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15,300 | Biatrial pacing improves atrial haemodynamics and atrioventricular timing compared with pacing from the right atrial appendage. | Patients with interatrial conduction delay may have suboptimal left atrioventricular (AV) timing due to delayed contraction of the left atrium with foreshortening of ventricular filling. This may be an issue in pacemaker patients, especially those requiring resychronization therapy. Pacing from the high interatrial septum (IAS) or the distal or proximal coronary sinus (CSD and CSP) may improve left AV synchrony compared with pacing from the right atrial appendage (RAA). Our aim was to compare haemodynamics of these pacing sites.</AbstractText>A total of 24 patients undergoing radiofrequency ablation for paroxysmal atrial fibrillation were studied. Left atrial pressures were recorded in sinus rhythm, and during pacing from the RAA, IAS, CSD, CSP, and with biatrial (BiA) pacing from the IAS + CSD. Amplitudes, +dP/dT(max), and timing of the a-wave were compared between recordings. Left atrial contractility, measured by +dP/dT(max), was greatest during BiA pacing (P ≤ 0.03 for all comparisons). There was a marked reduction in delay to peak a-wave when pacing from all sites compared with the RAA, with BiA pacing yielding the shortest delay (P ≤ 0.001). However, AV conduction was shortened by all alternative pacing sites, which mitigated the anticipation of left atrial contraction with respect to ventricular activation, except for BiA pacing (P < 0.001). Pacing of the IAS did not result in any improvement in haemodynamics or AV synchrony.</AbstractText>Multisite atrial pacing results in favourable acute atrial haemodynamics and left AV synchrony. This may be a solution in pacemaker patients with interatrial conduction delay.</AbstractText> |
15,301 | The Dublin cardiac arrest registry: temporal improvement in survival from out-of-hospital cardiac arrest reflects improved pre-hospital emergency care. | Out-of-hospital cardiac arrest (OOHCA) survival remains poor, estimated at 3-7%. We aim to describe the incidence of OOHCA, survival from OOHCA, and the impact of improved pre-hospital care on survival from OOHCA.</AbstractText>A retrospective registry was established using multi-source information to assess survival from cardiac arrest following the introduction of several improvements in pre-hospital emergency medical care from 2003. Survival from OOHCA, from asystole/pulseless electrical activity, and from ventricular tachycardia/ventricular fibrillation was estimated. Adjusted per 100 000 population annual incidence rates from national population census data were calculated. Mean and median emergency medical services (EMS) response times to OOHCA calls were assessed. A total of 962 OOHCAs occurred from 1 January 2003 until 31 December 2008. Sixty-nine per cent (69%, n = 664) were male. Seventy-two per cent (72%, n = 693) occurred at home with 28% occurring in a public venue. Of these public venues, 33.9% (91 of 268) had an automated external defibrillator available. Bystander cardiopulmonary resuscitation (CPR) was in progress when emergency services arrived in 11% (n = 106) of the cases. Nineteen per cent (19.4%, n = 187) had a known prior cardiac history or chest pain prior to circulatory collapse. Overall survival to hospital discharge improved significantly from 2.6 to 11.3%, P = 0.001. Survival from ventricular fibrillation (VF) to hospital admission, rose from 28.6 to 86.3%, P = 0.001. Survival to hospital discharge from VF improved from 21.4 to 33%, P = 0.007. Mean EMS response times to the scene of arrest decreased from 9.18 to 8.34 min. Emergency medical services scene time, reflecting acute pre-hospital medical care, rose from 14.46 to 18.12 min. The adjusted incidence of OOHCA for our catchment population declined from 109.4 to 88.2 per 100,000 population between 2003 and 2008.</AbstractText>The incidence of OOHCA has declined but importantly, survival to hospital discharge has improved dramatically. Reduction in ambulance response time, resulting in earlier initiation of basic and advanced life support and earlier defibrillation, was associated with an increase in the proportion of victims found in VF rather than asystole and likely accounted for most of the improvement. Further improvements in response times and public education to improve bystander CPR rates should remain a priority.</AbstractText> |
15,302 | Relationship of sustained ventricular tachyarrhythmias to outcomes in patients undergoing primary percutaneous coronary intervention with varying underlying baseline risk. | The association of sustained ventricular tachycardia/fibrillation (VT/VF) with mortality in patients undergoing primary percutaneous coronary intervention (PCI) may vary with baseline patient risk and may be associated with higher mortality in patients who have high-risk baseline features but not in the low-risk patient cohort undergoing this procedure.</AbstractText>Among the 5,259 ST Elevation Myocardial Infarction (STEMI) patients presenting for primary PCI from the APEX AMI trial, we evaluated the association of VT/VF with outcomes according to underlying risk for 90-day mortality estimated using baseline variables and with a Cox regression model.</AbstractText>Ventricular tachycardia/fibrillation occurred in 3.6% (63/1,736), 4.9% (87/1,788), and 8.1% (141/1,735) of patients in the low-, intermediate-, and high-tertiles of 90-day predicted death, respectively. Ninety-day death was between 3.2- and 4.8-fold higher in patients with VT/VF compared with those without it in the 3 risk groups (low risk 1.6% vs 0.5%, intermediate risk 5.7% vs 1.2%, high risk 33.6% vs 7.7%). Both early (during cardiac catheterization) and late VT/VF (after cardiac catheterization) were associated with high risk of death regardless of baseline risk category.</AbstractText>The incidence of VT/VF and mortality increased as patients' baseline risk increased, and VT/VF remained an important prognostic marker for the increased risk of clinical adverse events and 90-day mortality irrespective of underlying baseline risk in patients undergoing primary PCI. Thus, even in otherwise low-risk patients, occurrence of VT/VF helps to further identify higher risk cohort that may warrant closer monitoring.</AbstractText>Copyright © 2011 Mosby, Inc. All rights reserved.</CopyrightInformation> |
15,303 | Hospital racial composition: a neglected factor in cardiac arrest survival disparities. | Racial disparities in survival after out-of-hospital cardiac arrest have been reported, but their causes remain uncertain. We sought to determine if hospital racial composition accounted for survival differences for patients hospitalized after cardiac arrest.</AbstractText>We evaluated hospitalizations of white and black Medicare beneficiaries (2000-2007) admitted from the emergency department to the intensive care unit with a diagnosis of cardiac arrest or ventricular fibrillation. We examined unadjusted survival rates and developed a multivariable logistic regression model that included patient and hospital factors.</AbstractText>We analyzed 68,115 cardiac arrest admissions. Unadjusted survival to hospital discharge was worse for blacks (n = 7,942) compared with whites (n = 60,173) (30% vs 33%, P < .001). In multivariate analyses accounting for patient and hospital factors, adjusted probability of survival was worse for black patients at hospitals with higher proportions of black patients (31%, 95% CI 29%-32%) compared with predominately white hospitals (46%, 95% CI 36%-57%; P = .003). Similarly, whites had worse risk-adjusted survival at hospitals with higher proportions of black patients (28%, 95% CI 27%-30%) compared with predominately white hospitals (32%, 95% CI 31%-33%, P = .006). Blacks were more likely to be admitted to hospitals with low survival rates (23% vs 15%, P < .001).</AbstractText>Hospitals with large black patient populations had worse cardiac arrest outcomes than predominantly white hospitals, and blacks were more likely to be admitted to these high-mortality hospitals. Understanding these differences in survival outcomes may uncover the causes for these disparities and lead to improved survival for all cardiac arrest victims.</AbstractText>Copyright © 2011 Mosby, Inc. All rights reserved.</CopyrightInformation> |
15,304 | Impact of therapeutic hypothermia in the treatment of patients with out-of-hospital cardiac arrest from the J-PULSE-HYPO study registry. | Mild hypothermia is an effective therapy for patients with return of spontaneous circulation (ROSC) after out-of-hospital cardiac arrest. However, evidence of the effectiveness of therapeutic hypothermia (TH) remains unclear.</AbstractText>A multicenter registry in Japan (J-PULSE-HYPO study registry) was conducted to investigate the effectiveness of TH for post-resuscitation neurological dysfunction developing after out-of-hospital cardiac arrest from 14 institutions, between January 2005 and December 2009. The committee entrusted each hospital with the timing of cooling, cooling methods, target temperature, duration, and rewarming. There were 452 patients (375 men) enrolled into the registry. The mean age was 58.6 ± 13.5 years. Initial electrocardiogram rhythm at the time of occurrence of the cardiac arrest showed 68.9% had ventricular fibrillation or pulseless ventricular tachycardia, 13.7% had pulseless electrical activity, and 9.1% had asystole. The median interval from the occurrence of cardiac arrest to ROSC was 26 min. The target core temperature during TH was 33.9 ± 0.4°C and the mean duration of cooling was 31.5 ± 13.9 h. Intra-aortic balloon pumping was used in 40.1% and percutaneous cardiopulmonary support in 22.6% of patients. At 30 days after cardiac arrest, the proportion of survival was 80.1% and the proportion of patients with favorable neurological functions, with a cerebral performance category score of 1 or 2, was 55.3%.</AbstractText>The J-PULSE-HYPO study registry showed a clinical aspect of TH.</AbstractText> |
15,305 | Cardiac electrophysiological assessment in patients with sarcoidosis. | Sarcoidosis is a multisystem granulomatous disease of unknown origin that can cause sudden death.</AbstractText>Electrophysiological evaluation of patients with suspected sarcoidosis with cardiac involvement.</AbstractText>We studied 22 patients with mean age of 55.32 ± 13.13 years, diagnosed with sarcoidosis and suspected cardiac involvement. These patients underwent clinical evaluation, laboratory tests, electrocardiogram, echocardiogram, 24-hour Holter, technetium or gallium scintigraphy and electrophysiological study. In selected cases, we performed positron emission tomography or magnetic resonance imaging. Patients were followed up in the outpatient care service with quarterly visits.</AbstractText>Cardiac involvement was confirmed in four (18.2%) patients. Ventricular extrasystoles with density > 100/24 h were documented in 24-Holter monitoring in 12 (54.5%) patients. Electrophysiological studies revealed an increased HV interval in seven patients (31.8%) and increased Wenckebach point in four (18.2%) patients. There was induction of atrial fibrillation in seven patients (31.8%) and sustained ventricular tachycardia in one patient (4.5%). Four patients with confirmed cardiac sarcoidosis had documented ventricular extrasystoles with density > 100/24 h. Out of these, two had prolonged HV interval and atrial fibrillation was induced in two of them. Sustained ventricular tachycardia was not induced in any of these patients. After mean follow-up period of 20.9 ± 15.7 months, one patient with cardiac sarcoidosis had sudden death.</AbstractText>Patients with sarcoidosis and suspected cardiac involvement have a high prevalence of ventricular extrasystoles (VEs) and conduction system disorders.</AbstractText> |
15,306 | Electrical storm: Incidence, Prognosis and Therapy. | Implantable defibrillators are lifesavers and have improved mortality rates in patients at risk of sudden death, both in primary and secondary prevention. However, they are unable to modify the myocardial substrate, which remains susceptible to life-threatening ventricular arrhythmias. Electrical storm is a clinical entity characterized the recurrence of hemodynamically unstable ventricular tachycardia and/or ventricular fibrillation, twice or more in 24 hours, requiring electrical cardioversion or defibrillation. With the arrival of the implantable cardioverter-defibrillator, this definition was broadened, and electrical storm is now defined as the occurrence of three or more distinct episodes of ventricular tachycardia or ventricular fibrillation in 24 hours, requiring the intervention of the defibrillator (anti-tachycardia pacing or shock). Clinical presentation can be very dramatic, with multiple defibrillator shocks and hemodynamic instability. Managing its acute presentation is a challenge, and mortality is high both in the acute phase and in the long term. In large clinical trials involving patients implanted with a defibrillator both for primary and secondary prevention, electrical storm appears to be a harbinger of cardiac death, with notably high mortality soon after the event. In most cases, the storm can be interrupted by medical therapy, though transcatheter radiofrequency ablation of ventricular arrhythmias may be an effective treatment for refractory cases.This narrative literature review outlines the main clinical characteristics of electrical storm and emphasises critical points in approaching and managing this peculiar clinical entity. Finally focus is given to studies that consider transcatheter ablation therapy in cases refractory to medical treatment. |
15,307 | Prolongation of the corrected QT complex--a cause of sudden cardiac death in the mountain environment? | In the mountain environment sudden cardiac death (SCD) has been shown to be responsible for the deaths of up to 52% of downhill skiers and 30% of hikers. The majority of SCD's are precipitated by a ventricular arrhythmia. Although most are likely to result from structural abnormalities associated with conditions such as ischaemic heart disease, a small but significant number may be due to abnormalities in ion channel activity, commonly known as, "channelopathies". Channelopathies have the potential to lengthen the time between ventricular depolarisation and repolarisation that can result in prolongation of the corrected QT interval (QTc) and episodes of polymorphic ventricular tachycardia (PVT) and eventually, ventricular fibrillation. This review examines the factors that prolong the QTc interval in the mountain environment and outlines a practical framework for preventing the life threatening arrhythmias that are associated with this condition. |
15,308 | Associations between outpatient heart failure process-of-care measures and mortality. | Assessment of the quality of care for outpatients with heart failure (HF) has focused on the development and use of process-based performance measures, with the supposition that these care process measures are associated with clinical outcomes. However, this association has not been evaluated for current and emerging outpatient HF measures.</AbstractText>Performance on 7 HF process measures (4 current and 3 emerging) and 2 summary measures was assessed at baseline in patients from 167 US outpatient cardiology practices with patients prospectively followed up for 24 months. Participants included 15 177 patients with reduced left ventricular ejection fraction (≤35%) and chronic HF or post-myocardial infarction. Multivariable analyses were performed to assess the process-outcome relationship for each measure in eligible patients. Vital status was available for 11 621 patients. The mortality rate at 24 months was 22.1%. Angiotensin-converting enzyme inhibitor or angiotensin receptor blocker use, β-blocker use, anticoagulant therapy for atrial fibrillation, cardiac resynchronization therapy, implantable cardioverter-defibrillators, and HF education for eligible patients were each independently associated with improved 24-month survival, whereas aldosterone antagonist use was not. The all-or-none and composite care summary measures were also independently associated with improved survival. Each 10% improvement in composite care was associated with a 13% lower odds of 24-month mortality (adjusted odds ratio, 0.87; 95% confidence interval, 0.84 to 0.90; P<0.0001).</AbstractText>Current and emerging outpatient HF process measures are positively associated with patient survival. These HF measures may be useful for assessing and improving HF care.</AbstractText><AbstractText Label="CLINICAL TRIAL REGISTRATION- URL" NlmCategory="BACKGROUND">http://www.clinicaltrials.gov. Unique identifier: NCT00303979.</AbstractText> |
