after PCI. The primary end point was the composite of death from all causes, ventricular fibrillation occurring more than 48 hours after randomization, cardiogenic shock, and congestive heart failure during the first 90 days after randomization.</AbstractText>A total of 2452 patients were randomly assigned to a treatment group. Significantly more patients had early ST-segment resolution with combination-facilitated PCI (43.9%) than with abciximab-facilitated PCI (33.1%) or primary PCI (31.0%; P=0.01 and P=0.003, respectively). The primary end point occurred in 9.8%, 10.5%, and 10.7% of the patients in the combination-facilitated PCI group, abciximab-facilitated PCI group, and primary-PCI group, respectively (P=0.55); 90-day mortality rates were 5.2%, 5.5%, and 4.5%, respectively (P=0.49).</AbstractText>Neither facilitation of PCI with reteplase plus abciximab nor facilitation with abciximab alone significantly improved the clinical outcomes, as compared with abciximab given at the time of PCI, in patients with ST-segment elevation myocardial infarction. (ClinicalTrials.gov number, NCT00046228 [ClinicalTrials.gov].)</AbstractText>Copyright 2008 Massachusetts Medical Society.</CopyrightInformation> |
7,657 | Enhanced left atrial reservoir, increased conduit, and weakened booster pump function in hypertensive patients with paroxysmal atrial fibrillation. | The aim of this study was to evaluate whether paroxysmal atrial fibrillation (PAF) has an impact on left atrial (LA) function in hypertensive patients and, if so, to select clinical factors influencing this relationship. Sixty-four essential hypertensive patients with PAF (group EHf) and fifty-five patients without PAF (group EH) were enrolled. Using acoustic quantification, the maximal and minimum LA volume (LAVmax, LAVmin), the LA volume at the end of rapid emptying (EREV), and the LA volume at the onset of atrial emptying (OAEV) were measured. The LA total emptying volume (TE; TE=LAVmax-LAVmin), LA rapid emptying volume (RE; RE=LAVmax-EREV), and left atrial ejection fraction (LAEF)=(OAEV-LAVmin)/OAEVx100% were calculated. LAVmax, LAVmax indexed to body surface area (LAVmaxI), TE and RE were significantly increased in group EHf. LAEF was clearly lower in group EHf than in group EH. The linear regression analysis showed that the frequency and total number of PAF episodes were the factors with the greatest influence on LAVmaxI (r=0.787, p<0.05). TE and frequency of PAF episodes were the most influential factors on RE (r=0.902, p<0.01). These results suggest that the occurrence of PAF in hypertensive patients is associated with enhanced LA reservoir and conduit function and worse booster pump function. The enhancement of LA reservoir function may be related to the frequency and total number of PAF episodes, and the increased LA conduit function may be related to the LA total emptying volume and frequency of PAF episodes. |
7,658 | Attenuating the defibrillation dosage decreases postresuscitation myocardial dysfunction in a swine model of pediatric ventricular fibrillation. | The optimal biphasic defibrillation dose for children is unknown. Postresuscitation myocardial dysfunction is common and may be worsened by higher defibrillation doses. Adult-dose automated external defibrillators are commonly available; pediatric doses can be delivered by attenuating the adult defibrillation dose through a pediatric pads/cable system. The objective was to investigate whether unattenuated (adult) dose biphasic defibrillation results in greater postresuscitation myocardial dysfunction and damage than attenuated (pediatric) defibrillation.</AbstractText>Laboratory animal experiment.</AbstractText>University animal laboratory.</AbstractText>Domestic swine weighing 19 +/- 3.6 kg.</AbstractText>Fifty-two piglets were randomized to receive biphasic defibrillation using either adult-dose shocks of 200, 300, and 360 J or pediatric-dose shocks of approximately 50, 75, and 85 J after 7 mins of untreated ventricular fibrillation. Contrast left ventriculograms were obtained at baseline and then at 1, 2, 3, and 4 hrs postresuscitation. Postresuscitation left ventricular ejection fraction and cardiac troponins were evaluated.</AbstractText>By design, piglets in the adult-dose group received shocks with more energy (261 +/- 65 J vs. 72 +/- 12 J, p < .001) and higher peak current (37 +/- 8 A vs. 13 +/- 2 A, p < .001) at the largest defibrillation dose needed. In both groups, left ventricular ejection fraction was reduced significantly at 1, 2, and 4 hrs from baseline and improved during the 4 hrs postresuscitation. The decrease in left ventricular ejection fraction from baseline was greater after adult-dose defibrillation. Plasma cardiac troponin levels were elevated 4 hrs postresuscitation in 11 of 19 adult-dose piglets vs. four of 20 pediatric-dose piglets (p = .02).</AbstractText>Unattenuated adult-dose defibrillation results in a greater frequency of myocardial damage and worse postresuscitation myocardial function than pediatric doses in a swine model of prolonged out-of-hospital pediatric ventricular fibrillation cardiac arrest. These data support the use of pediatric attenuating electrodes with adult biphasic automated external defibrillators to defibrillate children.</AbstractText> |
7,659 | Mild therapeutic hypothermia in patients after out-of-hospital cardiac arrest due to acute ST-segment elevation myocardial infarction undergoing immediate percutaneous coronary intervention. | Mild therapeutic hypothermia (MTH) has been integrated into international resuscitation guidelines. In the majority of patients, sudden cardiac arrest is caused by myocardial infarction. This study investigated whether a combination of MTH with primary percutaneous coronary intervention (PCI) is feasible, safe, and potentially beneficial in patients after cardiac arrest due to acute myocardial infarction.</AbstractText>Single-center observational study with a historical control group.</AbstractText>University clinic.</AbstractText>Thirty-three patients after cardiac arrest with ventricular fibrillation as initial rhythm and restoration of spontaneous circulation who remained unconscious at admission and presented with acute ST elevation myocardial infarction (STEMI).</AbstractText>In 16 consecutive patients (2005-2006), MTH was initiated immediately after admission and continued during primary PCI. Seventeen consecutive patients who were treated in a similar 2-yr observation interval before implementation of MTH (2003-2004) served as a control group. Feasibility, safety, mortality, and neurologic outcome were documented.</AbstractText>Initiation of MTH did not result in longer door-to-balloon times compared with the control group (82 vs. 85 mins), indicating that implementation of MTH did not delay the onset of primary PCI. Target temperature (32-34 degrees C) in the MTH group was reached within 4 hrs, consistent with previous trials and suggesting that primary PCI did not affect the velocity of cooling. Despite a tendency to increased bleeding complications and infections, patients treated with MTH tended to have a lower mortality after 6 months (25% vs. 35%, p = .71) and an improved neurologic outcome as determined by a Glasgow-Pittsburgh Cerebral Performance Scale score of 1 or 2 (69% vs. 47% in the control group, p = .30).</AbstractText>MTH in combination with primary PCI is feasible and safe in patients resuscitated after cardiac arrest due to acute myocardial infarction. A combination of these therapeutic procedures should be strongly considered as standard therapy in patients after out-of-hospital cardiac arrest due to STEMI.</AbstractText> |