15,309 | Risk assessment of R-on-T event based on modeled QT-RR relationship. | R-on-T event is a well-known trigger of ventricular tachycardia (VT) and ventricular fibrillation (VF). We propose a method to estimate the risk of R-on-T event from the inter-beat (RR) intervals based on modeled QT-RR relationship.</AbstractText>We retrospectively analyzed the Spontaneous Ventricular Tachyarrhythmia Database and the HAWAI Registry, which include a total of 397 RR interval recordings from 116 implantable cardioverter defibrillator patients. For each RR interval time series, QT intervals were estimated from the weighted average of preceding RR intervals using Bazett, Fridericia, and linear formulas. The risk score (RS) of each cycle was calculated to quantify the probability of R-on-T event based on the timing of R-wave relative to the estimated T-end. We identified 52,440 ectopic beats (EBs) episodes, 280 nonsustained VT (NSVT) episodes, and 352 sustained VT/VF episodes. The RS of episode onset and the prematurity index (PMI) of the initiating beat were compared.</AbstractText>Using different QT-RR models, R-on-T events were respectively detected in 9% EB, 45% NSVT, 69% VT/VF (Bazett); in 6% EB, 41% NSVT, 65% VT/VF (Fridericia); and in 7% EB, 42% NSVT, 66% VT/VF (linear). No R-on-T event was found in normal beats. Consistent among three QT-RR models, the RS of episode onset rises sharply from EB to NSVT and to VT/VF episodes. In contrast, no trend in PMI is found.</AbstractText>The risk of R-on-T can be estimated from RR intervals, based on modeled QT-RR relationship. An episode onset with higher RS has increased risk of developing into NSVT or VT/VF.</AbstractText>©2011, The Authors. Journal compilation ©2011 Wiley Periodicals, Inc.</CopyrightInformation> |
15,310 | Myocardial substrate in secondary ventricular fibrillation: insights from quantitative waveform measures. | Some patients presenting with nonshockable cardiac arrest rhythms will subsequently manifest ventricular fibrillation. Their prognosis remains poor despite transition to a shockable rhythm. Quantitative waveform measures assess the electrophysiologic status of the fibrillating heart and predict outcome.</AbstractText>To use waveform measures to compare those who presented initially with ventricular fibrillation (primary group) with those who manifested ventricular fibrillation after initially presenting with a nonshockable arrest rhythm (secondary group).</AbstractText>We conducted an observational study using a convenience sample to compare waveform measures of amplitude spectrum area (AMSA), cardioversion output predictor (COP), and detrended fluctuation analysis (DFA) prior to initial shock between the primary (n = 178) and secondary (n = 28) groups. We produced a primary group matched to the secondary group based on the average waveform values to evaluate the observed versus expected outcomes in the secondary group.</AbstractText>Survival was 42% in the primary group and 0% in the secondary group. There was a trend toward more favorable waveform values in the primary compared with the secondary group (9.48 versus 9.29, p = 0.10 for AMSA; 13.75 versus 14.12, p = 0.003 for COP; and 0.36 versus 0.44, p = 0.09 for DFA). The restricted, matched primary group experienced a survival of 37%, compared with 0% for the secondary group.</AbstractText>Taken together, the findings suggest that the electrophysiologic status of the heart may be suitable for resuscitation in at least some secondary ventricular fibrillation cases and that other pathophysiology may contribute substantially to the poor prognosis. Alternately, waveform measures may not predict clinical outcomes in secondary ventricular fibrillation.</AbstractText> |
15,311 | Genetic predisposition for sudden cardiac death in myocardial ischaemia: the Arrhythmia Genetics in the NEtherlandS study. | Sudden cardiac death from ventricular fibrillation during myocardial infarction is a leading cause of total and cardiovascular mortality. This multifactorial, complex condition clusters in families, suggesting a substantial genetic cause. We carried out a genomewide association study (GWAS) for sudden cardiac death, in the AGNES (Arrhythmia Genetics in the Netherlands) population, consisting of patients with (cases) and without (controls) ventricular fibrillation during a first ST-elevation myocardial infarction. The most significant association was found at chromosome 21q21 (rs2824292; odds ratio = 1.78, 95% CI 1.47-2.13, P = 3.3 × 10(-10)), 98 kb proximal of the CXADR gene, encoding the Coxsackie and adenovirus receptor. This locus has not previously been implicated in arrhythmia susceptibility. Further research on the mechanism of this locus will ultimately provide novel insight into arrhythmia mechanisms in this condition. |
15,312 | Therapeutic hypothermia after cardiac arrest: where are we now? | Therapeutic hypothermia is widely recommended after cardiac arrest. In this review, we present publications reflecting the current discussion and opinions related to use of therapeutic hypothermia in comatose adult cardiac arrest survivors.</AbstractText>The clinical outcome benefit of therapeutic hypothermia found in recent effectiveness studies is similar to that found in previous randomized trials. No single cooling method has been shown to be superior in terms of clinical outcomes. Therapeutic hypothermia is easy to perform and lacks severe side-effects or complications associated with mortality. Prehospital and intra-arrest cooling are being explored as a way to further improve outcome, although no clear relationship between timing of cooling and outcome has been documented.</AbstractText>Although only proven beneficial for patients with ventricular fibrillation, the majority of centres today use therapeutic hypothermia also for comatose survivors with other initial rhythms. Some controversies still exist; the optimal target temperature, timing and duration of cooling have not yet been defined, and some researchers still think that the concept of therapeutic hypothermia is not satisfactorily proven scientifically. A new randomized study comparing temperature management to 36°C with 33°C is therefore underway.</AbstractText> |
15,313 | Effects of aldosterone and mineralocorticoid receptor antagonism on cardiac ion channels in the view of upstream therapy of atrial fibrillation. | Atrial fibrillation (AF) is the most common sustained arrhythmia in man. Over the past years, importance of the renin-angiotensin-aldosterone system in AF pathophysiology has been recognized. Lately, the role of aldosterone in AF pathophysiology and mineralocorticoid receptor (MR) antagonism in "upstream" AF treatment is discussed with special regards concerning the effects on AF-induced structural remodeling. However, there is more and more evidence that MR antagonism also influences atrial electrophysiology and, respectively, AF-induced electrical remodeling, whereas the molecular mechanisms are almost unknown. The aim of this mini-review is to give an overview about the role of aldosterone in AF pathophysiology in principle and to summarize current available data concerning affection of cardiac ion channels by aldosterone and MR antagonism. Finally, as modulation of oxidative stress is discussed as one main therapy principle of "upstream" treatment of AF, potential mechanisms how modulation of oxidative stress by aldosterone and accordingly MR antagonism might alter atrial ion currents are delineated. Summarized, publications concerning potential mechanisms of aldosterone- and MR antagonism-modulated cardiac ion channels in various experimental settings are almost exclusively limited to the ventricular level and, partly, they are also contradictorily. Translation of these data to the atria is problematic because atrial and ventricular electrophysiology exhibit remarkable differences. It can be concluded that further research on the "atrial level" is needed in order to clarify the potential impact of the affection of atrial ion channels by aldosterone and accordingly MR antagonism in "upstream" therapy of AF. |
15,314 | Tetrahydrobiopterin depletion and NOS2 uncoupling contribute to heart failure-induced alterations in atrial electrophysiology. | Heart failure is a common antecedent to atrial fibrillation; both heart failure and atrial fibrillation are associated with increased myocardial oxidative stress. Chronic canine heart failure reduces atrial action potential duration and atrial refractoriness. We hypothesized that inducible nitric oxide synthase 2 (NOS2) contributes to atrial oxidative stress and electrophysiologic alterations.</AbstractText>A 16-week canine tachypacing model of heart failure was used (n= 21). At 10 weeks, dogs were randomized to either placebo (n = 12) or active treatment (n = 9) with NOS cofactor, tetrahydrobiopterin (BH(4), 50 mg), and NOS substrate (L-arginine, 3 g) twice daily for 6 weeks. A group of matched controls (n = 7) was used for comparison. Heart failure increased atrial NOS2 and reduced atrial BH(4), while L-arginine was unchanged. Treatment reduced inducible atrial fibrillation and normalized the heart failure-induced shortening of the left atrial myocyte action potential duration. Treatment increased atrial [BH(4)] while [L-arginine] was unchanged. Treatment did not improve left ventricular function or dimensions. Heart failure-induced reductions in atrial [BH(4)] resulted in NOS uncoupling, as measured by NO and superoxide anion (O(2)(·-)) production, while BH(4) and L-arginine treatment normalized NO and O(2)(·-). Heart failure resulted in left atrial oxidative stress, which was attenuated by BH(4) and L-arginine treatment.</AbstractText>Chronic non-ischaemic heart failure results in atrial oxidative stress and electrophysiologic abnormalities by depletion of BH(4) and uncoupling of NOS2. Modulation of NOS2 activity by repletion of BH(4) may be a safe and effective approach to reduce the frequency of atrial arrhythmias during heart failure.</AbstractText> |
15,315 | Amiodarone-induced acute respiratory distress syndrome masquerading as acute heart failure. | Amiodarone use has been rarely associated with the development of acute respiratory distress syndrome (ARDS), usually in association with surgery or pulmonary angiography. In patients with preexisting left ventricular dysfunction, the diagnosis may be overlooked.</AbstractText>A 92-year-old woman with a history of atrial fibrillation who was on low-dose amiodarone presented to the Emergency Department with sudden onset of shortness of breath. The patient was started on treatment for acute heart failure based on the physical examination and the elevated brain natriuretic peptide level. Despite adequate diuresis, the patient showed no improvement. A chest computed tomography scan revealed acute interstitial pneumonitis. The patient received corticosteroids due to suspected amiodarone-induced acute interstitial pneumonitis resulting in ARDS. She returned to her baseline activity within 2 weeks of the therapy.</AbstractText>Although rare, clinicians should be vigilant for amiodarone-induced acute interstitial pneumonitis resulting in ARDS, as delay in treatment may result in a high risk of mortality. In addition, the development of ARDS occurred in our patient in the absence of precipitating factors such as surgery or pulmonary angiography.</AbstractText>Copyright © 2012. Published by Elsevier Inc.</CopyrightInformation> |
15,316 | The effect of comorbidity on the competing risk of sudden and nonsudden death in an ambulatory heart failure population. | Sudden death (SD) and non-sudden cardiac death are responsible for the majority of deaths in patients with heart failure. We sought to identify the influence of comorbid illness (Charlson Comorbidity Index [CCI]) on competing modes of death in heart failure.</AbstractText>A retrospective analysis of 824 patients followed in a tertiary care heart failure clinic was performed. We analyzed the cumulative incidence of sudden and nonsudden death. Competing risk regression was used to examine the association between medical comorbidities and mode of death. The outcomes of interest were overall mortality, SD, SD and/or appropriate implantable cardioverter-defibrillator therapy (ICD), and non-SD.</AbstractText>Mean age of the study population was 64.1 ± 14.7 years, 68.6% were male, and mean ejection fraction was 32.8% ± 13.5%. Over a mean follow-up of 4.4 years, 229 patients (27.8%) died. SD accounted for 33 deaths (14.4%), whereas SD/appropriate ICD therapy occurred in 56 patients (24.5%). The risk of non-SD and total mortality increased (P < .0001) as the CCI increased, whereas the risk of SD decreased (P = .03). The cumulative incidence of SD, SD and/or ventricular tachycardia/fibrillation, and non-SD at 5 years was 5.6%, 9.1%, and 27.8%, respectively. In multivariate competing risk analysis, advancing age, New York Heart Association class, and a CCI >4 were significantly associated with non-SD.</AbstractText>Patients with heart failure with significant comorbidities are much more likely to sustain non-SD. These findings may have implications in optimal selection of patients with heart failure for interventions such as prophylactic ICD therapy.</AbstractText>Copyright © 2011. Published by Elsevier Inc.</CopyrightInformation> |
15,317 | Left atrial stiffness relates to left ventricular diastolic dysfunction and recurrence after pulmonary vein isolation for atrial fibrillation. | An increased left atrial (LA) stiffness reflects the structural remodeling and deterioration of the LA function. This study was designed to estimate LA stiffness by measuring a combination of the strain and LA pressure in patients undergoing pulmonary vein isolation (PVI) of atrial fibrillation (AF) and to evaluate the influence of the LA stiffness on the cardiac function, serum markers, and recurrence of AF after PVI.</AbstractText>In 155 consecutive patients with AF, the brain natriuretic peptide (BNP) and aminoterminal procollagen type III propeptide (PIIIP) plasma levels were measured before the PVI. The difference between the minimum and maximum LA systolic pressures was directly measured by a transseptal puncture. The ratio of the difference in the LA pressures to the peak systolic LA strain evaluated by speckle-tracking echocardiography was used as an index of the LA stiffness.</AbstractText>The calculated LA stiffness index was related to the BNP level (r(s) = 0.444, P < 0.001), E/E' ratio (r(s) = 0.444, P < 0.001), LA volume index (r(s) = 0.370, P < 0.001), and PIIIP level (r(s) = 0.305, P = 0.002). During a mean follow-up period of 33.8 ± 12.2 months, 45 patients (29%) presented with AF recurrences. A Cox proportional hazard regression analysis showed the LA stiffness index was an independent predictor of recurrence of AF (HR 2.88; 95% CI 1.75 to 4.73, P < 0.001).</AbstractText>In patients with AF, the LA stiffness index is related to left ventricular diastolic dysfunction, LA dilatation, and collagen synthesis and may predict AF recurrences after PVI.</AbstractText>© 2011 Wiley Periodicals, Inc.</CopyrightInformation> |
15,318 | Obstructive sleep apnea syndrome and cardiovascular diseases. | Obstructive sleep apnea syndrome (OSAS) is a chronic disease characterized by recurrent episodes of partial or complete upper airway collapse and obstruction during sleep, associated with intermittent oxygen desaturation, sleep fragmentation, and symptoms of disruptive snoring and daytime sleepiness. Increasing focus is being placed on the relationship between OSAS and all-cause and cardiovascular disease-related mortality, but it still largely unclear whether this association is causative or simply speculative and epidemiological. Basically, reliable clinical evidence supports the hypothesis that OSAS might be associated with essential and resistant hypertension, as well as with an incremental risk of developing stroke, cardiac rhythm perturbations (e.g., atrial fibrillation, bradyarrhythmias, supraventricular and ventricular arrhythmias), coronary artery disease, acute myocardial infarction, and heart failure. Although it is still unclear whether OSAS might represent an independent risk factor for several acute or chronic conditions, or rather might trigger cardiovascular disease in the presence of traditional cardiovascular risk factors (e.g., obesity, diabetes, and dyslipidemia), there is a plausible biological background underlying this association, in that most of the mechanisms implicated in the pathogenesis of OSAS (i.e., hypoxia, hypercapnia, negative intrathoracic pressure, micro-arousal, sympathetic hyperactivity, metabolic and hormonal changes, oxidative stress, phlogosis, endothelial dysfunction, hypercoagulability, and genetic predisposition) might also be involved in the pathogenesis of cardiovascular disorders. In this article we discuss the different aspects of the relationship between OSAS and pathogenically different conditions such as systemic hypertension, coronary artery disease, stroke, metabolic abnormalities, arrhythmias, and heart failure, and we also discuss the kaleidoscope of phenomena implicated in the pathogenesis of this challenging disease. |
15,319 | Delayed and indirect effects of antiarrhythmic drugs in reducing sudden cardiac death. | In the USA, two-thirds of sudden cardiac deaths (SCDs) are caused by sustained ventricular tachycardia and ventricular fibrillation. Implantable cardioverter defibrillator (ICD) therapy has been demonstrated to decrease mortality caused by these arrhythmias, when used both for primary and secondary prevention. However, ICD use is expensive, has proarrhythmic effects and does not prevent ventricular arrhythmias. Antiarrhythmic drugs (AADs) can be used for acute or chronic therapy to prevent ventricular arrhythmias and SCD. Most commonly, AADs are often used in patients with an ICD who have recurrent ICD shocks due to ventricular arrhythmias. Class I AADs are used in patients with a structurally normal heart and are contraindicated in patients with structural heart disease. β-blockers have been demonstrated to be beneficial in preventing mortality and malignant tachyarrhythmias in postmyocardial infarction and congestive heart failure patients, and in patients who have an ICD. Amiodarone has a neutral effect on mortality, while other class III drugs may increase mortality in certain subgroups of patients. Dronedarone, a new class III drug, may reduce mortality, but sufficient data are not available to allow for its use in the prevention of malignant tachyarrhythmias. Few drugs that are not classified as AADs can also prevent arrhythmias, via their beneficial effects on cardiovascular remodeling. These non-ADDs have delayed and indirect effects, which are mediated by the renin-angiotensin-aldosterone system and lipid metabolism - n-3 polyunsaturated fatty acids (fish oil), and statins, and can thus can reduce the likelihood of future malignant ventricular arrhythmias in patients with coronary artery disease or congestive heart failure. The role of chronic drug therapy alone for primary and secondary prevention of SCD is less than desirable because of proarrhythmic and adverse side effects. The non-ADDs are well tolerated and have no proarrhythmic actions, thus their benefit could outweigh risks, although currently there are no concrete data to suggest this. |
15,320 | A case of takotsubo cardiomyopathy with ventricular fibrillation after gastroenterological endoscopy. | We describe a case of takotsubo cardiomyopathy with ventricular fibrillation after gastroenterological endoscopy in a 66-year-old woman. Ten minutes after the upper and lower gastrointestinal endoscopic examinations, the patient lost consciousness, went into respiratory arrest, and became cyanotic; an electrocardiogram (ECG) showed ventricular fibrillation. Electrical defibrillation was applied three times resulting in the patient's recovery. Subsequently, the ECG showed ST elevation in V2-V3; ultrasound cardiography showed a severely hyperkinetic base of the left ventricle, with the rest of the ventricle akinetic; and cardiac catheterization disclosed a normal coronary artery and normal contraction of the left ventricle. |
15,321 | Long-term changes in the incidence of out-of-hospital ventricular fibrillation. | To report the long-term changes in the incidence of out-of-hospital ventricular fibrillation (VF), and also to report concurrent changes in the possible explanatory factors for the change.</AbstractText>This was a retrospective observational study. All bystander-witnessed out-of-hospital cardiac arrests (with a known initial rhythm) in Helsinki, Finland during 1.1.1994-31.12.2007 were included in the study. High (years 1994-1996) and low (2002-2004) incidence periods for VF were defined and compared.</AbstractText>There were 3131 bystander-witnessed out-of-hospital cardiac arrests of which 3118 (99.6%) had a known initial rhythm. During 2000-2007 the annual incidence of bystander witnessed ventricular fibrillation (VF) was 11.6 (95% CI 9.7-13.5) per 100,000 inhabitants. In 1994-1996 VF was 1.8 times more likely than in 2002-2004, after adjustment for several patient related factors and EMS related factors. Arrests with cardiac aetiology became less common, as 54.8% arrests had a cardiac cause in 1994-1996 compared to 45.2% in 2002-2004 (p<0.001). Of cardiac arrests with cardiac aetiology, 60.6% presented with VF in 1994-1996 compared to 45.7% in 2002-2004 (p<0.001). There were major changes in the possible explanatory factors during the study period.</AbstractText>The decline in the incidence of out-of-hospital VF seems to have ended, and the annual incidence of VF has stabilised to 11.6 (95% CI 9.7-13.5) per 100,000 inhabitants. During the period of lower incidence of VF, cardiac aetiology caused fewer arrests, and these arrests did not present with VF as often as previously.</AbstractText>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
15,322 | MOG1: a new susceptibility gene for Brugada syndrome. | Brugada syndrome (BrS) is caused mainly by mutations in the SCN5A gene, which encodes the α-subunit of the cardiac sodium channel Na(v)1.5. However, ≈ 20% of probands have SCN5A mutations, suggesting the implication of other genes. MOG1 recently was described as a new partner of Na(v)1.5, playing a potential role in the regulation of its expression and trafficking. We investigated whether mutations in MOG1 could cause BrS.</AbstractText>MOG1 was screened by direct sequencing in patients with BrS and idiopathic ventricular fibrillation. A missense mutation p.Glu83Asp (E83D) was detected in a symptomatic female patient with a type-1 BrS ECG but not in 281 controls. Wild type (WT)- and mutant E83D-MOG1 were expressed in HEK Na(v)1.5 stable cells and studied using patch-clamp assays. Overexpression of WT-MOG1 alone doubled sodium current (I(Na)) density compared to control conditions (P<0.01). In contrast, overexpression of mutant E83D alone or E83D+WT failed to increase I(Na) (P<0.05), demonstrating the dominant-negative effect of the mutant. Microscopy revealed that Na(v)1.5 channels failed to properly traffic to the cell membrane in the presence of the mutant. Silencing endogenous MOG1 demonstrated a 54% decrease in I(Na) density.</AbstractText>Our results support the hypothesis that dominant-negative mutations in MOG1 can impair the trafficking of Na(v)1.5 to the membrane, leading to I(Na) reduction and clinical manifestation of BrS. Moreover, silencing MOG1 reduced I(Na), demonstrating that MOG1 is likely to be important in the surface expression of Na(v)1.5 channels. All together, our data support MOG1 as a new susceptibility gene for BrS.</AbstractText> |
15,323 | Defibrillation testing at the time of implantable cardioverter defibrillator implantation: results of the European Heart Rhythm Association survey. | This survey assesses the current practices of testing defibrillation function at the time of the first implanted cardioverter defibrillator placement. Responses have been collected from 57 European heart rhythm management centres. The results of the survey show an extraordinary inconsistency in the approaches to defibrillation testing (19.3% of responders report no testing at the time of implantation). A policy statement on this topic would help to improve patient care and unify the procedure according to evidence based data. |
15,324 | Complex cardiac anatomy and catheter access: the role of imaging in patients referred for catheter ablation. | A 66-year-old man with Kartagener's syndrome, situs inversus totalis, and recurrent supraventricular tachycardia and a 49-year-old man with atrial fibrillation and drug-refractory rapid ventricular rate response were referred for catheter ablation. In the first case, the mirrored anatomy of the right atrium was reconstructed using three-dimensional electroanatomical mapping, which guided successful ablation of a typical atrioventricular nodal reentrant tachycardia. In the second case, computerized tomography showed the presence of left atrial isomerism with interruption of the inferior vena cava and azygous continuation into the superior vena cava, guiding advancement of the ablation catheter for access into the positionally right atrial ablation site. These cases illustrate the role of imaging in patients with unusual anatomy of the cardiac chambers and major blood vessels guiding optimal catheter access for catheter ablation. |
15,325 | The use of antiarrhythmic drugs for adult cardiac arrest: a systematic review. | In adult cardiac arrest, antiarrhythmic drugs are frequently utilized in acute management and legions of medical providers have memorized the dosage and timing of administration. However, data supporting their use is limited and is the focus of this comprehensive review.</AbstractText>Databases including PubMed, Cochrane Library (including Cochrane database for systematic reviews and Cochrane Central Register of Controlled Trials), Embase, and AHA EndNote Master Library were systematically searched. Further references were gathered from cross-references from articles and reviews as well as forward search using SCOPUS and Google scholar. The inclusion criteria for this review included human studies of adult cardiac arrest and anti-arrhythmic agents, peer-review. Excluded were review articles, case series and case reports.</AbstractText>Of 185 articles found, only 25 studies met the inclusion criteria for further review. Of these, 9 were randomised controlled trials. Nearly all trials solely evaluated Ventricular Tachycardia (VT) and Ventricular Fibrillation (VF), and excluded Pulseless Electrical Activity (PEA) and asystole. In VT/VF patients, amiodarone improved survival to hospital admission, but not to hospital discharge when compared to lidocaine in two randomized controlled trials.</AbstractText>Amiodarone may be considered for those who have refractory VT/VF, defined as VT/VF not terminated by defibrillation, or VT/VF recurrence in out of hospital cardiac arrest or in-hospital cardiac arrest. There is inadequate evidence to support or refute the use of lidocaine and other antiarrythmic agents in the same settings.</AbstractText>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
15,326 | Massively dilated right atrium masquerading as a mediastinal tumor. | Severe tricuspid valve insufficiency causes right atrial dilatation, venous congestion, and reduced atrial contractility, and may eventually lead to right heart failure. We report a case of a patient with severe tricuspid valve insufficiency, right heart failure, and a massively dilated right atrium. The enormously dilated atrium compressed the right lung, resulting in a radiographic appearance of a mediastinal tumor. Tricuspid valve repair and reduction of the right atrium was performed. Follow up examination revealed improvement of liver function, reduced peripheral edema and improved New York Heart Association (NYHA) class. The reduction of the atrial size and repair of the tricuspid valve resulted in a restoration of the conduit and reservoir function of the right atrium. Given the chronicity of the disease process and the long-standing atrial fibrillation, there is no impact of this operation on right atrial contraction. In combination with the reconstruction of the tricuspid valve, the reduction atrioplasty will reduce the risk of thrombembolic events and preserve the right ventricular function. |
15,327 | Characteristics of high-echoic objects in the hepatic vessels of patients with cardiopulmonary arrest: a prospective cohort study. | High-echoic objects in the hepatic vessels of patients with cardiopulmonary arrest (CPA) are frequently detected by ultrasonography.</AbstractText>To demonstrate this phenomenon and clarify its clinical characteristics.</AbstractText>In a tertiary care academic medical centre, 203 CPA patients were evaluated by ultrasonography. CT determined the origin and location of high-echoic objects detected in the liver. The frequency and characteristics of this phenomenon were investigated. The background, laboratory data and survival rate were compared between patients with and without high-echoic objects.</AbstractText>High-echoic objects were seen in 73 (36.0%) patients and could clearly be detected in the hepatic veins of 41 (56.2%) patients. CT confirmed that these were gas in 27 of 53 patients, and were clearly visible in the hepatic veins in 12 (44.4%) patients. Hepatic portal venous gas was not identified. Compared to patients without high-echoic objects, witnessed arrest (p<0.001), bystander cardiopulmonary resuscitation (p=0.005), ventricular fibrillation or pulseless electrical activity (p=0.012) and return of spontaneous circulation (p=0.018) were significantly less frequent in patients with high-echoic objects. These patients had a lower incidence of survival to discharge (1.4% vs 7.7%, p=0.100). Multivariate analysis showed that absence of high-echoic objects was a marginally significant factor in association with return of spontaneous circulation (p=0.052).</AbstractText>High-echoic objects were often observed on ultrasonography in CPA patients; these objects were considered hepatic venous gas. The presence of high-echoic objects may be a poor prognostic sign in patients with CPA.</AbstractText> |
15,328 | Atrial fibrillation in emergency department: prevalence of sinus rhythm 1 week after discharge. | Current guidelines do not provide definitive indications about the treatment in emergency departments (ED) of patients with recent-onset atrial fibrillation (AF).</AbstractText>A multicentre observational study involving four general hospitals of the same metropolitan area was conducted. All consecutive adult patients admitted to the ED with recent symptoms of AF (<48 h duration) and discharged home were considered. Patients who underwent ED early cardioversion were enrolled in group A. Patients managed with ventricular rate control were enrolled in group B.</AbstractText>On the 24 h Holter recordings at 1-week follow-up, stable sinus rhythm was detected in 46/58 (79.3%; 95% CI 68.9 to 89.7) patients in group A and 8/33 (24.2%; 95% CI 9.6 to 38.9) patients in group B (p<0.01).</AbstractText>According to the study results, rhythm at the time of ED discharge is a poor indicator of the short-term evolution of AF.</AbstractText> |
15,329 | Chronic electrical neuronal stimulation increases cardiac parasympathetic tone by eliciting neurotrophic effects. | Recently, we provided a technique of chronic high-frequency electric stimulation (HFES) of the right inferior ganglionated plexus for ventricular rate control during atrial fibrillation in dogs and humans. In these experiments, we observed a decrease of the intrinsic ventricular rate during the first 4 to 5 months when HFES was intermittently shut off.</AbstractText>We thus hypothesized that HFES might elicit trophic effects on cardiac neurons, which in turn increase baseline parasympathetic tone of the atrioventricular node.</AbstractText>In mongrel dogs atrial fibrillation was induced by rapid atrial pacing. Endocardial HFES of the right inferior ganglionated plexus, which contains abundant fibers to the atrioventricular node, was performed for 2 years. Sham-operated nonstimulated dogs served as control. In chronic neurostimulated dogs, we found an increased neuronal cell size accompanied by an increase of choline acetyltransferase and unchanged tyrosine hydroxylase protein expression as compared with unstimulated dogs. Moreover, β-nerve growth factor (NGF) and neurotrophin (NT)-3 were upregulated in chronically neurostimulated dogs. In vitro, HFES of cultured neurons of interatrial ganglionated plexus from adult rats increased neuronal growth accompanied by upregulation of NGF, NT-3, glial-derived neurotrophic factor (GDNF), ciliary neurotrophic factor (CNTF) and brain-derived neurotrophic factor (BDNF) expression. NGF was identified as the main growth-inducing factor, whereas NT-3 did not affect HFES-induced growth. However, NT-3 could be identified as an important acetylcholine-upregulating factor.</AbstractText>HFES of cardiac neurons in vivo and in vitro causes neuronal cellular hypertrophy, which is mediated by NGF and boosters cellular function by NT-3-mediated acetylcholine upregulation. This knowledge may contribute to develop HFES techniques to augment cardiac parasympathetic tone.</AbstractText> |
15,330 | Echocardiographic predictors of left atrial appendage thrombus formation. | Although transesophageal echocardiography is the definitive test for the detection of left atrial (LA) appendage thrombus, transthoracic echocardiography has yet to prove useful for the determination of increased risk for LA appendage thrombus formation. The authors hypothesized that higher LA volume and/or lower left ventricular ejection fraction (LVEF) might prove valuable as markers of increased risk for LA appendage thrombus formation and tested this hypothesis in a consecutive retrospective series of patients with atrial fibrillation undergoing both transthoracic and transesophageal echocardiography.</AbstractText>Three hundred thirty-four consecutive patients with atrial fibrillation undergoing transesophageal echocardiography for the detection of LA appendage thrombus were studied. Anticoagulation status, CHADS(2) scores, and echocardiographic parameters were catalogued. The relationship between the presence of LA appendage thrombus and covariates was analyzed using binary logistic regression.</AbstractText>LA appendage thrombus was detected in 52 patients (15.6%). A higher CHADS(2) score (odds ratio, 1.45; P < .004), increased LA volume index (odds ratio, 1.02; P = .018), and lower LVEF (odds ratio, 1.02; P = .05) were significant predictors of LA appendage thrombus formation. LA appendage thrombus was not seen in patients with CHADS(2) scores ≤ 1, LVEFs > 55%, and a LA volume indexes < 28 mL/m(2). A ratio of LVEF to LA volume index ≤ 1.5 produced 100% sensitivity for the presence of LA appendage thrombus.</AbstractText>The presence of LA appendage thrombus is related to both clinical and echocardiographic variables. Although no single echocardiographic variable discriminated between the presence and absence of LA thrombus, a normal LVEF and normal LA volume index were associated with the absence of LA appendage thrombus formation. For patients with atrial fibrillation with CHADS(2) scores ≤ 1, normal left ventricular systolic function and normal LA volume in combination may be a useful measure for the identification of patients at low risk for LA appendage thrombus formation.</AbstractText>Copyright © 2011 American Society of Echocardiography. Published by Mosby, Inc. All rights reserved.</CopyrightInformation> |