7,660 | Study of nycthemeral variations in blood pressure in patients with heart failure. | The objective of this study was to describe and analyse the nycthemeral variations in blood pressure (BP) by ambulatory BP monitoring (ABPM) over 24 h in patients with heart failure (HF).</AbstractText>The study population included 50 stable HF patients hospitalized in a cardiology department for acute pulmonary oedema. Parameters studied were: New York Heart Association class, clinical resting BP and heart rate in sitting and then standing positions, ABPM parameters, distance covered during a 6-min walking test, echographic left ventricular ejection fraction (LVEF), natremia, kaliemia, creatininemia, plasma haemoglobin and N-terminal fragment of brain-type natriuretic peptide levels.</AbstractText>Clinical hypertension was noted in 20% of patients (10/50) and orthostatic hypotension in 16% (8/50). Nine of 50 patients (18%) were hypertensive during the day and 21 (42%) at night. Thirty-nine of the 50 patients (78%) are nondippers. Nondipper patients are more prevalent when the HF has been present for more than 24 months (95 vs. 67%, P=0.04). This prevalence does not differ depending on New York Heart Association class or LVEF. Furthermore, there exists: (i) a significant positive relationship (R=0.46, P=0.02) between the diastolic BP (DBP) over 24 h and the distance covered during the walking test; (ii) a significant negative relationship between the day-night differences (in mmHg) of the systolic BP (SBP) (R=-0.46, P=0.01) and DBP (R=-0.33, P=0.03) and the duration of HF, between the day-night difference of the DBP and the LVEF (R=-0.34, P=0.02) and (iii) between the day-night differences of the SBP (R=-0.48, P=0.001) and the DBP (R=-0.32, P=0.03) and natremia. The day-night difference of the SBP has a positive correlation with plasma haemoglobin level (R=0.32, P=0.03).</AbstractText>This study confirms the feasibility of carrying out ABPM with an adapted device in HF patients with atrial fibrillation. ABPM allows diagnosis to be more precise than the clinical measuring of BP abnormalities, which have a pejorative prognosis (e.g. hypertension, hypotension, nondipper status).</AbstractText> |
7,661 | Association between statin therapy and reductions in atrial fibrillation or flutter and inappropriate shock therapy. | In patients without implantable cardioverter defibrillators (ICDs), statins have been shown to reduce the incidence of atrial fibrillation and atrial flutter (AF/AFL). We sought to determine if statin therapy could reduce the occurrence of AF/AFL with rapid ventricular rates with and without inappropriate shock therapy among a large heterogeneous ICD cohort.</AbstractText>We prospectively followed 1445 consecutive patients receiving an ICD for the primary (n = 833) or secondary (n = 612) prevention from December 1997 through January 2007. Outcome measures include incidence of AF/AFL that initiated ICD therapy or was detected during ICD interrogation. Cox hazard regression analyses were conducted to determine the predictors of AF/AFL with and without inappropriate shock delivery and did not include inappropriate shocks resulting from lead dysfunction or other exogenous factors. Patients in this study (n = 1445) were followed over a mean follow-up period of (mean +/- SD) 874 +/- 805 days. There were 563 episodes of AF/AFL detected, with 200 episodes resulting in inappropriate shock therapy. Overall, 745 patients received statin therapy and 700 did not. The use of statin therapy was associated with an adjusted hazard ratio of 0.472 [95% confidence interval (CI), 0.349-0.638, P < 0.001] for the development of AF/AFL with shock therapy and 0.613 (95% CI, 0.496-0.758, P < 0.001) without shock therapy when compared with the group without statin use.</AbstractText>Among a cohort with ICDs at high risk for cardiac arrhythmias, statin therapy was associated with a reduction in AF/AFL tachyarrhythmia detection and inappropriate shock therapy.</AbstractText> |
7,662 | Severe diffuse coronary artery spasm in the early phase of cardiogenic shock. | Coronary artery vasospasm rarely appears as a diffuse phenomenon that involves all the coronary tree. We present a clinical case of acute myocardial infarction complicated by ventricular fibrillation and cardiogenic shock. Urgent coronary angiography showed occlusion of proximal Circumflex coronary artery and a TIMI I flow in the left anterior descending artery due to severe, diffuse coronary vasospasm. Patient was successfully treated with intra-aortic balloon pump and intracoronary bolus of nitroglycerin with restoration of flow in left coronary branches and complete resolution of shock. |
7,663 | Minimal model for human ventricular action potentials in tissue. | Modeling the dynamics of wave propagation in human ventricular tissue and studying wave stability require models that reproduce realistic characteristics in tissue. We present a minimal ventricular (MV) human model that is designed to reproduce important tissue-level characteristics of epicardial, endocardial and midmyocardial cells, including action potential (AP) amplitudes and morphologies, upstroke velocities, steady-state action potential duration (APD) and conduction velocity (CV) restitution curves, minimum APD, and minimum diastolic interval. The model is then compared with three previously published human ventricular cell models, the Priebe and Beuckelmann (PB), the Ten Tusscher-Noble-Noble-Panfilov (TNNP), and the Iyer-Mazhari-Winslow (IMW). For the first time, the stability of reentrant waves for all four models is analyzed, and quantitative comparisons are made among the models in single cells and in tissue. The PB, TNNP, and IMW models exhibit quantitative differences in APD and CV rate adaptation, as well as completely different reentrant wave dynamics of quasi-breakup, stability, and breakup, respectively. All the models have dominant frequencies comparable to clinical values except for the IMW model, which has a large range of frequencies extending beyond the clinical range for both ventricular tachycardia (VT) and ventricular fibrillation (VF). The TNNP and IMW models possess a large degree of short-term memory and we show for the first time the existence of memory in CV restitution. The MV model also can be fitted to reproduce the dynamics of other models and is computationally more efficient: the times required to simulate the MV, TNNP, PB and IMW models follow the ratio 1:31:50:8084. |
7,664 | Predicting drug-induced changes in QT interval and arrhythmias: QT-shortening drugs point to gaps in the ICHS7B Guidelines. | The regulatory guidelines (ICHS7B) recommending inhibition of the delayed rectifier K(+) current (I(Kr)), carried by human ether-a-go-go-related gene (hERG) channels in cardiac cells (the hERG test), as a 'first line' test for identifying compounds inducing QT prolongation, have limitations, some of which are outlined here.</AbstractText>hERG current was measured in HEK293 cells, stably transfected with hERG channels; action potential duration (APD) and arrhythmogenic effects were measured in isolated Purkinje fibres and perfused hearts from rabbits.</AbstractText>576 compounds were screened in the hERG test: 58% were identified as hERG inhibitors, 39% had no effect and 3% were classified as stimulators. Of the hERG inhibitors, 92 were tested in the APD assay: 55.4% of these prolonged APD, 28.3% had no effect and 16.3% shortened APD. Of the 70 compounds without effect on hERG channels, 54.3% did not affect APD, 25.7% prolonged, while 20% significantly shortened APD. Dofetilide (hERG inhibitor; IC(50), 29 nM) prolonged QT and elicited early after-depolarizations and/or torsade de pointes (TdP) in isolated hearts. Mallotoxin and NS1643 (hERG current stimulators at 3 microM), levcromakalim and nicorandil (no effect on hERG current), all significantly shortened APD and QT, and elicited ventricular fibrillation (VF) in isolated hearts.</AbstractText>The hERG assay alone did not adequately identify drugs inducing QT prolongation. It is also important to detect drug-induced QT shortening, as this effect is associated with a potential risk for ventricular tachycardia and VF, the latter being invariably fatal, whereas TdP has an approximately 15-25% incidence of death.</AbstractText> |
7,665 | Tako-Tsubo syndrome in a pregnant woman. | We describe a rare case of Tako-Tsubo syndrome which occurred in a young woman at the beginning of pregnancy, who presented cardiac arrest at onset. In this case, the transient left ventricular ballooning involving both mid and apical segments, in absence of coronary artery disease, produced a severe impairment of cardiac function with typical echocardiographic and electrocardiographic findings. The favourable outcome, despite the sudden cardiac death at the beginning, raises further questions on this new kind of cardiomyopathy. |
7,666 | Left atrial reservoir function as a potent marker for first atrial fibrillation or flutter in persons > or = 65 years of age. | The aim of this prospective study was to evaluate the incremental value of left atrial (LA) function for the prediction of risk for first atrial fibrillation (AF) or atrial flutter. Maximum and minimum LA volumes were quantitated by echocardiography in 574 adults (mean age 74 +/- 6 years, 52% men) without a history or evidence of atrial arrhythmia. During a mean follow-up period of 1.9 +/- 1.2 years, 30 subjects (5.2%) developed electrocardiographically confirmed AF or atrial flutter. Subjects with new AF or atrial flutter had lower LA reservoir function, as measured by total LA emptying fraction (38% vs 49%, p <0.0001) and higher maximum LA volumes (47 vs 40 ml/m(2), p = 0.005). An increase in age-adjusted risk for AF or atrial flutter was evident when the cohort was stratified according to medians of LA emptying fraction (< or =49%: hazard ratio 6.5, p = 0.001) and LA volume (> or =38 ml/m(2): hazard ratio 2.0, p = 0.07), with the risk being highest for subjects with concomitant LA emptying fractions < or =49% and LA volume > or =38 ml/m(2) (hazard ratio 9.3, p = 0.003). LA emptying fraction (p = 0.002) was associated with risk for first AF or atrial flutter after adjusting for baseline clinical risk factors for AF or atrial flutter, left ventricular ejection fraction, diastolic function grade, and LA volume. In conclusion, reduced LA reservoir function markedly increases the propensity for first AF or atrial flutter, independent of LA volume, left ventricular function, and clinical risk factors. |