15,331 | Investigation of the safety of irreversible electroporation in humans. | A single-center prospective nonrandomized cohort study was performed to investigate the safety of irreversible electroporation (IRE) for tumor ablation in humans.</AbstractText>Thirty-eight volunteers with advanced malignancy of the liver, kidney, or lung (69 separate tumors) unresponsive to alternative treatment were subjected to IRE under general anesthesia. Clinical examination, biochemistry, and computed tomography (CT) scans of the treated organ were performed before, immediately after, and at 1 month and 3 months after the procedure.</AbstractText>No mortalities occurred at 30 days. Transient ventricular arrhythmia occurred in four patients, and electrocardiographically (ECG) synchronized delivery was used subsequently in the remaining 30 patients, with two further arrhythmias (supraventricular tachycardia and atrial fibrillation). One patient developed obstruction of the upper ureter after IRE. One adrenal gland was unintentionally directly electroporated, which produced transient severe hypertension. There was no other evidence of adjacent organ damage related to the electroporation. Other adverse events were not directly related to IRE, but two patients developed temporary neurapraxia as a result of arm extension during a prolonged period of anesthesia. Although not a primary aim of this preliminary study, complete target tumor ablation verified by CT was achieved in 46 of the 69 tumors treated with IRE (66%). Most treatment failures occurred in renal and lung tumors. Biopsy in three patients showed coagulative necrosis in the regions treated by IRE.</AbstractText>IRE appears to be safe for human clinical use provided ECG-synchronized delivery is used. Comparative evaluation with alternative ablative technologies is warranted.</AbstractText>Copyright © 2011 SIR. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
15,332 | Public access defibrillation. | In the United States, 250,000 people die from a cardiac arrest every year. Despite a well established emergency medical response system, survival from out-of-hospital cardiac arrest remains poor in United States cities. Paramount to achieving successful resuscitation of a cardiac arrest victim is provision of early defibrillation. Among patients that arrest due to a ventricular fibrillation, the likelihood of survival decreases by 10% for every minute of delay in defibrillation. In 1995, the American Heart Association challenged the medical industry to develop a defibrillator that could be placed in public settings, used safely by lay responders, and provide earlier defibrillation to cardiac arrest victims. Over the last decade, there have been significant technological advancements in automated external defibrillators (AEDs), and clinical studies have demonstrated their benefits and limitations in various public locations. This article discusses the technologic features of the modern AED and the current data available on the use of AEDs in public settings. |
15,333 | Device features for managing patients with heart failure. | Implanted devices in heart failure patients improve survival, but requires correct prescription, programming, and monitoring. Requirements change since heart failure is a dynamic condition. Repeated episodes of acute decompensation increase mortality. Events involve several processes converging to manifest with fluid congestion. Implantable devices identify changes such as those in rhythm, device function or hemodynamics. Incorporation of remote monitoring technology (TRUST Trial), enables tracking of these parameters and prompt notification of deviations, even if the patient remains asymptomatic. This may facilitate management of large patient volumes and enable pre-emptive treatment to improve outcomes in these high-risk patients. |
15,334 | Reduction of right ventricular pacing with advanced atrioventricular search hysteresis: results of the PREVENT study. | Right ventricular pacing predisposes to the development of heart failure and atrial fibrillation. Automatic atrioventricular search hysteresis (AVSH) is a commonly used strategy to decrease the percentage of right ventricular pacing (%VP) in patients without permanent AV block, but the results have not been optimal.</AbstractText>The randomized, crossover PREVENT study evaluated whether an enhanced AVSH with two new features can reduce %VP compared with standard AVSH. The new features are the repetitive hysteresis [switch from extended to basic AV delay after a consistent loss of intrinsic AV conduction (IAVC) lasting for six consecutive atrial cycles] and the scan hysteresis (periodic IAVC search extension over six consecutive atrial cycles). Both standard AVSH and enhanced AVSH performed a periodic IAVC search every 180 cardiac cycles and operated with a basic AV-delay of 225 ms and a rate-independent maximum AV-delay of 300 ms for paced and sensed atrial events.</AbstractText>Among 178 patients, 53.4% had no evidence of AV block at enrollment and 46.6% had history of intermittent AV block. The median %VP was decreased by enhanced AVSH compared to standard AVSH (4.0% vs 5.5%, P < 0.001), particularly in patients with a history of AV block (21.4% vs 25.5%, P < 0.001). The primary study hypothesis that 25% of all patients would experience > 20% relative %VP reduction was not met as 46 (25.8%) patients (95% confidence interval, 20.5-31.8%) presented such relative reduction.</AbstractText>The enhanced AVSH algorithm reduces %VP compared with standard AVSH in patients with intermittent AV block.</AbstractText>©2011, The Authors. Journal compilation ©2011 Wiley Periodicals, Inc.</CopyrightInformation> |
15,335 | Ablation of ventricular fibrillation in an orthotopic heart lung transplant. | Arrhythmia is well described following cardiac transplantation. We report a case of recurrent ventricular fibrillation (VF) originating from an orthotopic cardiac allograft. VF was consistently initiated on each occasion by a relatively early-coupled monomorphic ventricular ectopic. Antiarrhythmic agents failed to suppress the arrhythmia. Electrophysiological testing with noncontact mapping showed a high-frequency potential at the earliest activation site. Radiofrequency ablation resulted in abolition of ventricular ectopy with no further VF recurrence. Although there is substantial experience with ablation of atrial tachycardias in this setting, experience with ablation for ventricular arrhythmias is limited and ablation of VF not described. |
15,336 | WCD LifeVest: risk stratification in a case of Tako-Tsubo cardiomyopathy with QT interval prolongation. | A 50-year-old woman with arterial hypertension suffered from recurrent syncope. On admission, recurrent torsades de pointes tachycardia, ventricular flutter, and ventricular fibrillation with the necessity of cardiopulmonary resuscitation were documented. After administration of β-blocking agents, amiodarone, and magnesium, heart rhythm was stabilized. Coronary angiography excluded coronary artery disease. Echocardiography revealed apical ballooning with reduced ventricular function. The ECG showed left bundle-branch block and profound QT prolongation. A WCD (wearable cardioverter-defibrillator) LifeVest was prescribed for the patient, and, thereafter, no arrhythmias were experienced. The ECG gradually normalized; echocardiography revealed slight anteroapical hypokinesia with overall normal left ventricular function. After a period of 3 months, the patient was no longer asked to wear the LifeVest; 6 months later the patient is without any complaints. |
15,337 | Wogonin suppresses arrhythmias, inflammatory responses, and apoptosis induced by myocardial ischemia/reperfusion in rats. | Wogonin is a flavonoid isolated from Scutellaria baicalensis Georgi, a traditional Chinese medicine, and it possesses antioxidant and anti-inflammatory effects. The aim of this study is to investigate the in vivo effect of wogonin on myocardial ischemia/reperfusion injury in an open-chest anesthetized rat model, which was induced by 45-minute left coronary artery occlusion and 2-hour reperfusion. Rats were treated with wogonin (5, 10, and 20 mg/kg, intraperitoneal) 40 minutes before ischemia or treatment with 10 mg/kg of wogonin 15 minutes after occlusion. Pretreatment with 10 mg/kg of wogonin significantly delayed the occurrence of ventricular premature contractions and tachycardia, and it suppressed the incidence of ventricular tachycardia and ventricular fibrillation, and mortality elicited by ischemia when compared with that in the control group, accompanied by reducing the arrhythmia scores. After 2-hour reperfusion, pretreatment and posttreatment with wogonin significantly reduced the infarct size and plasma levels of creatine kinase muscle-brain fraction and lactate dehydrogenase. Wogonin also significantly reduced the elevation of plasma tissue necrosis factor-α and superoxide anion production in the myocardium with ischemia/reperfusion. The expression of monocyte chemoattractant protein-1, phosphorylated p38 mitogen-activated protein kinase, p65 and IκBα, and active caspase-3 in ischemic myocardium pronouncedly increased in the control group; these were significantly attenuated by treatment with wogonin. In conclusion, wogonin demonstrated in vivo cardioprotective effects by the attenuation of the severity of ischemia-induced arrhythmias and irreversible ischemia/reperfusion injury, which is associated with its antioxidant capacity and anti-inflammatory effects. The suppression of nuclear factor-κB and p38 mitogen-activated protein kinase activation and the inhibition of monocyte chemoattractant protein-1 expression contribute to the beneficial effects of wogonin. |
15,338 | Report from the Japanese registry of CPR for in-hospital cardiac arrest (J-RCPR). | In-hospital cardiopulmonary arrest (CPA) is an important issue, but data in Japan are limited.</AbstractText>To investigate in-hospital CPA, we conducted a prospective multicenter observational registry of in-hospital CPA and resuscitation in Japan (J-RCPR). During January 2008 to December 2009, patients were registered from 12 participating hospitals. All patients, visitors and employees within the facility campus who experience a cardiopulmonary resuscitation event defined as either a pulseless or a pulse with inadequate perfusion requiring chest compressions and/or defibrillation of ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT) were registered. Data were collected in 6 major categories of variables: facility data, patient demographic data, pre-event data, event data, outcome data, and quality improvement data. Data for 491 adults were analyzed. The prevalence of pulseless VT/VF as first documented rhythm was 28.1%, asystole was 29.5% and pulseless electrical activity was 41.1%. Immediate causes of event were arrhythmia 30.6%, acute respiratory insufficiency 26.7%, and hypotension 15.7%. Return of spontaneous circulation was 64.7%; the proportion of survival 24h after CPA was 49.8%, the proportion of survival to hospital discharge was 27.8% and proportion of favorable neurological outcome at 30 days was 21.4%.</AbstractText>This is the first report of the registry for in-hospital CPA in Japan and shows that the registry provides important observational data.</AbstractText>All rights are reserved to the Japanese Circulation Society.</CopyrightInformation> |
15,339 | Clinical trials update from the American Heart Association meeting 2010: EMPHASIS-HF, RAFT, TIM-HF, Tele-HF, ASCEND-HF, ROCKET-AF, and PROTECT. | This article provides information and a commentary on key trials relevant to the pathophysiology, prevention, and treatment of heart failure presented at the annual meeting of the American Heart Association held in Chicago in 2010. Unpublished reports should be considered as preliminary, since analyses may change in the final publication. In patients with mild heart failure (HF), EMPHASIS-HF showed that the addition of eplerenone to standard therapy was well tolerated and reduced both the risk of death and hospitalization. The addition of cardiac resynchronization therapy to implantable cardioverter defibrillator (ICD) therapy reduced the incidence of all-cause mortality and HF hospitalizations in patients with NYHA class II-III HF compared with ICD alone in RAFT. Telemonitoring failed to improve outcome compared with a high standard of conventional care in patients with chronic HF (TIM-HF study) and a telephone-based interactive voice response system failed to improve outcome in patients recently hospitalized for HF (Tele-HF study). ASCEND-HF suggested that nesiritide was ineffective but safe in patients with acute decompensated HF. ROCKET-AF suggests that the factor-Xa inhibitor rivaroxaban may be as effective as warfarin in patients with atrial fibrillation. The PROTECT study provided more data to suggest that amino-terminal B-type natriuretic peptide guided therapy may be beneficial in patients with left ventricular systolic dysfunction. |
15,340 | Mitral annular calcification predicts cardiovascular morbidity and mortality in middle-aged patients with atrial fibrillation: the Belgrade Atrial Fibrillation Study. | Mitral annular calcification (MAC) has been suggested as a reliable, time-averaged marker of atherosclerosis and is associated with coronary artery disease, heart failure, ischemic stroke, and increased mortality. Data on the relationship between MAC and cardiovascular morbidity and mortality in atrial fibrillation (AF) are sparse, with the exception of the relationship between MAC and stroke. We investigated the association of MAC with cardiovascular morbidity, stroke, cardiovascular mortality, and all-cause death in a cohort of middle-aged patients with AF with a mean 10-year follow-up.</AbstractText>This was an observational study of patients with nonvalvular AF between 1992 and 2007.</AbstractText>Of 1,056 patients, 33 (3.1%) had MAC; they were more likely to be older and female and to have a dilated left atrium, reduced left ventricular ejection fraction, permanent AF, hypertension, and/or diabetes mellitus (all P < .05). Total follow-up was 10,418.5 years (mean, 9.9 ± 5.9 years), and the mean age was 52.7 ± 12.2 years. In univariate analysis, MAC was associated with all-cause death, cardiovascular death, stroke, new cardiac morbidity (all P < .05), and the composite end point of ischemic stroke, myocardial infarction (MI), and all-cause death (P < .001). In multivariate analyses, MAC was related to all-cause death (hazard ratio [HR], 4.3; 95% CI, 1.8-10.0; P < .001), cardiovascular death (HR, 3.5; 95% CI, 1.2-10.4; P = .025), the composite end point (HR, 2.1; 95% CI, 1.0-4.3; P = .048), and new cardiac morbidity (HR, 2.4; 95% CI, 1.3-4.5; P = .005). There was no significant relationship between MAC and stroke or MI in the multivariate analyses.</AbstractText>MAC is associated with increased cardiovascular morbidity, cardiovascular mortality, and all-cause mortality of patients with AF. MAC should be acknowledged as a marker of increased cardiovascular risk in middle-aged patients with AF.</AbstractText> |
15,341 | Polymorphisms of the angiotensin-converting enzyme and angiotensinogen gene in patients with atrial fibrillation. | Activation of the renin-angiotensin system (RAS) is associated with atrial fibrillation (AF). The aim of this study was to investigate the relation between AF and polymorphisms in RAS. One hundred and fifty patients with AF, 100 patients with no documented episode of AF and 100 healthy subjects were consecutively recruited into the study. The angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism, and the M235T, A-20C, and G-6A polymorphisms of the angiotensinogen gene were genotyped. Patients with AF had significantly lower frequency of II genotype of ACE I/D and higher frequency of angiotensinogen M235T polymorphism T allele and TT genotype and G-6A polymorphism G allele and GG genotype compared with the controls. AF patients had significantly larger left atrium, higher left ventricular mass index (LVMI) and higher frequency of significant valvular pathology. ACE I/D polymorphism II genotype, angiotensinogen M235T polymorphism TT genotype and G allele and GG genotype of angiotensinogen G-6A polymorphism were still independently associated with AF when adjusted for left atrium, LVMI and presence of significant valvular pathology. Genetic predisposition might be underlying the prevalence of acquired AF. Patients with a specific genetic variation in the RAS genes may be more liable to develop AF. |