7,667 | Left ventricular systolic function in the prognosis of patients hospitalized due to worsening heart failure. | Preserved left ventricular systolic function (LVSF) is observed in up to 50% of patients with heart failure (HF). We aimed to determine the prognostic value of LVSF and identify prognostic indices in patients hospitalized due to HF with preserved and depressed LVSF.</AbstractText>We evaluated clinical records of 304 patients admitted due to decompensated HF, with ECG, echocardiogram and plasma NT-proBNP determination. The endpoint was death or hospital readmission within 6 months.</AbstractText>Patients with preserved LVSF were more frequently women (72.9% vs. 45.0%, p < 0.001) and were more frequently in atrial fibrillation (56.3% vs. 35.6%, p < 0.001). NT-proBNP values at discharge were higher in patients with depressed LVSF (median 5291 [2050-10306] vs. 2146 [1048-4052] pg/ml, p < 0.001). Among patients with preserved LVSF, predictors of adverse events were male ender, hemoglobin, serum creatinine and serum sodium levels at discharge. Among patients with depressed LVSF, predictors of adverse events were male gender, atrial fibrillation, non-prescription of ACE inhibitors at discharge and NT-proBNP levels at discharge. Death or hospital readmission occurred in 40 patients with preserved LVSF and 95 with depressed LVSF (HR = 1.20 [95% CI: 0.83-1.73]).</AbstractText>Our results show an ominous prognosis of acute HF, regardless of LVSF, in an elderly HF population. Patients with preserved LVSF presented weaker neurohumoral activation, These results reinforce the need for closer follow-up and aggressive strategies irrespective of systolic function in HF patients.</AbstractText> |
7,668 | Familial and sporadic hypertrophic myopathy: differences and similarities in a genotyped population. A long follow-up study. | Hypertrophic cardiomyopathy (HCM) is a genetic disease associated with mutations in genes encoding cardiac sarcomere proteins. A mutation is identified in two-thirds of cases, and more frequently in familial forms. Doubts remain concerning the true identity of the sporadic form.</AbstractText>To compare, in a genotyped population, the phenotypic expression of the disease over time in patients with familial and sporadic HCM.</AbstractText>79 patients with HCM, aged 39 +/- 17.8 years at diagnosis, were followed for 12 +/- 9.5 (1-30) years and divided into two groups: G1 (familial)--68 patients (24 unrelated index patients, 44 relatives), follow-up time (FUP) 12 +/- 9.8 (1-30) years; G2 (sporadic)1 index patients (no phenotypic disease in first-degree relatives), FUP 10.8 +/- 8 (2-24) years. Fabry disease was excluded in G2. The two groups were compared regarding clinical, ECG and echocardiographic (echo) features at diagnosis and after FUP. Five sarcomere genes (MYH7, MYBPC3, TNNT2, MYL2 and TNNI3) were screened for mutations by direct sequencing, after PCR amplification with intronic sets of oligonucleotide primers designed according to the published genomic sequence of the genes.</AbstractText>A) Thirteen different mutations (in 3 genes) were identified in 14 index patients in G1; only in one patient in G2 was a mutation found. B) The two groups differed clinically in age at diagnosis (G1: 37.18 (4-79) years; G2: 51 +/- 14 (19-67) years; p = 0.02), and family history of sudden cardiac death (G1: 12/24 families; G2: 1/11 families; p = 0.04). Age, gender, FUP, symptoms, need for medical treatment, cardiovascular (CV) hospitalization and mortality (CV or any cause) were similar. C) ECG patterns did not differ, although significant (but similar) changes occurred in 45% (G1) and 36% (G2) of patients (p = 0.75). These changes were in the same direction, with a trend in both groups toward the development of atrial fibrillation and/or advanced conduction disease. D) Echo features (only considered in adults) were similar despite significant changes during FUP (in 68% of G1, and 82% of G2; p = 0.48). These changes also followed the same tendency: progression to a more diffuse pattern of ventricular hypertrophy (G1: 52%; G2: 73%; p = 0.33) and development of left atrial dilatation (G1: 37%; G2: 45%; p = 0.52).</AbstractText>The similar phenotypic expression and behavior over time in familial and sporadic forms of HCM strongly indicate that the disease is one and the same. Differences in genetic findings, age at diagnosis and family history of sudden death suggest that sporadic forms may be caused by low penetrance de novo mutations in sarcomeric genes other than those associated with familial disease.</AbstractText> |
7,669 | [The utility of assaying the N-terminal of brain natriuretic peptide precursor (NT pro-BNP) to predict the clinical outcome in patients with supraventricular tachyarrhythmias observed and treated in the emergency room]. | Many patients arrive at the emergency room (ER) with recent-onset atrial fibrillation or other forms of supraventricular tachyarrhythmia (SV Ta) or tachycardia. The restoration of sinus rhythm (SR) is always desirable and, in addition, can enable many hospitalisations to be avoided, thereby achieving considerable savings in financial and healthcare resources. Even in haemodynamically stable cases, it is clearly useful to be able to evaluate which subjects will benefit most from attempts to restore SR, even when few truly diagnostic means are on hand (such as echocardiography, which is not always promptly available in the ER setting). We evaluated the brain natriuretic peptide precursor (N terminal pro-BNP) in 105 patients arriving at the ER. We observed that SR was restored in a low percentage of patients with values > 4500, while the vast majority of those with values < 1500 was normalised even by means of antiarrhythmic drugs alone. It is therefore probable that a medium-low value of the hormone indicates only an acute response to the distension of the atrial tissue induced by the arrhythmia; by contrast, decidedly elevated values are probably also caused by ventricular dysfunction and therefore indicate a lesser likelihood of restoring SR. The routine evaluation of NT pro-BNP could be used as an alternative to echocardiography in order to rapidly select patients in whom cardioversion should be attempted in the ER or Brief Observation Unit. |
7,670 | Mobile biatrial thrombus in a patient with mitral stenosis under heparin infusion. | A 58-year-old female patient with complaints of sudden presenting pain and pallor on her left foot was referred to our clinic for urgent embolectomy. On her cardiovascular examination there was an apical grade 2/6 systolic murmur and a grade 2/4 diastolic murmur. The presenting electrocardiography revealed atrial fibrillation with rapid ventricular response. She underwent emergent femoro-popliteal embolectomy. Transthoracic echocardiography showed a mobile 1.4 x 1.7-cm sized left atrial thrombus, mild mitral regurgitation and 9 mmHg mean gradient on mitral valve after embolectomy. Unfractioned (UF) heparin infusion was initiated immediately after surgery. After three days, the control transthoracic echocardiography revealed left atrial thrombus and also a large 'snake-like' thrombus waving in right atrium. The patient underwent biatrial thrombectomy and mitral valve replacement. When she became haemodynamically stable, a bilateral lower limb venous Doppler ultrasonographic study was performed. This study indicated a thrombus formation in the deep veins of the left leg. The origin of the right atrial thrombus was probably a snapped piece of thrombus from the calf deep-veins after the initiation of intravenous UF heparin. In summary, we have reported an extremely rare case of biatrial thrombus in a patient under UF heparin infusion. |
7,671 | Using within-patient correlation to improve the accuracy of shock outcome prediction for cardiac arrest. | Analysis of the electrocardiogram (ECG) can to a certain extent predict if a cardiac arrest patient in ventricular fibrillation will get return of spontaneous circulation (ROSC) if defibrillated. The accuracy of such methods determines how useful it is clinically and for retrospective analysis.</AbstractText>We have tested the accuracy of a new shock outcome prediction algorithm that is the first to use an updating algorithm capable of learning from previous shocks within a resuscitation effort. The algorithm relies on known predictive features from the pre-shock ECG, but for each delivered shock it re-estimates the patient-dependent relationship between predictive feature value and probability of ROSC by incorporating the information from the already performed shocks. The predictive features mean-slope, median-slope, cardioversion-outcome-predictor and amplitude-spectrum-analysis originally had areas under the receiver operating characteristics curve of 0.843, 0.846, 0.837 and 0.819, respectively. The improvements in areas after applying the algorithm were (bootstrap estimate of mean improvement, 95% confidence interval in parentheses): mean-slope, 0.019 (0.00036, 0.042); median-slope, 0.024 (0.0013, 0.048); cardioversion-outcome-predictor, 0.021 (0.0010, 0.051); amplitude-spectrum-analysis, 0.026 (0.0016, 0.051). The predictions for the first shock to each patient were not included when calculating the areas, as for the first shocks the new algorithm has no previous shocks to learn from and give predictions identical to those of the original features.</AbstractText>It is possible to improve current shock prediction methods by using an updating algorithm capable of learning from previous shocks within a resuscitation effort.</AbstractText> |
7,672 | ST-T wave changes in a patient complicated with vasospastic angina and Brugada syndrome: differential responses to acetylcholine in right and left coronary artery. | A 49-year-old man with chest pain and syncope presented saddleback or occasionally coved type ST elevation in V1-V3. Coronary spasm in the left anterior descending artery was induced by acetylcholine injection and ST elevation changed from saddleback to coved type in V2-V3 together with ST depression in V4-V5, whereas acetylcholine injection into the right coronary artery did not provoke spasm, but induced augmented and coved type ST elevation in V2 without ST-T changes in V4-V5. These electrocardiographic changes in response to acetylcholine administration into each coronary artery are compatible with pathogenesis of vasospastic angina and Brugada syndrome, respectively. |
7,673 | Prehospital cardiac arrest: a marker for higher mortality in patients with acute myocardial infarction and moderately reduced left ventricular function: results from the MITRA plus registry. | According to the current guidelines for acute myocardial infarction, ventricular fibrillation during the acute phase of myocardial infarction is no indication for specific treatment like ICD implantation. Primary objective of our study was to evaluate the prognostic significance of cardiac arrest within the acute phase of myocardial infarction in patients with moderately reduced left ventricular function.</AbstractText>From 1994 until 2004, we included 7111 patients with acute STEMI and an LVEF >30% from the MITRA plus registry who were discharged alive from hospital and had a complete follow up. We compared long term prognosis on total mortality in patients with and without prehospital cardiac arrest. 286 out of 7111 patients (4%) with moderately reduced LVEF >30% after STEMI had prehospital cardiac arrest and were discharged alive from hospital. In these patients, total mortality during a mean follow up of 13 months was 13.6% compared to 8.7% in patients without cardiac arrest, although patients with cardiac arrest were younger and had less risk factors. Higher mortality after cardiac arrest was independent from gender, risk factors and medical treatment. Only in patients with preserved LVEF >55% after STEMI, mortality was equal in patients with and without cardiac arrest.</AbstractText>Prehospital cardiac arrest in the acute phase of STEMI is an independent risk indicator for higher mortality in patients with moderately reduced left ventricular function (LVEF 30-55%). To evaluate the prognostic impact of the implantation of an ICD in these patients, further investigation is needed.</AbstractText> |
7,674 | Immediate post-shock chest compressions improve outcome from prolonged ventricular fibrillation. | This study was designed to test the hypothesis that immediate post-shock chest compressions improve outcome from prolonged ventricular fibrillation (VF) compared with typical "hands off" period (i.e., delayed post-shock compressions) associated with AED use.</AbstractText>After 7.5 min of untreated VF, 36 domestic swine (26+/-1 kg) were treated with 200 J biphasic shocks and randomly assigned to: (1) 1 min of immediate post-shock chest compressions or (2) simulated pre-hospital automated external defibrillator (AED) care with delays in post-shock chest compressions. Return of spontaneous circulation (ROSC) occurred in 7/18 immediate chest compressions animals within 2 min of the first shock versus 0/18 AED animals (P<0.01). Ten of 18 immediate chest compressions animals attained ROSC compared with 3/18 AED animals (P<0.05). Nine of 18 immediate chest compressions swine were alive at 24 and 48 h compared with 3/18 AED swine (P<0.05). All 48-h survivors had good neurologic outcomes. Among the 21 animals that defibrillated with the first shock, ROSC was attained in 7/10 immediate chest compressions animals within 2 min of the first shock compared with 0/11 AED animals (P=0.001), and 48-h survival was attained in 8/10 versus 3/11, respectively (P<0.05).</AbstractText>Immediate post-shock chest compressions can substantially improve outcome from prolonged VF compared with simulated pre-hospital AED care.</AbstractText> |
7,675 | Rationale, development and implementation of the Resuscitation Outcomes Consortium Epistry-Cardiac Arrest. | To describe the development, design and consequent scientific implications of the Resuscitation Outcomes Consortium (ROC) population-based registry; ROC Epistry-Cardiac Arrest.</AbstractText>The ROC Epistry--Cardiac Arrest is designed as a prospective population-based registry of all Emergency Medical Services (EMSs)-attended 9-1-1 calls for patients with out-of-hospital cardiac arrest occurring in the geographical area described by the eight US and three Canadian regions. The dataset was derived by an North American interdisciplinary steering committee. Enrolled cases include individuals of all ages who experience cardiac arrest outside the hospital, with evaluation by organized EMS personnel and: (a) attempts at external defibrillation (by lay responders or emergency personnel), or chest compressions by organized EMS personnel; (b) were pulseless but did not receive attempts to defibrillate or CPR by EMS personnel. Selected data items are categorized as mandatory or optional and undergo revisions approximately every 12 months. Where possible all definitions are referenced to existing literature. Where a common definition did not exist one was developed. Optional items include standardized CPR process data elements. It is anticipated the ROC Epistry--Cardiac Arrest will enroll between approximately 9000 and 13,500 treated all rhythm arrests and 4000 and 5000 ventricular fibrillation arrests annually and approximately 8000 EMS-attended but untreated arrests.</AbstractText>We describe the rationale, development, design and future implications of the ROC Epistry--Cardiac Arrest. This paper will serve as the reference for subsequent ROC manuscripts and for the common data elements captured in both ROC Epistry--Cardiac Arrest and the ROC trials.</AbstractText> |
7,676 | Intracoronary infusion of catecholamines causes focal arrhythmias in pigs. | Acute ischemia causes myriad changes including increased catecholamines. We tested the hypothesis that elevated catecholamines alone are arrhythmogenic.</AbstractText>A 504 electrode sock was placed over both ventricles in six open-chest pigs. During control infusion of saline through a catheter in the left anterior descending coronary artery (LAD), no sustained arrhythmias occurred, and the refractory period estimated by the activation recovery interval (ARI) was 175 +/- 14 ms in the LAD bed below the catheter. After infusion of isoproterenol at 0.1 microg/kg/min through the catheter, the ARI in this bed was significantly reduced to 109 +/- 10 ms. A sharp gradient of refractoriness of 43 +/- 10 ms was at the border of the perfused bed. Sustained monomorphic ventricular tachycardia occurred after drug infusion in the perfused bed or near its boundary in all animals with a cycle length of 329 +/- 26 ms and a focal origin. The maximum slope of the ARI restitution curve at the focal origins of the tachyarrhythmias was always <1 (0.62 +/- 0.15). Similar results with a focal arrhythmia origin occurred in two additional pigs in which intramural mapping was performed with 36 plunge needle electrodes in the left ventricular perfused bed.</AbstractText>Regional elevation of a catecholamine, which is one of the alterations produced by acute ischemia, can by itself cause tachyarrhythmias. These arrhythmias are closely associated with a shortened refractory period and a large gradient of the spatial distribution of refractoriness but not with a steep restitution curve.</AbstractText> |