15,342 | Azygous vein coil lowers defibrillation threshold in patients with high defibrillation threshold. | Implantable cardioverter defibrillators (ICDs) reduce sudden death in patients at high risk. High defibrillation thresholds (DFTs) are not uncommon and may be the cause of failed defibrillation in patients with ICDs. Addition of a coil in the azygous vein posterior to the heart lowers the DFT in most patients by altering the electrical vector during defibrillation. This can be accomplished fairly easily and expeditiously using standard equipment in the laboratory. It also avoids the difficulties and complications associated with other methods such as the use of a subcutaneous array.</AbstractText>This series of three cases illustrates the type of patients who may benefit from this technique. The addition of an azygous coil successfully lowered the DFT to <10 J in each case. A brief description of the technique used to implant the azygous coil follows.</AbstractText>This simple and elegant solution can be highly useful as part of the armamentarium in tackling the problem of high DFTs.</AbstractText> |
15,343 | The effects of sex on out-of-hospital cardiac arrest outcomes. | We examined the effects of sex on out-of-hospital cardiac arrest outcomes. There is evidence that women are more likely to survive cardiac arrest than men. However, few large studies have examined these sex differences in detail. It is unknown whether the female survival advantage is age-specific or whether sex affects neurologic outcomes after cardiac arrest events.</AbstractText>Data were analyzed from a nationwide population-based out-of-hospital cardiac arrest database (between January 2005 and December 2007) involving 318,123 patients (male: 188,357, female: 129,766) to assess the effects of sex on out-of-hospital cardiac arrest outcomes in Japan. We selected 276,590 patients aged 20 to 89 years with out-of-hospital cardiac arrest and compared the frequencies of initial cardiac rhythms, 1-month survival rates, and favorable neurologic outcome rates between sexes.</AbstractText>The incidence of out-of-hospital cardiac arrest was higher in men than in women (men: 0.12%; women: 0.07%). Men were witnessed more often while out-of-hospital cardiac arrest was occurring (men: 42.1% and women: 36.9%), typically presented with initial ventricular fibrillation/ventricular tachycardia rhythms, and had a higher 1-month survival rate overall after out-of-hospital cardiac arrest events (men: 5.2% and women: 4.3%). However, the rate of survival with a favorable neurologic outcome for women aged 30 to 49 years was significantly higher than that for men within the same age range. Among patients initially presenting with ventricular fibrillation/ventricular tachycardia, the rate of survival with favorable neurologic outcome was higher for women than men in the group aged 40 to 59 years.</AbstractText>Our results suggest that men have a higher 1-month survival rate after out-of-hospital cardiac arrest because of a higher frequency of ventricular fibrillation/ventricular tachycardia presentation compared with women. Although patients of both sexes with out-of-hospital cardiac arrest initially presenting with ventricular fibrillation/ventricular tachycardia exhibited similar overall survival rates, the rate of survival with favorable neurologic outcome was significantly higher for women than men in the group aged 40 to 59 years.</AbstractText>Copyright © 2011 Elsevier Inc. All rights reserved.</CopyrightInformation> |
15,344 | Clinical and classic echocardiographic features of patients with, and without, left ventricle reverse remodeling following the introduction of cardiac resynchronization therapy. | The aim of the study was to assess clinical and classic echocardiographic data in patients with different cardiac resynchronization therapy (CRT) outcomes.</AbstractText>Sixty consecutive patients (aged 66.3 ± 8.7 years, 57 men) with chronic heart failure (CHF) in New York Heart Association (NYHA) classes III-IV despite optimized pharmacotherapy, with left ventricular end-diastolic diameter (LVEDD) > 55 mm, left ventricular ejection fraction £ 35% and wide QRS complex (≥ 120 ms), including individuals with permanent atrial fibrillation (AF) and single- and dual-chamber pacing, were assessed firstly before, and secondly three months after, biventricular heart stimulator implantation (excluding three patients who died during the follow-up). Patients developing ≥ 10% reduction of left ventricular end-systolic volume (LVESV) were classified as responders to CRT.</AbstractText>The group of responders (n = 34, 59.7%) and the group of non-responders (n = 23, 40.3%) did not differ regarding baseline echocardiographic parameters or in terms of clinical data of age, gender, concomitant diseases, smoking or pharmacological treatment. The differences involved higher rates of ischemic CHF background, prevalence of hypertension and permanent AF, and a higher concentration of N-terminal pro-B-type natriuretic peptide (NT-proBNP) among the non-responders. In the multivariate logistic regression analysis, NT-proBNP, body mass index (BMI) and the presence of permanent AF correlated negatively with the magnitude of LVESV reduction following CRT introduction.</AbstractText>Classic echocardiographic data did not predict left ventricle reverse remodeling. Higher rates of ischemic CHF aetiology, hypertension, permanent AF and higher NT-proBNP concentration were found in the group without at least 10% LVESV reduction at the three month follow-up. NT-proBNP, BMI and the presence of permanent AF had negative effects on the magnitude of LVESV.</AbstractText> |
15,345 | Genetics of sudden cardiac death syndromes. | To survey recent developments in the field of genetics encompassing discovery of new candidate genes, new diagnostic strategies, and new therapies for sudden cardiac death (SCD) syndromes.</AbstractText>In addition to new mutations in known SCD genes, several novel genes not previously implicated in SCD causation have been found, particularly in long QT syndrome (e.g., KCNJ5, AKAP9, SNTA1), idiopathic ventricular fibrillation (e.g., DPP6, KCNJ8), dilated cardiomyopathy (e.g., NEBL), and hypertrophic cardiomyopathy (HCM; e.g., NEXN). Genetic SCD animal models have provided novel insights into the cellular mechanism and pathogenesis of nearly all the major SCD syndromes, which has led to several new drug therapies for patients with genetic arrhythmia syndromes (e.g., flecainide in catecholaminergic polymorphic ventricular tachycardia). Furthermore, genetic contributions to acquired heart diseases are increasingly being recognized. For example, a 21q21 locus is strongly associated with ventricular fibrillation after myocardial infarction. Near this locus is CXADR, a gene encoding a viral receptor implicated in myocarditis and dilated cardiomyopathy. Finally, common variants in cardiac ion channels and proteins likely contribute to common cardiac phenotypes.</AbstractText>Major strides have been made in uncovering new genes, mechanisms, and syndromes that have significantly advanced the diagnosis and treatment of genetic SCD disorders.</AbstractText> |
15,346 | [Concealed Brugada syndrome that became apparent incidentally during atrial fibrillation therapy]. | A 31-year-old male patient was admitted to the emergency department with acute atrial fibrillation. After diltiazem infusion, a single oral dose of 600 mg propafenone was given to the patient for medical cardioversion. Approximately four hours later, sinus rhythym was restored. Re-evaluation of the admission ECG revealed right bundle branch block and saddleback-type ST-segment elevation of about 2 mm in V1-2 leads. Following propafenone, this type 2 Brugada ECG pattern turned to the coved type 1 Brugada pattern with ST elevation of more than 2 mm. After disappearance of propafenone effect, the ECG pattern turned to the type 2 Brugada pattern. Considering that the patient also had a family history of sudden cardiac death, electrophysiological study was conducted. During ventricular tachycardia stimulation, no ventricular arrhythmia was observed, thus the patient was scheduled to a close follow-up program. |
15,347 | Percutaneous transatrial access to the pericardial space for epicardial mapping and ablation. | Puncture of the atrial appendage may provide access to the pericardial space. The aim of this study was to evaluate the feasibility of epicardial mapping and ablation through an endocardial transatrial access in a swine model.</AbstractText>An 8-F Mullins sheath was used to perforate the right (n=16) or left (n=1) atrial appendage in 17 pigs (median weight, 27.5 kg; first and third quartiles [Q1, Q3], 25.2, 30.0 kg). A 7-F ablation catheter was introduced into the pericardial space to perform epicardial mapping and deliver radiofrequency pulses on the atria. The pericardial space was entered in all 17 animals. In 15 (88%) animals, there was no hemodynamic instability (mean blood pressure monitoring, initial median, 80 mm Hg; Q1, Q3, 70, 86 mm Hg; final median, 88 mm Hg; Q1, Q3, 80, 96 mm Hg; P=0.426). In these 15, a mild hemorrhagic pericardial effusion was identified and aspirated (median, 20 mL; Q1, Q3, 15, 30 mL) during the procedure, and postmortem gross analysis revealed that the atrial perforation was closed in these animals. In 2 (12%) of the 17 animals, there was major pericardial bleeding with hemodynamic collapse. On gross examination, it was found that pericardial space was accessed through right ventricular perforation in 1 animal and the tricuspid annulus in the other. After the initial study, we used an occlusion device in 3 other animals to attempt to seal the puncture (2 at the right atrial appendage and 1 at the right ventricle). These 3 animals had no significant pericardial bleeding.</AbstractText>Transatrial endovascular right atrial appendage puncture may provide a potential alternative route for pericardial access. Further studies are needed to evaluate its safety with longer and more-complex procedures before being applied in clinical settings.</AbstractText> |
15,348 | A novel lead configuration for optimal spatio-temporal detection of intracardiac repolarization alternans. | Electric alternans is a pattern of variation in the shape of ECG waveform that occurs every other beat. In humans, alternation in ventricular repolarization, known as repolarization alternans (RA), has been associated with increased vulnerability to ventricular tachycardia/fibrillation and sudden cardiac death.</AbstractText>This study investigates the spatio-temporal variability of intracardiac RA and its relationship to body surface RA in an acute myocardial ischemia model in swine. We developed a real-time multichannel repolarization signal acquisition, display, and analysis system to record ECG signals from catheters in the right ventricle, coronary sinus, left ventricle, and epicardial surface before and after circumflex coronary artery balloon occlusion. We found that RA is detectable within 4 minutes after the onset ischemia and is most prominently seen during the first half of the repolarization interval. Ischemia-induced RA was detectable on unipolar and bipolar leads (both in near- and far-field configurations) and on body surface leads. Far-field bipolar intracardiac leads were more sensitive for RA detection than body surface leads, with the probability of body surface RA detection increasing as the number of intracardiac leads detecting RA increased, approaching 100% when at least three intracardiac leads detected RA. We developed a novel, clinically applicable intracardiac lead system based on a triangular arrangement of leads spanning the right ventricular and coronary sinus catheters, which provided the highest sensitivity for intracardiac RA detection when compared with any other far-field bipolar sensing configurations.</AbstractText>In conclusion, intracardiac alternans, a complex spatio-temporal phenomenon associated with arrhythmia susceptibility and sudden cardiac death, can be reliably detected through a novel triangular right ventricular-coronary sinus lead configuration.</AbstractText> |
15,349 | Cardiac sarcoidosis and giant cell myocarditis as causes of atrioventricular block in young and middle-aged adults. | Cardiac sarcoidosis (CS) and giant cell myocarditis (GCM) may present as high-degree atrioventricular block (AVB), but their proportion of the causal spectrum of AVB is not well-known. We investigated the prevalence of biopsy-verified CS and GCM in young and middle-aged adults undergoing pacemaker (PM) implantation for AVB.</AbstractText>We used the PM registry of Helsinki University Central Hospital to identify all patients aged 18 to 55 years who underwent PM implantation for AVB between January 1999 and April 2009 and reviewed their medical records. In total, 133 patients had either second- or third-degree AVB as an indication for PM. Of them, 61 had a known cause for AVB, and they were excluded from further analyses. Among the remaining 72 patients with initially unexplained AVB, biopsy-verified CS or GCM was found in 14 (19%) and 4 (6%) patients, respectively. The majority (16/18, 89%) were women. Among the adult patients aged <55 years, the prevalence of CS and GCM combined was 14% (95% CI, 7.7% to 19.3%) of the whole AVB population and 25% (95% CI, 15% to 35%) of those with an initially unexplained AVB. Over an average of 48 months of follow-up, 7 (39%) of 18 patients with CS or GCM versus 1 of the 54 patients in whom AVB remained idiopathic, experienced either cardiac death, cardiac transplantation, ventricular fibrillation, or treated sustained ventricular tachycardia (P<0.001).</AbstractText>CS and GCM explain ≥25% of initially unexplained AVB in young and middle-aged adults. These patients are at high risk for adverse cardiac events.</AbstractText> |
15,350 | Atrioventricular junction ablation and pacemaker implantation for heart failure associated with atrial fibrillation: potential issues and therapies in the setting of acute heart failure syndrome. | Atrial fibrillation is the most common arrhythmia and is especially clinically important in patients with heart failure. Prolonged atrial fibrillation with high ventricular rate response may lead to development or worsening of left ventricular function. If adequate heart rate control cannot be obtained medically, often patients will undergo pacemaker implant and catheter ablation of the atrioventricular junction. This intervention can have profound effects on the course of heart failure. This article reviews the technique, complications, outcome data, and alternatives to this management strategy. The potential role of this therapeutic modality in those hospitalized with acute heart failure syndromes is discussed. |
15,351 | Predictors of occult paroxysmal atrial fibrillation in cryptogenic strokes detected by long-term noninvasive cardiac monitoring. | Background and Purpose. Paroxysmal Atrial fibrillation/Flutter (PAF) detection rates in cryptogenic strokes have been variable. We sought to determine the percentage of patients with cryptogenic stroke who had PAF on prolonged non-invasive cardiac monitoring. Methods and Results. Sixty-two consecutive patients with stroke and TIA in a single center with a mean age of 61 (+/- 14) years were analyzed. PAF was detected in 15 (24%) patients. Only one patient reported symptoms of shortness of breath during the episode of PAF while on monitoring, and 71 (97%) of these 73 episodes were asymptomatic. A regression analysis revealed that the presence of PVCs (ventricular premature beats) lasting more than 2 minutes (OR 6.3, 95% CI, 1.11-18.92; P = .042) and strokes (high signal on Diffusion Weighted Imaging) (OR 4.3, 95% CI, 5-36.3; P = .041) predicted PAF. Patients with multiple DWI signals were more likely than solitary signals to have PAF (OR 11.1, 95% CI, 2.5-48.5, P < .01). Conclusion. Occult PAF is common in cryptogenic strokes, and is often asymptomatic. Our data suggests that up to one in five patients with suspected cryptogenic strokes and TIAs have PAF, especially if they have PVCs and multiple high DWI signals on MRI. |