7,677 | Effects of procainamide and sotalol on restitution properties, dispersion of refractoriness, and ventricular fibrillation activation patterns in pigs. | Interest in combining antiarrhythmic drugs has been prompted by the lack of efficacy of monotherapies and the toxicity resulting from high doses of individual agents.</AbstractText>We tested the hypothesis that procainamide and sotalol combined have greater beneficial effects on restitution, on the dispersion of refractoriness, and on decreasing the complexity of ventricular fibrillation (VF) than either drug alone.</AbstractText>Six open-chest pigs received intravenous procainamide (15 mg/kg load and 50 microg/kg/min maintenance) followed by sotalol (1.5 mg/kg). Another six pigs received sotalol first and procainamide second. Before drugs and after each drug, 20-second episodes of electrically induced VF were recorded from a 21 x 24 unipolar electrode plaque (2 mm spacing) sutured on the lateral posterior left ventricular epicardium. Restitution properties and dispersion of refractoriness were estimated from activation recovery intervals during pacing.</AbstractText>The combination of the two drugs reduced the maximum slope of the restitution curve and during VF reduced the number of wavefronts, the activation rate, the percentage of wavefront families exhibiting reentry, and the conduction velocity more than either drug alone. In addition, in the group that received sotalol first, both drugs together reduced the SD and the coefficient of variation of the spatial dispersion of refractoriness compared with baseline.</AbstractText>Procainamide and sotalol combined have greater beneficial effects on restitution properties, dispersion of refractoriness, and the complexity of VF than either drug alone compared with baseline.</AbstractText> |
7,678 | Hypertrophic cardiomyopathy with preexcitation: insights from noninvasive electrocardiographic imaging (ECGI) and catheter mapping. | Hypertrophic Cardiomyopathy and Preexcitation.</AbstractText>Fasciculoventricular pathway has been described as an unusual variant of preexcitation. Electrocardiographic imaging (ECGI) is a novel imaging modality for noninvasive electroanatomic mapping of epicardial activation and repolarization.</AbstractText>We present a case of an 18-year-old male with hypertrophic cardiomyopathy (HCM) and an electrocardiogram (ECG)-based diagnosis of Wolff-Parkinson-White (WPW) syndrome, who underwent a noninvasive ECGI study to image ventricular activation, followed by an electrophysiology study (EPS). The ECGI electroanatomic isochrone map showed early activation of the epicardial aspect of the atrioventricular (A-V) groove and an aberrant posterior-base-to-apex progression of activation in the left ventricular (LV) epicardium. The EPS showed a likely fasciculoventricular pathway (FVP) without any inducible tachycardia.</AbstractText>While FVP has been described before, this is the first report of detailed quantitative three-dimensional characterization of electrical activation sequence of a heart with this type of preexcitation, using a novel noninvasive imaging modality (ECGI). In spite of abnormal ventricular activation, the EPS demonstrated that the FVP is not capable of supporting reentrant supraventricular tachycardia or rapidly conducted atrial fibrillation.</AbstractText> |
7,679 | Effect of ranolazine on ventricular vulnerability and defibrillation threshold in the intact porcine heart. | Extensive in vitro studies and clinical evidence (MERLIN trial) indicate an antiarrhythmic potential of ranolazine, a novel antianginal agent. Programmed electrophysiologic testing was performed to quantify ranolazine's effects on ventricular vulnerability and defibrillation thresholds and to gain insights into mechanisms.</AbstractText>Effects of ranolazine (9.2 +/- 2.1 microM, plasma level) on surface ECG, right ventricular effective refractory period (ERP), and repetitive extrasystole (RE), ventricular fibrillation (VF), and defibrillation (DFT) thresholds were determined in 29 normal closed-chest anesthetized pigs. The single extrastimulus method was employed for ERP and for RE and VF thresholds. DFT(50) was determined using an up-down testing protocol with an implantable cardioverter-defibrillator. Ranolazine increased rate-corrected QT interval from 490 +/- 30 to 527 +/- 24 ms (P < 0.05) but did not alter T(peak)-T(end) interval (59 +/- 8 to 62 +/- 11, P = 0.65). ERP increased by 40 +/- 6 ms (P < 0.001). Compared with baseline, ranolazine raised RE threshold from 20 +/- 6 to 34 +/- 9 mA (P < 0.001) and VF threshold from 38 +/- 4 to 48 +/- 10 mA (P < 0.05). DFT(50) was unchanged (baseline: 14 +/- 2 J; ranolazine: 14 +/- 2 J; P = 0.6), whereas diastolic pacing threshold increased from baseline pulse width of 0.07 +/- 0.03 to 0.17 +/- 0.07 ms (P < 0.01) with 1V pulse amplitude.</AbstractText>Ranolazine, at therapeutic concentrations, produces a mild increase in QT interval and a marked increase in both RE and VF thresholds. Thus, ranolazine does not augment and may improve dispersion of ventricular repolarization, suggesting a potential antiarrhythmic action. Ranolazine is unlikely to affect the margin of safety of defibrillation, given no significant effect on DFT, but could result in a mild increase in pacing threshold.</AbstractText> |
7,680 | Clinical use of cooled radiofrequency ablation. | Irrigated (cooled) radiofrequency (RF) ablation has become our primary ablation tool for treating atrial fibrillation, macroreentrant atrial tachycardias, and scar-related ventricular tachycardias. As with any technology that increases ablation lesion size, there is the potential for increased risk. The methods described are a cautious approach to power titration that considers the risks of excessive heating and the lesion size needed for a particular site. Future methods of assessing lesion creation will hopefully refine energy titration to improve safety and efficacy of cooled RF ablation. |
7,681 | Improved survival after an out-of-hospital cardiac arrest using new guidelines. | An out-of-hospital cardiac arrest (OHCA) is associated with a poor prognosis. We hypothesized that the implementations of 2005 European Resuscitation Council resuscitation guidelines were associated with improved 30-day survival after OHCA.</AbstractText>We prospectively recorded data on all patients with OHCA treated by the Mobile Emergency Care Unit of Copenhagen in two periods: 1 June 2004 until 31 August 2005 (before implementation) and 1 January 2006 until 31 March 2007 (after implementation), separated by a 4-month period in which the above-mentioned change took place.</AbstractText>We found that 30-day survival increased after the implementation from 31/372 (8.3%) to 67/419 (16%), P=0.001. ROSC at hospital admission, as well as survival to hospital discharge, were obtained in a significantly higher proportion from 23.4% to 39.1%, P<0.0001, and from 7.9% to 16.3%, P=0.0004, respectively. Treatment after implementation was confirmed as a significant predictor of better 30-day survival in a logistic regression analysis.</AbstractText>The implementation of new resuscitation guidelines was associated with improved 30-day survival after OHCA.</AbstractText> |
7,682 | Thyrotoxic cardiomyopathy and encephalopathy in a paraplegic man. | Case report.</AbstractText><AbstractText Label="BACKGROUND/OBJECTIVE" NlmCategory="OBJECTIVE">Thyrotoxicosis complicating spinal cord injury is more common than generally appreciated. To raise the level of awareness, the following case of fatal thyrotoxicosis is presented.</AbstractText>A 77-year-old man, paralyzed at the T12 level for 46 years, developed a sudden 42 lb weight loss, dyspnea, interscapular pain, 120/40 mm Hg blood pressure, a nodular thyroid gland, atrial fibrillation, progressive cardiac enlargement, left ventricular ejection fraction diminishing from 30 to 10% and a persistently low level of thyrotropic hormone, 0.05-0.2 microU ml(-1) (normal 0.35-5.5 microU ml(-1)). As coronary artery bypass grafting had been carried out 6 years earlier and other signs of thyrotoxicosis-exophthalmos, lid lag, sweating, tremor and diarrhea-were absent, recurrent arteriosclerotic heart disease was assumed and a trial of thyroid suppression not attempted. He eventually developed depression and memory loss and died in heart failure after a 4-year course of this illness.</AbstractText>This case probably represented a toxic multinodular goiter in an elderly paraplegic man with potentially treatable cardiovascular and nervous system complications.</AbstractText> |
7,683 | Double rhythm in double heart. | We describe the case of a patient with heterotopic transplantation, sinus rhythm originating from the donor heart, ventricular fibrillation of the native heart and right severe decompensation. The double rhythm was easily detected with a surface ECG and the transthoracic echocardiogram, both performed in the left conventional and in the right modified mode. The patient was successfully treated with direct current shock with quick restoration of native heart synchronization and clinical relief of symptoms. |
7,684 | C-reactive protein but not atrial dysfunction predicts recurrences of atrial fibrillation after cardioversion in patients with preserved left ventricular function. | Maintenance of sinus rhythm after cardioversion of atrial fibrillation is a major clinical challenge also in patients with preserved left ventricular function. Subclinical inflammation and atrial strain have been recognized as important contributors to atrial fibrillation onset and perpetuation. Aim of the study was to compare the predictive role of C-reactive protein (CRP) and indices of atrial dysfunction in relation to subacute arrhythmic recurrence rate in patients with persistent atrial fibrillation and normal left ventricular ejection fraction (LVEF).</AbstractText>We studied 53 patients with a mean LVEF of 58.7 +/- 6%. Left atrial diameter and area, left atrial auricle emptying velocity, N-terminal pro-b-type natriuretic peptide (NT-proBNP) and CRP levels were determined few hours before electrical cardioversion. NT-proBNP and CRP levels were also measured 1 h and 3 weeks after cardioversion.</AbstractText>Subacute atrial fibrillation recurrences were documented in 18 (33.9%) patients. Whereas none of the parameters reflecting atrial dysfunction predicted arrhythmic outcome, higher CRP levels (>3.0 mg/l) were significantly associated with atrial fibrillation recurrences [odds ratio (OR): 1.6; 95% confidence interval (CI): 1.4-2.5; P = 0.031]. No changes in CRP levels were evident after cardioversion independently of underlying rhythm. On the contrary, NT-proBNP levels, which were correlated with left atrial auricle emptying velocity, significantly decreased only in patients who maintained sinus rhythm (from 638 +/- 329 to 295 +/- 261 pg/ml; P < 0.001).</AbstractText>The present study demonstrates that in patients with persistent atrial fibrillation and preserved LVEF, CRP level is an independent predictor of atrial fibrillation subacute recurrence rate, whereas none of the indices of atrial dysfunction is associated with arrhythmic outcome. NT-proBNP levels reflect, instead, the hemodynamic alterations secondary to arrhythmia presence.</AbstractText> |
7,685 | Safety of myocardial flash-contrast echocardiography in combination with dobutamine stress testing for the detection of ischaemia in 5250 studies. | The purpose of the present study was to provide evidence regarding the safety of real-time flash-contrast echocardiography combined with dobutamine-atropine stress echo (DASE).</AbstractText>The combination of perfusion assessment using myocardial contrast echocardiography (MCE) with DASE has shown very promising results for the diagnosis of coronary artery disease. Concerns have, however, been expressed regarding the safety of the use of echo-contrast agents in echocardiography.</AbstractText>5250 individuals (70.8% men, aged 64.6 years (SD 10.6)) were submitted to DASE, with concurrent MCE using a low mechanical index technique with the administration of high-energy impulses in order to assess replenishment time.</AbstractText>No deaths or myocardial infarctions were observed. Sustained ventricular tachycardia (VT) or fibrillation requiring resuscitation occurred in two cases (0.04%). The incidence of other arrhythmic events was: sustained VT not requiring resuscitation, 10 (0.18%); non-sustained VT, 18 (0.34%); atrial tachycardia, 4 (0.08%); atrial fibrillation, 25 (0.48%). Other observed adverse events included: intense headache, 52 (1%); intense back pain, 26 (0.5%). Vagal reactions with marked systolic blood pressure falls were observed in 45 cases (0.9%). Hypersensitivity reactions were reported in 23 cases (0.44%), although no serious cases of hypersensitivity requiring hospitalisation were recorded. The sensitivity, specificity and overall accuracy of DASE/MCE were 92%, 61% and 85%, respectively.</AbstractText>This report of safety data regarding stress-contrast echocardiography in a large series of subjects suggests that this is an exceptionally safe technique, given that in 5250 studies no study-related deaths or myocardial infarctions were encountered, whereas serious adverse events requiring hospitalisation were extremely rare (one in 2625 studies).</AbstractText> |
7,686 | Perioperative management of a 7-year-old child with Brugada syndrome. | Brugada syndrome results from abnormalities in the myocardial transmembrane conduction of sodium, resulting in the characteristic electrocardiographic changes of ST segment elevation in the precordial leads and incomplete right bundle branch block in an otherwise structurally normal heart. Affected patients are frequently asymptomatic until their presentation with potentially lethal arrhythmias including ventricular fibrillation. The youngest reported patient with Brugada syndrome to undergo anesthetic management is presented in this article; the pathophysiology of the syndrome is reviewed, and its perioperative implications are discussed. |
7,687 | The synergism between atrial fibrillation and heart failure. | Atrial fibrillation (AF) is a common comorbidity in heart failure (HF) patients and is classically associated with acceleration in the rate of HF progression. The precise mechanism for this interaction is unclear, but comprises "bidirectional" aspects in which AF promotes HF and HF also increases the likelihood of AF. We therefore studied the relationship between AF in an ovine model of pacing-induced congestive HF, in an attempt to identify the mechanisms that underpin the apparent synergistic relationship between AF and HF.</AbstractText>Sixteen adult sheep were paced at 190 beats/min for 21 days (HF). AF was induced in 8 of these animals at 14 days' pacing using programmed extrastimuli (HF + AF). Left ventricular hemodynamics and the pattern of cardiac neurohormonal activation, via coronary sinus (CS) sampling, were determined at rest and during submaximal exercise testing in both groups at 21 days and after AF reversion (by atrial defibrillation) at 21 days. CS norepinephrine (NE), endothelin (ET-1), and brain natriuretic peptide (BNP) levels were significantly increased in HF + AF animals, whereas LV end-diastolic pressure (EDP) and LV dP/dt max were significantly reduced compared with moderate HF alone. Cardioversion significantly reduced CS NE and BNP levels and improved contractility in AF + HF animals. In a further 6 animals, we explored the mechanism by which HF increases susceptibility to AF, with specific emphasis on the influence of functional mitral regurgitation. The elimination of MR in HF animals using a percutaneous mitral annular reduction device significantly decreased the inducibility of AF.</AbstractText>AF induction significantly depresses left ventricular function and causes activation of myocardial neurohormones. In conjunction, the presence of functional MR increases susceptibility to AF and this may be attenuated by MR reduction by percutaneous mitral annular reduction.</AbstractText> |