15,352 | Endurance exercise training reduces cardiac sodium/calcium exchanger expression in animals susceptible to ventricular fibrillation. | Increased sodium/calcium exchanger activity (NCX1, an important regulator of cardiomyocyte cystolic calcium) may provoke arrhythmias. Exercise training can decrease NCX1 expression in animals with heart failure improving cytosolic calcium regulation, and could thereby reduce the risk for ventricular fibrillation (VF).</AbstractText>To test this hypothesis, a 2-min coronary occlusion was made during the last minute of exercise in dogs with healed myocardial infarctions; 23 had VF (S, susceptible) and 13 did not (R, resistant). The animals were randomly assigned to either 10-week exercise training (progressively increasing treadmill running; S n = 9; R n = 8) or 10-week sedentary (S n = 14; R n = 5) groups. At the end of the 10-week period, the exercise + ischemia test provoked VF in sedentary but not trained susceptible dogs. On a subsequent day, cardiac tissue was harvested and NCX1 protein expression was determined by Western blot.</AbstractText>In the sedentary group, NCX1 expression was significantly (ANOVA, P < 0.05) higher in susceptible compared to resistant dogs. In contrast, NCX1 levels were similar in the exercise trained resistant and susceptible animals.</AbstractText>These data suggest that exercise training can restore a more normal NCX1 level in dogs susceptible to VF, improving cystolic calcium regulation and could thereby reduce the risk for sudden death following myocardial infarction.</AbstractText> |
15,353 | Autonomic remodeling in the left atrium and pulmonary veins in heart failure: creation of a dynamic substrate for atrial fibrillation. | Atrial fibrillation (AF) is commonly associated with congestive heart failure (CHF). The autonomic nervous system is involved in the pathogenesis of both AF and CHF. We examined the role of autonomic remodeling in contributing to AF substrate in CHF.</AbstractText>Electrophysiological mapping was performed in the pulmonary veins and left atrium in 38 rapid ventricular-paced dogs (CHF group) and 39 control dogs under the following conditions: vagal stimulation, isoproterenol infusion, β-adrenergic blockade, acetylcholinesterase (AChE) inhibition (physostigmine), parasympathetic blockade, and double autonomic blockade. Explanted atria were examined for nerve density/distribution, muscarinic receptor and β-adrenergic receptor densities, and AChE activity. In CHF dogs, there was an increase in nerve bundle size, parasympathetic fibers/bundle, and density of sympathetic fibrils and cardiac ganglia, all preferentially in the posterior left atrium/pulmonary veins. Sympathetic hyperinnervation was accompanied by increases in β(1)-adrenergic receptor R density and in sympathetic effect on effective refractory periods and activation direction. β-Adrenergic blockade slowed AF dominant frequency. Parasympathetic remodeling was more complex, resulting in increased AChE activity, unchanged muscarinic receptor density, unchanged parasympathetic effect on activation direction and decreased effect of vagal stimulation on effective refractory period (restored by AChE inhibition). Parasympathetic blockade markedly decreased AF duration.</AbstractText>In this heart failure model, autonomic and electrophysiological remodeling occurs, involving the posterior left atrium and pulmonary veins. Despite synaptic compensation, parasympathetic hyperinnervation contributes significantly to AF maintenance. Parasympathetic and/or sympathetic signaling may be possible therapeutic targets for AF in CHF.</AbstractText> |
15,354 | New drugs vs. old concepts: a fresh look at antiarrhythmics. | Common arrhythmias, particularly atrial fibrillation (AF) and ventricular tachycardia/fibrillation (VT/VF) are a major public health concern. Classic antiarrhythmic (AA) drugs for AF are of limited effectiveness, and pose the risk of life-threatening VT/VF. For VT/VF, implantable cardiac defibrillators appear to be the unique, yet unsatisfactory, solution. Very few AA drugs have been successful in the last few decades, due to safety concerns or limited benefits in comparison to existing therapy. The Vaughan-Williams classification (one drug for one molecular target) appears too restrictive in light of current knowledge of molecular and cellular mechanisms. New AA drugs such as atrial-specific and/or multichannel blockers, upstream therapy and anti-remodeling drugs, are emerging. We focus on the cellular mechanisms related to abnormal Na⁺ and Ca²⁺ handling in AF, heart failure, and inherited arrhythmias, and on novel strategies aimed at normalizing ionic homeostasis. Drugs that prevent excessive Na⁺ entry (ranolazine) and aberrant diastolic Ca²⁺ release via the ryanodine receptor RyR2 (rycals, dantrolene, and flecainide) exhibit very interesting antiarrhythmic properties. These drugs act by normalizing, rather than blocking, channel activity. Ranolazine preferentially blocks abnormal persistent (vs. normal peak) Na⁺ currents, with minimal effects on normal channel function (cell excitability, and conduction). A similar "normalization" concept also applies to RyR2 stabilizers, which only prevent aberrant opening and diastolic Ca²⁺ leakage in diseased tissues, with no effect on normal function during systole. The different mechanisms of action of AA drugs may increase the therapeutic options available for the safe treatment of arrhythmias in a wide variety of pathophysiological situations. |
15,355 | Comparison of the usefulness of cardiac resynchronization therapy in three age-groups (<65, 65-74 and ≥75 Years) (from the InSync/InSync ICD Italian Registry). | Chronic heart failure is one of the most important geriatric syndromes, associated with disability, increased hospital admissions, and high mortality. The aim of this study was to evaluate the existence of age-related differences in clinical effectiveness and outcomes of cardiac resynchronization therapy (CRT), alone or in combination with an implantable cardioverter-defibrillator (CRT-D), in a large, real-world registry. A total of 1,787 patients admitted for CRT or CRT-D to the 117 centers participating in the InSync/InSync ICD Italian Registry from 1999 to 2005 were evaluated. Patients were divided into 3 age groups: <65 years (n = 571), 65 to 74 years (n = 740), and ≥75 years (n = 476). The left ventricular ejection fraction did not differ in the 3 groups (26 ± 8% vs 26 ± 7% vs 27 ± 8%, p = 0.123). Atrial fibrillation prevalence demonstrated an age-related increase. The use of recommended medical therapy for chronic heart failure decreased with age, as well as CRT-D implantation (p <0.001). The percentage of echocardiographic responders to CRT was similar in the 3 groups, and New York Heart Association class significantly improved independent of age. During the follow-up period (19 ± 13 months), all-cause mortality was higher in patients aged ≥75 years than in those aged <65 years (p = 0.005). In the whole population, mortality was associated with the nonresponder condition, the presence of atrial fibrillation and the lack of prescription of recommended medical therapy. In conclusion, CRT improved left ventricular performance and functional capacity independent of age. The proportion of the responder condition to CRT was the same in all groups. Pharmacologic undertreatment is an important issue in a "real-world" geriatric population. |
15,356 | Ventricular tachycardia without apparent heart disease: long-term follow-up. | The purpose of the study was to evaluate the long-term prognosis of ventricular tachycardia (VT) in patients without structural heart disease (HD).</AbstractText>Holter monitoring, exercise test, echocardiography, right angiography, coronary angiography, and electrophysiologic study were performed in 810 patients with VT.</AbstractText>Eighty patients (mean age, 45 ± 17 years) had no apparent HD. VT was reproduced at electrophysiologic study in 62 patients. Mean follow-up was 9.7 ± 7 years. Initially, 91% were treated with drugs. Defibrillator was implanted in 4, including 2 for arrhythmogenic right ventricular cardiomyopathy diagnosed later. VT ablation was performed in 3 patients. Three patients older than 70 years died of nonarrhythmic cause. Other patients are alive without antiarrhythmic drug treatment in 50%. Three developed a dilated cardiomyopathy; and 2, atrial fibrillation.</AbstractText>Invasive treatment was rarely required in patients with VT without HD. The prognosis was only dependent on the age and the pattern of electrocardiogram in VT.</AbstractText>Copyright © 2011 Elsevier Inc. All rights reserved.</CopyrightInformation> |
15,357 | Characteristics of J wave-associated idiopathic ventricular fibrillation: role of drugs. | A storm of J wave-associated idiopathic ventricular fibrillation (VF) was observed in a 49-year-old man. Multiform premature ventricular complexes initiated the episodes of VF. Intravenous isoproterenol attenuated the J wave and suppressed the VF storm. After the implantation of a cardioverter defibrillator, VF was induced by programmed electrical stimulation at baseline, and it was terminated by a 25-J shock after an unsuccessful 15-J shock. During oral treatment with quinidine sulfate, 600 mg daily, the J wave was attenuated and VF became noninducible by programmed electrical stimulation. VF induced by a shock delivered on the T wave was terminated by a single 10-J shock. Mean F-F interval and dominant frequency of the VF were 162 ms and 6.8 Hz at baseline, and 210 ms and 5.0 Hz during the quinidine sulfate treatment. |
15,358 | An impaired renal function: a predictor of ventricular arrhythmias and mortality in patients with nonischemic cardiomyopathy and heart failure. | This study investigated the overall mortality and the incidence of ventricular tachyarrhythmia (VT) in 99 patients with nonischemic cardiomyopathy (NICM) and with an implantable cardioverter defibrillator (ICD) suffering from heart failure.</AbstractText>We performed a stepwise regression model to identify independent risk factors for the occurrence of ventricular arrhythmias. Using a Cox regression model, independent risk factors for total mortality were evaluated and, subsequently, a Kaplan-Meier analysis was applied. The primary endpoint of this study was the identification of independent predictors of overall mortality and the incidence of malignant arrhythmias.</AbstractText>One hundred twenty-five VT (≥310 ms), 51 fast VT (between 310 ms and 240 ms), and 48 episodes of ventricular fibrillation (≤240 ms) were documented in 32 patients. Independent predictors of arrhythmias detected and treated by the ICD included female gender (odds ratio [OR] 3.4), lack of statin therapy (OR 3.5), and increased serum creatinine (OR 3.7). The Kaplan-Meier analysis showed no difference in survival between participants with or without VT. Total mortality was predicted by increased age (OR 2.3) and an impaired renal function (OR 1.9), independently.</AbstractText>In this cohort of NICM patients with heart failure, female gender, lack of statin therapy, and increased creatinine represented independent risk factors for the incidence of malignant arrhythmias. Furthermore, renal insufficiency and age favored total mortality. Considering these results, impaired renal function might represent a valuable noninvasive tool to identify NICM patients who, despite ICD implantation, have the highest risk of mortality and therefore require a particularly thorough follow-up.</AbstractText>©2011, The Authors. Journal compilation ©2011 Wiley Periodicals, Inc.</CopyrightInformation> |
15,359 | Clinical experience with a novel subcutaneous implantable defibrillator system in a single center. | Implantable cardioverter-defibrillators (ICDs) reduce mortality in both primary and secondary prevention, but are associated with substantial short- and long-term morbidity. A totally subcutaneous ICD (S-ICD) system has been developed. We report the initial clinical experience of the first 31 patients implanted at our hospital.</AbstractText>All patients had an ICD indication according to the ACC/AHA/ESC guidelines. The first 11 patients were part of the reported CE trial. The implantation was performed without fluoroscopy. The device was implanted subcutaneously in the anterior axillary line, with a parasternal lead tunneled from the xiphoid to the manubrial-sternal junction. Ventricular fibrillation (VF) was induced to assess detection accuracy and defibrillation efficacy using 65 J shocks.</AbstractText>Post-implant, 52 sustained episodes of VF were induced. Sensitivity was 100% and induced conversion efficacy was 100% (with standard polarity in 29 patients). Mean time to therapy was 13.9 ± 2.5 s (range 11-21.6 s). Late procedure-related complications were observed in 2 of the first 11 implantations (lead migration). During follow-up, spontaneous ventricular arrhythmias occurred in four patients, with accurate detection of all episodes. Inappropriate therapy was observed in five patients. Recurrences were prevented with reprogramming.</AbstractText>The S-ICD system can be implanted without the use of fluoroscopy by using anatomical landmarks only. Episodes of VF were accurately detected using subcutaneous signals, and all induced and clinical episodes were successfully converted. The S-ICD system is a viable alternative to conventional ICD systems for selected patients.</AbstractText> |
15,360 | Contribution of comorbidities to functional impairment is higher in heart failure with preserved than with reduced ejection fraction. | Comorbidities negatively affect prognosis more strongly in heart failure with preserved (HFpEF) than with reduced (HFrEF) ejection fraction. Their comparative impact on physical impairment in HFpEF and HFrEF has not been evaluated so far.</AbstractText>The frequency of 12 comorbidities and their impact on NYHA class and SF-36 physical functioning score (SF-36 PF) were evaluated in 1,294 patients with HFpEF and 2,785 with HFrEF. HFpEF patients had lower NYHA class (2.0 ± 0.6 vs. 2.4 ± 0.6, p < 0.001) and higher SF-36 PF score (54.4 ± 28.3 vs. 54.4 ± 27.7, p < 0.001). All comorbidities were significantly (p < 0.05) more frequent in HFrEF, except hypertension and obesity, which were more frequent in HFpEF (p < 0.001). Adjusting for age and gender, COPD, anemia, hyperuricemia, atrial fibrillation, renal dysfunction, cerebrovascular disease and diabetes had a similar (p for interaction > 0.05) negative effect in both groups. Obesity, coronary artery disease and peripheral arterial occlusive disease exerted a significantly (p < 0.05) more adverse effect in HFpEF, while hypertension and hyperlipidemia were associated with fewer (p < 0.05) symptoms in HFrEF only. The total impact of comorbidities on NYHA (AUC for prediction of NYHA III/IV vs. I/II) and SF-36 PF (r(2)) in multivariate analyses was approximately 1.5-fold higher in HFpEF, and also much stronger than the impact of a 10% decrease in ejection fraction in HFrEF or a 5 mm decrease in left ventricular end-diastolic diameter in HFpEF.</AbstractText>The impact of comorbidities on physical impairment is higher in HFpEF than in HFrEF. This should be considered in the differential diagnosis and in the treatment of patients with HFpEF.</AbstractText> |
15,361 | Trabectedin has a low cardiac risk profile: a comprehensive cardiac safety analysis. | This analysis provides a cross-study evaluation of the cardiac safety of trabectedin.</AbstractText>Drug-related cardiac adverse events (CAEs) were retrieved from phase I-III clinical trials, pharmacovigilance databases, and spontaneously reported cases. Left ventricular ejection fraction (LVEF) was monitored in combination phase I studies with doxorubicin or pegylated liposomal doxorubicin (PLD) and in a phase III trial (with PLD).</AbstractText>CAEs [grade 4 cardiac arrest with severe pancytopenia and sepsis (n = 1 patient), grade 4 atrial fibrillation (n = 2), and grade 1 tachycardia (n = 1)] occurred in 4/283 patients (1.4%) in 6 single-agent phase I trials. CAEs (grade 1 sinus tachycardia in a hypertensive patient and grade 1 ventricular dysfunction) occurred in 2/155 patients (1.3%) in 4 phase I combination trials. Results from 19 single-agent phase II trials showed CAEs in 20/1,132 patients (1.8%): arrhythmias (tachycardia/palpitations; n = 13; 1.1%) were the most common. A rather similar rate of symptomatic CAEs was observed in both arms of a phase III trial in recurrent ovarian cancer: 6/330 patients (1.8%; PLD) and 11/333 patients (3.3%; trabectedin/PLD). No clinically relevant LVEF changes occurred in phase I combination trials. In the phase III trial, LVEF decreases from baseline were similar: 9% of patients (PLD) and 7% (trabectedin/PLD), with no relevant symptoms. During postmarketing experience in soft tissue sarcoma (2,046 patients treated), 4 CAEs (2 cardiac arrest, 2 cardiac failure; ~0.2%) occurred in patients with preexisting conditions.</AbstractText>Trabectedin has a low incidence of CAEs, consisting mainly of arrhythmias. This extensive data review indicates a low cardiac risk profile for trabectedin.</AbstractText> |
15,362 | Rhythm control should be better for the management of patients with atrial fibrillation and heart failure--rhythm control vs. rate control: which is better in the management of atrial fibrillation? (Rhythm-side). | The incidence of atrial fibrillation (AF) increases with advancing NHYA cardiac functional class, and it significantly affects the cardiac function of a failing heart. In such situations, clinicians should aim to maintain sinus rhythm in these patients with heart failure (HF) in order to improve their prognosis. However, according to various randomized clinical studies demonstrating the non-superiority of rhythm control over rate control, many clinicians seem to prefer to take the line of least resistance (ie, rate control). Curative catheter ablation mainly based on isolation procedure of the pulmonary veins in patients with AF and HF has demonstrated a significant improvement in left ventricular function, even in the presence of adequate ventricular rate control before the ablation. On the other hand, ablation and biventricular pacing therapy, which is an extreme rate control strategy, has not shown any beneficial effects for these patients. Therefore, a regular RR interval with an appropriate cycle length only is not sufficient to improve cardiac performance, and maintenance of sinus rhythm, which restores atrial contraction and the atrioventricular synchrony, is thought to be essential for an improvement in HF. Thoughtful clinicians should do their best to find a way to keep HF patients in sinus rhythm. |
15,363 | Rate control is a better initial treatment for patients with atrial fibrillation and heart failure--rhythm control vs. rate control: which is better in the management of atrial fibrillation? (Rate-side). | Congestive heart failure (CHF) and atrial fibrillation (AF) often coexist, and each increase the morbidity and mortality associated with the other. Until now, many studies have reported that a strategy of rate control, in combination with anticoagulation in patients at risk of thromboembolic events, appears to be at least equivalent to a strategy of maintaining sinus rhythm with currently available pharmacological therapeutic options. As compared to rhythm control therapy, rate control treatment is simple and relatively easy. Therefore, pharmacological rate control should be considered initially in patients with AF associated with CHF. However, cardiac symptoms associated with AF may continue after achieving reasonable ventricular rate control. Either pharmacological or non-pharmacological rhythm control needs to be considered at that time. Amiodarone is the only recommended antiarrhythmic drug in the recent therapeutic guidelines for CHF, and can be used for both rhythm and rate control of AF. However, there is no question that some patients require early non-pharmacological rhythm control instead of long-lasting rate control. Catheter ablation (CA) can be applicable even in AF associated with CHF, but the results of CA are closely associated with the clinical and electrophysiological characteristics in each patient, as well as with the experience with this procedure in each institution. Indications for and the appropriate period of CA need to be carefully examined in each individual. |
15,364 | [Neurology and cardiology: points of contact]. | Strokes resulting from cardiac diseases, and cardiac abnormalities associated with neuromuscular disorders are examples of the many points of contact between neurology and cardiology. Approximately 20-30% of strokes are related to cardiac diseases, including atrial fibrillation, congestive heart failure, bacterial endocarditis, rheumatic and nonrheumatic valvular diseases, acute myocardial infarction with left ventricular thrombus, and cardiomyopathies associated with muscular dystrophies, among others. Strokes can also occur in the setting of cardiac interventions such as cardiac catheterization and coronary artery bypass procedures. Treatment to prevent recurrent stroke in any of these settings depends on the underlying etiology. Whereas anticoagulation with vitamin K antagonists is proven to be superior to acetylsalicylic acid for stroke prevention in atrial fibrillation, the superiority of anticoagulants has not been conclusively established for stroke associated with congestive heart failure and is contraindicated in those with infective endocarditis. Ongoing trials are evaluating management strategies in patients with atrial level shunts due to patent foramen ovale. Cardiomyopathies and conduction abnormalities are part of the spectrum of many neuromuscular disorders including mitochondrial disorders and muscular dystrophies. Cardiologists and neurologists share responsibility for caring for patients with or at risk for cardiogenic strokes, and for screening and managing the heart disease associated with neuromuscular disorders. |
15,365 | Mutation analysis ion channel genes ventricular fibrillation survivors with coronary artery disease. | Observations from population-based studies demonstrated a strong genetic component of sudden cardiac death. The aim of this study was to test the hypothesis that ion channel genes mutations are more common in ventricular fibrillation (VF) survivors with coronary artery disease (CAD) compared to controls.</AbstractText>The entire coding sequence of KCNQ1, KCNH2, SCN5A, KCNE1, and KCNE2 genes was analyzed in 45 (five females) CAD individuals-survivors of documented VF and in 90 matched healthy controls. In another control group of 141 matched patients with CAD without malignant arrhythmias, the exons containing rare coding variants found in the VF survivors were sequenced.</AbstractText>The carrier frequency of all the rare sequence variants was significantly higher in the VF survivors (8/45, 17.8%) than in CAD controls (3/141, 2.2%, P = 0.001). In VF survivors, four coding variants in eight individuals were found. Three in KCNH2 gene: R148W and GAG186del are novel; P347S was previously related to long QT syndrome. In SCN5A gene, P2006A variant was found in five unrelated males. This variant has been demonstrated previously to have small effect on sodium channel kinetics. No rare coding variants were found in the healthy controls. The P2006A variant was found in three CAD controls.</AbstractText>The prevalence of selected, rare coding variants in five long QT genes was significantly higher in cases versus controls, confirming a mechanistic role for these genes among a subgroup of patients with coronary disease and VF.</AbstractText>©2011, The Authors. Journal compilation ©2011 Wiley Periodicals, Inc.</CopyrightInformation> |
15,366 | Clinical characteristics and long-term prognosis of vasospastic angina patients who survived out-of-hospital cardiac arrest: multicenter registry study of the Japanese Coronary Spasm Association. | Coronary artery spasm plays an important role in the pathogenesis of ischemic heart disease; however, its role in sudden cardiac death remains to be fully elucidated. We examined the clinical characteristics and outcomes of patients with vasospastic angina (VSA) in our nationwide multicenter registry by the Japanese Coronary Spasm Association.</AbstractText>Between September 2007 and December 2008, 1429 patients with VSA (male/female, 1090/339; median, 66 years) were identified. They were characterized by a high prevalence of smoking and included 35 patients who survived out-of-hospital cardiac arrest (OHCA). The OHCA survivors, as compared with the remaining 1394 non-OHCA patients, were characterized by younger age (median, 58 versus 66 years; P<0.001) and higher incidence of left anterior descending coronary artery spasm (72% versus 53%, P<0.05). In the OHCA survivors, 14 patients underwent implantable cardioverter-defibrillator (ICD) implantation while intensively treated with calcium channel blockers. Survival rate free from major adverse cardiac events was significantly lower in the OHCA survivors compared with the non-OHCA patients (72% versus 92% at 5 years, P<0.001), including appropriate ICD shocks for ventricular fibrillation in 2 patients. Multivariable analysis revealed that OHCA events were significantly correlated with major adverse cardiac events (hazard ratio, 3.25; 95% confidence interval, 1.39 to 7.61; P<0.01).</AbstractText>These results from the largest vasospastic angina cohort indicate that vasospasm patients who survived OHCA are high-risk population. Further studies are needed to determine whether implantable cardioverter-defibrillator therapy improves patient prognosis.</AbstractText> |
15,367 | Right ventricular mechanical dispersion is related to malignant arrhythmias: a study of patients with arrhythmogenic right ventricular cardiomyopathy and subclinical right ventricular dysfunction. | We evaluated if right ventricular (RV) mechanical dispersion by strain was related to ventricular arrhythmias (VT/VF) in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC) and if mechanical dispersion was increased in so far asymptomatic mutation carriers.</AbstractText>We included 69 patients, 42 had symptomatic ARVC and 27 were mutation positive asymptomatic family members. Forty healthy individuals served as controls. Myocardial strain was assessed in 6 RV and 16 left ventricular (LV) segments. Contraction duration (CD) in 6 RV and 16 LV segments were measured as the time from onset R on electrocardiogram to maximum myocardial shortening in each segment. The standard deviation of CD was defined as mechanical dispersion. Mechanical dispersion was more pronounced in ARVC patients with arrhythmias compared with asymptomatic mutation carriers and healthy individuals in RV [52(41,63) vs. 35(23,47) vs. 13(9,19)ms, P < 0.001]. Mechanical dispersion was more pronounced in asymptomatic mutation carriers compared with healthy individuals (P < 0.001). Right ventricular mechanical dispersion predicted VT/VF in a multivariate logistic regression analysis [odds ratio (OR), 1.66 (95% confidence interval (CI) 1.06-2.58), P < 0.03]. Right ventricular and LV function by strain were reduced in symptomatic ARVC patients and correlated significantly (R = 0.81, P < 0.001). Right ventricular and LV strain were reduced in asymptomatic mutation carriers compared with healthy individuals (P < 0.001).</AbstractText>Right ventricular mechanical dispersion was pronounced in patients with ARVC with VT/VF. Right ventricular mechanical dispersion was present in asymptomatic mutation carriers and may be helpful in risk stratification. Right ventricular and LV function correlated in ARVC patients implying that ARVC is a biventricular disease.</AbstractText> |
15,368 | Automaticity in acute ischemia: bifurcation analysis of a human ventricular model. | Acute ischemia (restriction in blood supply to part of the heart as a result of myocardial infarction) induces major changes in the electrophysiological properties of the ventricular tissue. Extracellular potassium concentration ([K(o)(+)]) increases in the ischemic zone, leading to an elevation of the resting membrane potential that creates an "injury current" (I(S)) between the infarcted and the healthy zone. In addition, the lack of oxygen impairs the metabolic activity of the myocytes and decreases ATP production, thereby affecting ATP-sensitive potassium channels (I(Katp)). Frequent complications of myocardial infarction are tachycardia, fibrillation, and sudden cardiac death, but the mechanisms underlying their initiation are still debated. One hypothesis is that these arrhythmias may be triggered by abnormal automaticity. We investigated the effect of ischemia on myocyte automaticity by performing a comprehensive bifurcation analysis (fixed points, cycles, and their stability) of a human ventricular myocyte model [K. H. W. J. ten Tusscher and A. V. Panfilov, Am. J. Physiol. Heart Circ. Physiol. 291, H1088 (2006)] as a function of three ischemia-relevant parameters [K(o)(+)], I(S), and I(Katp). In this single-cell model, we found that automatic activity was possible only in the presence of an injury current. Changes in [K(o)(+)] and I(Katp) significantly altered the bifurcation structure of I(S), including the occurrence of early-after depolarization. The results provide a sound basis for studying higher-dimensional tissue structures representing an ischemic heart. |
15,369 | Prevention of ventricular fibrillation episodes in Brugada syndrome by catheter ablation over the anterior right ventricular outflow tract epicardium. | The underlying electrophysiological mechanism that causes an abnormal ECG pattern and ventricular tachycardia/ventricular fibrillation (Vt/VF) in patients with the Brugada syndrome (BrS) remains unelucidated. However, several studies have indicated that the right ventricular outflow tract (RVOT) is likely to be the site of electrophysiological substrate. We hypothesized that in patients with BrS who have frequent recurrent VF episodes, the substrate site is the RVOT, either over the epicardium or endocardium; abnormal electrograms would be identified at this location, which would serve as the target site for catheter ablation.</AbstractText>We studied 9 symptomatic patients with the BrS (all men; median age 38 years) who had recurrent VF episodes (median 4 episodes) per month, necessitating implantable cardioverter defibrillator discharge. Electroanatomic mapping of the right ventricle, both endocardially and epicardially, and epicardial mapping of the left ventricle were performed in all patients during sinus rhythm. All patients had typical type 1 Brugada ECG pattern and inducible Vt/VF; they were found to have unique abnormal low voltage (0.94±0.79 mV), prolonged duration (132±48 ms), and fractionated late potentials (96±47 ms beyond QRS complex) clustering exclusively in the anterior aspect of the RVOT epicardium. Ablation at these sites rendered Vt/VF noninducible (7 of 9 patients [78%]; 95% confidence interval, 0.40 to 0.97, P=0.015) and normalization of the Brugada ECG pattern in 89% (95% confidence interval, 0.52 to 0.99; P=0.008). Long-term outcomes (20±6 months) were excellent, with no recurrent Vt/VF in all patients off medication (except 1 patient on amiodarone).</AbstractText>The underlying electrophysiological mechanism in patients with BrS is delayed depolarization over the anterior aspect of the RVOT epicardium. Catheter ablation over this abnormal area results in normalization of the Brugada ECG pattern and prevents Vt/VF, both during electrophysiological studies as well as spontaneous recurrent Vt/VF episodes in patients with BrS.</AbstractText> |
15,370 | Termination of reentrant cardiac action potential propagation using far-field electrical pacing. | Several different types of rapid cardiac rhythm disorders, including atrial and ventricular fibrillation, are likely caused by multiple, rapidly rotating, action potential (AP) waves. Thus, an electrical pacing therapy, whose effectiveness is based on being delivered with a particular timing relative to one of these waves, is unlikely to be useful in terminating the remaining waves. Here, we develop pacing protocols that are designed to terminate rotating waves independently of when the sequences of stimuli are imposed or where each wave is in its rotation at the time the sequences are initiated. These protocols are delivered as far-field stimuli, and therefore are capable of simultaneously influencing all the waves present. The pacing intervals for these protocols are, in general, of unequal duration and are determined through examination of the dynamics of AP propagation in a 1-D ring model. Series of two or three stimuli with interstimulus intervals chosen in this way are shown to be effective in terminating these waves over a wide range of ring circumferences and AP dynamical parameters. Stimulus sequences of this type may form the basis for developing new defibrillation protocols to test in experiments or more realistic models of the electrical heart. |
15,371 | Outcome of patients aged over 75 years who received a pacemaker to treat sinus node dysfunction. | The prognosis for patients aged over 75 years who receive a pacemaker in the context of sinus node dysfunction is unclear.</AbstractText>We sought to evaluate the incidences of atrial fibrillation, heart failure and death in such patients, and the role of the pacing mode in their prognosis.</AbstractText>This was a retrospective study of 102 patients aged over 75 years (mean 82.2 ± 4.4 years) who received a pacemaker in the context of sinus node dysfunction.</AbstractText>During the follow-up period (mean 806 days), 36 patients (35.3%) experienced heart failure, 47 patients (46.1%) had an episode of paroxysmal atrial fibrillation, 19 patients (18.6%) progressed to chronic atrial fibrillation and 29 (28.4%) died, the fatal event being sudden death or of cardiac origin in almost half of these patients (44.8%). Patients assigned to dual-chamber minimal ventricular pacing showed significantly lower rates of heart failure episodes (P=0.023) and all-cause mortality (P<0.001) than those assigned to conventional dual-chamber pacing. In contrast, the two groups did not differ with regard to either paroxysmal or chronic atrial fibrillation.</AbstractText>In patients aged over 75 years, the use of dual-chamber pacemakers incorporating an algorithm minimizing ventricular pacing for sinus node dysfunction seems to decrease the number of heart failure episodes and mortality. On the basis of this finding, the implantation of such devices seems justifiable, even in this age group.</AbstractText>Copyright © 2010 Elsevier Masson SAS. All rights reserved.</CopyrightInformation> |