7,688 | Sub-clinical vascular disease in type 2 diabetic subjects: relationship with chronic complications of diabetes and the presence of cardiovascular disease risk factors. | We evaluated the association between a low ankle-brachial index (ABI), chronic complications of diabetes, and the presence of traditional cardiovascular disease risk factors in subjects with type 2 diabetes but without known cardiovascular disease.</AbstractText>We included diabetic subjects (n=923; 52% male; age range 50-85 years) without clinical evidence of coronary, cerebrovascular, or peripheral artery disease (PAD). A history of nephropathy, retinopathy, or neuropathy was collected from the medical records. A 12-lead electrocardiogram and ABI measurements were conducted on all study participants.</AbstractText>The mean duration of diabetes was 9.6 years. Prevalence of a low ABI (<0.9) was 26.2%. Multivariate analysis indicated that factors significantly associated with a low ABI were age (OR: 1.06; 95%CI: 1.033-1.084; p<0.001), plasma triglyceride concentration (OR: 1.002; 95%CI: 1.001-1.004; p=0.006), duration of diabetes (OR: 1.029; 95%CI: 1.008-1.051; p=0.007), and smoking habit (OR: 1.755; 95%CI: 1.053-2.925; p=0.03). The presence of nephropathy, neuropathy, retinopathy, left ventricular hypertrophy, left bundle branch block, and atrial fibrillation were all associated with a low ABI, but only renal disease remained significant after adjusting for age, duration of diabetes, and cardiovascular risk factors.</AbstractText>A low ABI is highly prevalent in subjects with diabetes and is related to age, duration of diabetes, smoking habit, and hypertriglyceridemia. Although chronic complications are frequently associated with a low ABI, only renal damage is independently associated with peripheral artery disease.</AbstractText> |
7,689 | Early repolarization syndrome and Brugada syndrome: is there any linkage? | Early repolarization syndrome (ERS) is characterized by the presence, in most cases in mid-to-lateral precordial leads, of a J wave on the downsloping portion of the QRS complex, followed by an elevation of the ST-segment with upward concavity. ERS is considered a benign electrocardiographic pattern of ventricular repolarization and, thus far, clinical interest in this syndrome has been confined to its differential diagnosis from myocardial infarction and pericarditis. Brugada syndrome (BS), an inherited cardiac disease first described in 1992, exhibits a characteristic electrocardiographic pattern consisting of a J wave mimicking a right bundle branch block with typical ST-segment elevation in the right precordial leads. Believed to be a normal repolarization variant for more than three decades, the syndrome is now known instead to be associated with a high incidence of life-threatening ventricular tachyarrhythmias and is responsible for a number of sudden deaths in young adults worldwide. Although clinical findings seem to differentiate the two syndromes, similarities between BS and ERS in terms of response to heart rate, pharmacologic agents, and neuromodulation could suggest a linkage in their pathophysiological mechanism. The authors review the clinical and experimental data in order to test this hypothesis. |
7,690 | Administration of the Rho-kinase inhibitor fasudil before ischemia or just after reperfusion, but not 30 min after reperfusion, protects the stunned myocardium in swine. | We assessed the effect of administration time for fasudil treatment of the stunned myocardium in 40 anesthetized open chest swine.</AbstractText>All swine were subjected to 12 min ischemia followed by reperfusion to generate stunned myocardium. Group A (n = 11) received saline in place of fasudil both before ischemia and after reperfusion. Group B (n = 10) received 30 min intravenous fasudil at a rate of 13 mug/kg/min starting 45 min before ischemia and received saline after reperfusion. Groups C (n = 10) and D (n = 9) received saline before ischemia, and received fasudil at a rate of 13 microg kg(-1) min(-1) starting just before reperfusion in group C and 30 min after reperfusion in group D. In both groups, treatment lasted 30 min. Myocardial contractility was assessed by percent segment shortening (%SS).</AbstractText>Three swine in group A, 2 swine in each of groups B and C, and one swine in group D had ventricular fibrillation or tachycardia after reperfusion and were excluded from further analysis. The changes of %SS from baseline at 90 min after reperfusion in groups B and C were 68 +/- 8% and 75 +/- 8%, respectively, which were significantly higher than in group A or D (47 +/- 10% or 43 +/- 8%).</AbstractText>We conclude that fasudil administered before ischemia or just after reperfusion, but not 30 min after reperfusion, protects the stunned myocardium.</AbstractText> |
7,691 | Cardiac fibrillation: from ion channels to rotors in the human heart. | Recent new information on the dynamics and molecular mechanisms of electrical rotors and spiral waves has increased our understanding of both atrial fibrillation and ventricular fibrillation. In this brief review, we evaluate the available evidence for the separate roles played by individual sarcolemmal ion channels in atrial fibrillation and ventricular fibrillation, assessing the clinical relevance of such findings. Importantly, although human data support the idea that rotors are a crucial mechanism for fibrillation maintenance in both atria and ventricles, there are clear inherent differences between the 2 chamber types, particularly in regard to the role of specific ion channels in fibrillation. But there also are similarities. This knowledge, together with new information on the changes that take place during disease evolution and between structurally normal and diseased hearts, may enhance our understanding of fibrillatory processes pointing to new approaches to improve disease outcomes. |
7,692 | Arrhythmias in cardiac catheterization laboratories. | Several kinds of arrhythmias, such as ventricular arrhythmias, atrial fibrillation, bradycardias and conduction disturbances can occur in cardiac catheterization laboratories. The patients' characteristics, the type of procedure, the features of the target vessel and the type of lesion play important roles in the occurrence of arrhythmia. A majority of the arrhythmias tend to revert spontaneously, but special treatment must be given promptly when necessary. In this paper, we will review the pathophysiology, clinical importance and treatment strategies for arrhythmias that occurred during diagnostic cardiac catheterization and PCI in cardiac catheterization laboratories. |
7,693 | Predicting defibrillation success. | Ventricular fibrillation is the primary rhythm in many cardiac arrest patients. Since the late 1980s, the surface electrocardiogram of ventricular fibrillation has been subjected to analysis to obtain reliable information about the likelihood of successful countershock and to estimate the duration of cardiac arrest. Considerable efforts were made in the past 2 years to further improve the predictive power of rescue shock measures.</AbstractText>In a retrospective clinical study, ventricular fibrillation single feature analysis was not able to reliably estimate duration between cardiac arrest onset and initial electrocardiogram. Combining ventricular fibrillation features in the time and frequency domain by employing neural networks did not further improve the best single feature prediction power taken from higher ventricular fibrillation frequency bands. Cardioversion outcome prediction based on the wavelet technique increased the specificity up to 66% at the 95% sensitivity level.</AbstractText>Recent results question the ventricular fibrillation feature analysis as a reliable tool to estimate the duration of human cardiac arrest. Animal and clinical studies confirmed that ventricular fibrillation waveform analysis contains information to reliably predict the countershock success rate and further improved countershock outcome prediction. Prospective clinical studies are highly warranted to demonstrate that ventricular fibrillation waveform analysis definitely improves survival after cardiac arrest.</AbstractText> |
7,694 | Thrombolysis and other drugs during cardiopulmonary resuscitation. | No specific drug therapy has been shown to improve long-term survival after cardiac arrest, and only few drugs have a proven benefit for short-term survival. This study reviews recent studies on drugs during cardiopulmonary resuscitation.</AbstractText>Epinephrine is the first-line vasopressor during cardiopulmonary resuscitation. Arginine vasopressin may be more effective than epinephrine in patients presenting with asystole or as a second vasopressor in refractory cardiac arrest. Sodium bicarbonate should not be 'blindly' administered during cardiopulmonary resuscitation unless an arterial blood gas analysis can be obtained or after prolonged unsuccessful cardiopulmonary resuscitation. Amiodarone may improve short-term survival. Thrombolytic therapy during cardiopulmonary resuscitation may be beneficial if a pulmonary embolism or acute myocardial infarction is suggested to be the cause of cardiac arrest.</AbstractText>Epinephrine is the vasopressor of first choice for routine use during cardiopulmonary resuscitation. Arginine vasopressin may be considered in patients presenting with asystole or who are unresponsive to initial treatment with epinephrine. Amiodarone should be used in shock-refractory ventricular fibrillation. Although not recommended for routine use, thrombolytic therapy during cardiopulmonary resuscitation may be considered in patients with suspected pulmonary embolism or after unsuccessful conventional cardiopulmonary resuscitation in patients with a presumably thrombotic cause of cardiac arrest.</AbstractText> |
7,695 | Atrial vs. dual-chamber cardiac pacing in sinus node disease: a register-based cohort study. | In patients with sinus node disease, dual-chamber pacing (DDD) possibly results in adverse effects on the ventricular function. We have compared the incidence of cardiovascular morbidity and mortality in patients with sinus node disease and with atrioventricular (AV) synchronous pacemakers, DDD vs. atrial pacing (AAI).</AbstractText>A nation-wide population-based cohort of 8777 patients with AAI- or DDD-mode pacemakers was followed during 12 years. The cohort was linked to national healthcare and census registers. Patients with DDD pacing and without any pre-implant admission for atrial fibrillation or flutter had an increased risk of post-implant fibrillation or flutter, in relation to corresponding AAA patients [hazard ratio (HR) = 1.30; 95% confidence interval (CI) 1.10-1.52]. A slight increase in the risk of any cardiovascular disease (HR = 1.07; CI, 1.00-1.15), and all-cause mortality (HR = 1.12; CI, 1.00-1.25), was seen among DDD patients, in relation to AAI patients, but there was no significant difference in the risk of ischaemic or unspecified stroke (HR = 1.14; CI, 0.94-1.37). Among DDD patients, the all-cause mortality did not differ from the general population [standardized mortality ratio (SMR) = 1.04; CI, 0.98-1.11]. Patients with AAI, however, had a decreased all-cause mortality risk (SMR = 0.89; CI, 0.82-0.97).</AbstractText>Our results support AAI as the preferred mode of pacing in patients with sinus node disease, and a normal AV node function.</AbstractText> |
7,696 | Improvement of left atrial function is associated with lower incidence of atrial fibrillation and mortality after cardiac resynchronization therapy. | Left atrial (LA) volume is a predictor of cardiovascular events in patients with heart failure. Improvement of LA function and reverse remodeling was observed after cardiac resynchronization therapy (CRT).</AbstractText>The purpose of this study was to explore the clinical significance of improvement in LA function after CRT.</AbstractText>Echocardiographic studies were performed before and 3 months after CRT in 97 patients (72 men and 25 women; age 63.8 +/- 13.3 years) with standard CRT indication but no history of atrial fibrillation (AF). LA active emptying fraction based on the change in volumes (LAV-EF) were calculated, and significant improvement in LA function (LA responder) was defined as a relative increase >/=50% from baseline LAV-EF. The primary end-points were newly developed AF detected by ECG or device and all-cause mortality.</AbstractText>After 1,200 +/- 705 days of follow-up, LA responders (n = 47 [48.5%]) had a significantly lower incidence of AF (12.8% vs 40%, P = .002) and mortality (17% vs 44%, P = .004) than did LA nonresponders. In Cox proportional hazard analysis, LA responders was the only independent predictor of lower risk of new-onset AF (hazard ratio 0.22, 95% confidence interval 0.08-0.61, P = .003), whereas both LA responders (hazard ratio 0.22, 95% confidence interval 0.09-0.53, P <.001) and left ventricular reverse remodeling (>10% reduction in left ventricular end-systolic volume at 3 months; hazard ratio 0.96, 95% confidence interval 0.93-0.99, P = .03) were independent predictors of lower risk of death after CRT.</AbstractText>Improvement of LA function after CRT was associated with a lower incidence of AF and mortality in AF naïve patients with severe heart failure.</AbstractText> |
7,697 | Advances in mechanisms of atrial fibrillation: structural remodeling, high-frequency fractionated electrograms, and reentrant AF drivers. | The mechanisms to explain atrial fibrillation (AF) have been widely debated. Although contemporary experimental techniques have provided more insight, hypotheses regarding AF propagation conceived in the early half of the century remain minimally altered and relevant today. Modern mapping technologies have implicated multiwavelet reentry as the electrophysiologic basis to explain AF propagation within the atrial myocardium; however, reentry has also been observed within pulmonary veins and may behave as a focal trigger. The ability to terminate AF by catheter ablation has provided additional clues to explain AF induction and sustenance. The presence of complex fractionated electrograms (CFAE) and subsequent successful CFAE-directed ablation suggest that diseased atrial myocardium is a necessary substrate for AF maintenance. Atrial remodeling creates differential areas of refractory periods and conduction velocity, which, in turn, creates a suitable environment for AF. This review addresses the complex relationship between remodeled atrial myocardium and reentry and explores the role of CFAEs in AF maintenance. |
7,698 | Sodium channel β1 subunit mutations associated with Brugada syndrome and cardiac conduction disease in humans. | Brugada syndrome is a genetic disease associated with sudden cardiac death that is characterized by ventricular fibrillation and right precordial ST segment elevation on ECG. Loss-of-function mutations in SCN5A, which encodes the predominant cardiac sodium channel alpha subunit NaV1.5, can cause Brugada syndrome and cardiac conduction disease. However, SCN5A mutations are not detected in the majority of patients with these syndromes, suggesting that other genes can cause or modify presentation of these disorders. Here, we investigated SCN1B, which encodes the function-modifying sodium channel beta1 subunit, in 282 probands with Brugada syndrome and in 44 patients with conduction disease, none of whom had SCN5A mutations. We identified 3 mutations segregating with arrhythmia in 3 kindreds. Two of these mutations were located in a newly described alternately processed transcript, beta1B. Both the canonical and alternately processed transcripts were expressed in the human heart and were expressed to a greater degree in Purkinje fibers than in heart muscle, consistent with the clinical presentation of conduction disease. Sodium current was lower when NaV1.5 was coexpressed with mutant beta1 or beta1B subunits than when it was coexpressed with WT subunits. These findings implicate SCN1B as a disease gene for human arrhythmia susceptibility. |
7,699 | Acute renal failure, gastrointestinal bleeding, and cardiac arrhythmia after administration of arsenic trioxide for acute promyelocytic leukemia. | The case of a patient who developed acute renal failure, gastrointestinal bleeding, and cardiac arrhythmia after receiving arsenic trioxide for the treatment of acute promyelocytic leukemia (APL) is described.</AbstractText>An 84-year-old Caucasian woman with a history of osteoarthritis sought medical attention for relapse of her APL, which had initially been diagnosed approximately 30 months earlier. Complete remission was accomplished with three cycles of i.v. daunorubicin for 3 days and oral tretinoin for 28 days. After 19 months in remission, she was noted to have increased bruising and blood test values consistent with APL relapse. Two additional trials of oral tretinoin were unsuccessful, and arsenic trioxide was initiated at a daily dosage of 0.15 mg/kg of actual body weight. Less than 24 hours after receiving arsenic trioxide, the patient had "bile-like emesis" and her hemoglobin level decreased. Upper gastrointestinal bleeding was suspected and managed aggressively with transfusions of platelets and fresh frozen plasma and i.v. desmopressin. She became anuric, and her serum creatinine level more than doubled. Hemodialysis was started due to a sudden increase in potassium and fluid overload that did not respond to i.v. furosemide. One hour after hemodialysis, the patient was found pulseless and unresponsive by nursing staff. The cardiac arrest team rapidly responded and noted atrial fibrillation with a fast ventricular rate. Postresuscitation, the patient was transferred to the intensive care unit. Despite aggressive life-support therapy, the patient remained unresponsive.</AbstractText>An 84-year-old woman developed acute renal failure, gastrointestinal bleeding, and cardiac arrhythmia after receiving arsenic trioxide for the treatment of APL.</AbstractText> |
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