15,372 | Arrhythmogenic substrate in hearts of rats with monocrotaline-induced pulmonary hypertension and right ventricular hypertrophy. | Mechanisms associated with right ventricular (RV) hypertension and arrhythmias are less understood than those in the left ventricle (LV). The aim of our study was to investigate whether and by what mechanisms a proarrhythmic substrate exists in a rat model of RV hypertension and hypertrophy. Rats were injected with monocrotaline (MCT; 60 mg/kg) to induce pulmonary artery hypertension or with saline (CON). Myocardial levels of mRNA for genes expressing ion channels were measured by real-time RT-PCR. Monophasic action potential duration (MAPD) was recorded in isolated Langendorff-perfused hearts. MAPD restitution was measured, and arrhythmias were induced by burst stimulation. Twenty-two to twenty-six days after treatment, MCT animals had RV hypertension, hypertrophy, and decreased ejection fractions compared with CON. A greater proportion of MCT hearts developed sustained ventricular tachycardias/fibrillation (0.83 MCT vs. 0.14 CON). MAPD was prolonged in RV and less so in the LV of MCT hearts. There were decreased levels of mRNA for K(+) channels. Restitution curves of MCT RV were steeper than CON RV or either LV. Dispersion of MAPD was greater in MCT hearts and was dependent on stimulation frequency. Computer simulations based on ion channel gene expression closely predicted experimental changes in MAPD and restitution. We have identified a proarrhythmic substrate in the hearts of MCT-treated rats. We conclude that steeper RV electrical restitution and rate-dependant RV-LV action potential duration dispersion may be contributing mechanisms and be implicated in the generation of arrhythmias associated with in RV hypertension and hypertrophy. |
15,373 | Differential clinical characteristics and outcome predictors of acute heart failure in elderly patients. | We determined the clinical-epidemiological characteristics and prognostic factors of early mortality and re-consultation in an elderly population attending the hospital emergency department (HED) for acute heart failure (AHF).</AbstractText>A prospective, observational, non interventional study including all the patients with AHF attended in the Spanish's HED. Two groups were defined: elderly (≥ 80 years) and controls (< 80 years).</AbstractText>demographic characteristics, comorbidity, degree of cardiac involvement, previous treatment, symptoms and signs of the AHF episode, precipitating factors, treatment in the HED and outcome.</AbstractText>mortality and re-consultation within 30 days.</AbstractText>Of the 942 patients included, 455 of whom were elderly (48.3%). In this elderly population female sex, auricular fibrillation and a history of ictus and a poor functional status predominated. The type of ventricular dysfunction was unknown in 70%. No main differences in the presentation of AHF were found between the two groups. Mortality and re-consultation to the HED within 30 days were similar in both groups. While several factors were identified to be related to mortality or re-consultation in control group, in the elderly group it was more difficult to identify patients who will die or re-consult to the HED within the following 30 days. Only respiratory insufficiency on arrival to the HED was found to predict a greater probability of death (OR 3.55; CI95% 1.39-9.11).</AbstractText>AHF in elderly patients presents some differential characteristics and, most importantly, it is more difficult to identify which of these patients will die or re-consult in the short-term.</AbstractText>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
15,374 | Performance of a rectilinear biphasic waveform in defibrillation of presenting and recurrent ventricular fibrillation: a prospective multicenter study. | We tested the hypothesis that shock success differs with initial and recurrent episodes of ventricular fibrillation (VF).</AbstractText>From September 2008 to March 2010 out-of-hospital cardiac arrest patients with VF as the initial rhythm at 9 study sites were defibrillated by paramedics using a rectilinear biphasic waveform. Shock success was defined as termination of VF within 5s post-shock. We used generalized estimating equation (GEE) analysis to assess the association between shock type (initial versus refibrillation) and shock success.</AbstractText>Ninety-four patients presented in VF. Mean age was 65.4 years, 78.7% were male, and 80.9% were bystander-witnessed. VF recurred in 75 (79.8%). There were 338 shocks delivered for initial (n = 90) or recurrent (n = 248) VF available for analysis. Initial shocks terminated VF in 79/90 (87.8%) and subsequent shocks in 209/248 (84.3%). GEE odds ratio (OR) for shock type was 1.37 (95% CI 0.68-2.74). After adjusting for potential confounders, the OR for shock type remained insignificant (1.33, 95% CI 0.60-2.53). We observed no significant difference in ROSC (54.7% versus 52.6%, absolute difference 2.1%, p = 0.87) or neurologically intact survival to hospital discharge (21.9% versus 33.3%, absolute difference 11.4%, p = 0.31) between those with and without VF recurrence.</AbstractText>Presenting VF was terminated with one shock in 87.8% of cases. We observed no significant difference in the frequency of shock success between initial versus recurrent VF. VF recurred in the majority of patients and did not adversely affect shock success, ROSC, or survival.</AbstractText>Copyright © 2011. Published by Elsevier Ireland Ltd.</CopyrightInformation> |
15,375 | Takotsubo cardiomyopathy: an Australian single centre experience with medium term follow up. | Takotsubo cardiomyopathy (TC) is increasingly recognised in patients presenting with features of acute coronary syndrome. We present a single centre experience of TC with medium term follow up.</AbstractText>Fifty-two consecutive patients presenting with a diagnosis of TC were included. The clinical presentation, complications, baseline and follow-up echocardiograms and cardiac magnetic resonance imaging were analysed.</AbstractText>Fifty-one patients were female. A stressful event preceded presentation in 37 (71%) patients. Chest pain was the most common symptom (83%). Two patients presented with an out-of-hospital cardiac arrest. ST segment elevation (40%) and global T wave inversion (44%) were the most frequent electrocardiogram changes. Left ventricular assessment demonstrated typical apical ballooning in 41 patients and 11 patients demonstrated the mid-wall variant. In-hospital complications occurred in 11 patients (21%) and included acute pulmonary oedema (n = 2), cardiogenic shock (n = 5); two of whom had a significant left ventricular outflow gradient, atrial fibrillation (n = 1), left ventricular thrombus (n = 2) and a cerebrovascular event (n = 2). Left ventricular function at presentation and follow up was compared in 40 patients. The mean ejection fraction in this group at presentation was 47% (20-70%) compared with that at follow up of 63% (44-76%). There were no significant complications or recurrences at follow up.</AbstractText>While TC is a reversible condition with low rates of complications and recurrence at follow up it is, as demonstrated in our cohort, associated with significant in-hospital morbidity in a proportion of patients.</AbstractText>© 2011 The Authors. Internal Medicine Journal © 2011 Royal Australasian College of Physicians.</CopyrightInformation> |
15,376 | Minimally invasive coronary artery bypass grafting via a small thoracotomy versus off-pump: a case-matched study. | The minimally invasive coronary artery bypass grafting (MICS CABG) operation performed via a small thoracotomy has not previously been examined in a direct comparison to sternotomy off-pump coronary artery bypass grafting (OPCAB).</AbstractText>We matched, according to age, gender, left ventricular function, and median number of distal anastomoses, 150 patients who underwent MICS CABG via small left thoracotomy, and 150 patients who received sternotomy OPCAB. All operations were performed by the same surgeon.</AbstractText>There was no perioperative mortality (0/300). In the MICS CABG group, pump assistance was used in 28/150 (19%) patients, and conversion to sternotomy occurred in 10/150 (6.7%) patients. In the OPCAB group, conversion to on-pump occurred in 3/150 (2.0%) patients. There were four (2.7%) reoperations for bleeding and one (0.7%) for anastomotic revision in each group. The median hospital length of stay was 5 days for MICS CABG (average 5.4), and 6 days for OPCAB (average 7.2) (P=0.02). New-onset atrial fibrillation occurred in 35 (23%) MICS CABG patients and in 42 (28%) OPCAB patients (P=0.3). No wound infection occurred with MICS CABG versus six (4.0%) with OPCAB (P=0.03). A self-limiting left pleural effusion developed in 22 (15%) MICS CABG patients and in six (4.0%) OPCAB patients (P=0.002). The median time to return to full physical activity was 12 days in MICS CABG patients versus >5 weeks in OPCAB patients (P<0.001).</AbstractText>MICS CABG is a valuable alternative for patients in need of multivessel CABG. The operation appears at least as safe as OPCAB, and associated with shorter hospital length of stay, less wound infections, and faster postoperative recovery than OPCAB.</AbstractText>Copyright © 2011 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved.</CopyrightInformation> |
15,377 | Ca2+/calmodulin-dependent protein kinase inhibition suppresses post-ischemic arrhythmogenesis and mediates sinus bradycardic recovery in reperfusion. | Ca(2+)/calmodulin-dependent protein kinase (CaMKII) activation is known to be associated with conditions where the incidence of arrhythmias is increased, and where cardiomyocyte Ca(2+)-overload occurs. The goal of this study was to determine whether CaMKII inhibition in the intact heart may be linked to the suppression of ventricular arrhythmias occurring during reperfusion after an ischemic insult.</AbstractText>Non-paced male rat hearts (n = 8-11) were treated with a CaMKII inhibitor (KN93, 2.5 μmol/L) 10 min prior to global ischemia (20 min) and for the initial 10 min of reperfusion. Cardiac mechanical and arrhythmic responses were evaluated under constant pressure perfusion conditions and myocyte damage assessed by measurement of coronary effluent lactate dehydrogenase (LDH).</AbstractText>Under basal conditions, KN93 increased coronary flow (41 ± 8% increase, p<0.05) and was negatively inotropic (29 ± 7% decrease, p<0.05), but did not affect heart rate. Ischemic contracture was significantly diminished in KN93-treated hearts (onset, min: 11.48 ± 0.50 vs 16.27 ± 1.23, p<0.05). CaMKII inhibition in early reperfusion almost completely abolished the incidence of ventricular tachycardia/fibrillation in reperfusion (11/11 control vs 1/8 KN93). In the absence of ventricular arrhythmias, heart rate was substantially reduced (% basal; 100 ± 3% vs 46 ± 8%, p<0.05) throughout reperfusion. Left ventricular developed pressure was initially low in KN93 hearts post-ischemia, but recovered to control levels by the end of 60 min reperfusion (68 ± 5% vs 56 ± 5%, p = ns). LDH was significantly reduced in KN93-treated hearts.</AbstractText>Although CaMKII inhibition diminishes contractile performance of the intact heart in the initial post-ischemic period, it provides crucial benefits through protection against potentially lethal reperfusion-induced arrhythmias and cardiomyocyte sarcolemmal rupture.</AbstractText>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
15,378 | Atrial fibrillation: pharmacological therapy. | Atrial fibrillation (AF) is the most common cardiac arrhythmia encountered in clinical practice. Although once considered a nuisance arrhythmia, recent clinical trial evidence suggests that the presence of AF is an important independent predictor of mortality and morbidity. The primary goals of AF treatment are relief of symptoms and prevention of stroke. The value of anticoagulation with warfarin has been proven unequivocally. Control of ventricular rate with atrioventricular nodal blocking agents-the so-called rate control strategy-is least cumbersome and sometimes the best approach. By contrast, efforts to restore and maintain sinus rhythm using antiarrhythmic drugs-the rhythm control approach-although tedious, may be ideal in patients who are young or highly symptomatic and in those with new-onset AF. The relative merits of both treatment strategies are discussed in this article, emphasizing the excellent clinical trial data that support each. |
15,379 | Ventricular fibrillation in a patient with Pompe disease: a cautionary tale. | Pompe disease is a rare genetic disorder resulting from a deficiency of the acid α-glucosidase enzyme. Although arrhythmias occur in these patients undergoing general anesthesia, they have not received sufficient emphasis in pediatric cardiology. We report a case of an infant with Pompe disease who experienced ventricular fibrillation during induction of anesthesia. |
15,380 | Variant angina and coronary artery spasm: the clinical spectrum, pathophysiology, and management. | Variant angina is a form of angina pectoris that shows transient ST-segment elevation on electrocardiogram during an attack of chest pain. Ischemic episodes of variant angina show circadian variation and often occur at rest from midnight to early morning. Ischemic episodes also occur during mild exercise in the early morning. However, they are not usually induced by strenuous exercise in the afternoon. Other important clinical features of variant angina include the high frequency of asymptomatic ischemic episodes and the syncope that sometimes occur during the ischemic episodes. Syncope is due to severe arrhythmias, including ventricular tachycardia, ventricular fibrillation, and high-degree atrioventricular block. Coronary artery spasm is the mechanism of ischemic episodes in variant angina. The incidence of coronary artery spasm shows a racial difference and is higher in Japanese than in Caucasians. Coronary arteriograms are normal or near-normal in most Japanese patients with variant angina. Deficient basal release of nitric oxide (NO) due to endothelial dysfunction, and enhanced vascular smooth muscle contractility with the involvement of the Rho/Rho-kinase pathway are reported to play important roles in the pathogenesis of coronary artery spasm. Other precipitating factors of coronary artery spasm include imbalance in autonomic nervous activity, increased oxidative stress, chronic low-grade inflammation, magnesium deficiency, and genetic susceptibility. The genetic risk factors associated with coronary artery spasm include gene polymorphisms of endothelial NO synthase (NOS), paraoxonase, and other genes. Calcium channel blockers are extremely effective in preventing coronary spasm. The long-acting nitrate, nicorandil, and Rho-kinase inhibitor are also useful for inhibiting coronary artery spasm. Because variant angina can lead to acute myocardial infarction, fatal arrhythmias, and sudden death, early treatment is important. The prognosis of patients with variant angina is favorable, if early complications can be overcome. However, because coronary artery spasm cannot be suppressed in some patients, even with multiple medications, medications to suppress intractable coronary artery spasm must be developed. |
15,381 | Use of Angiotensin receptor blockers in cardiovascular protection: current evidence and future directions. | To differentiate angiotensin II receptor blockers (ARBs) by vascular effects and outcomes in trials on cardio-protective endpoints.</AbstractText>MEDLINE searches were conducted from January 2003 to March 2009 using the following search terms: renin-angiotensin-aldosterone system (RAAS) blockade or inhibition; angiotensin II receptor blocker (ARBs); cardio-protection; vascular protection; end-organ protection; candesartan; eprosartan, irbesartan; losartan; olmesartan; telmisartan; and valsartan. Ongoing and recruiting clinical trials were identified via Clinicaltrials.gov (July 2008).</AbstractText>Pertinent basic science research and clinical trials with cardiovascular endpoints and information from reviews, American Heart Association 2009 statistics, and The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure guidelines were included in this review.</AbstractText>ARBs differ in their vascular protective pleiotropic effects and pharmacokinetic properties, which may contribute to their pharmacological protection to reduce cardiovascular morbidity and mortality, independently of their blood pressure (BP)-lowering effects.</AbstractText>Emerging data show that ARBs are effective in hypertension, left ventricular hypertrophy, postmyocardial infarction, and heart failure. To what extent their pleiotropic effects, independent of BP lowering, contribute to these outcomes will be the focus of research in the coming years. Well-designed, comparative-effectiveness studies are needed to clinically differentiate this class of agents. The future will be marked by multifunctional ARBs that will pharmacologically do more than antagonize the angiotensin type I (AT(1)) receptor.</AbstractText> |
15,382 | Epinephrine improves 24-hour survival in a swine model of prolonged ventricular fibrillation demonstrating that early intraosseous is superior to delayed intravenous administration. | Vasopressors administered IV late during resuscitation efforts fail to improve survival. Intraosseous (IO) access can provide a route for earlier administration. We hypothesized that IO epinephrine after 1 minute of cardiopulmonary resuscitation (CPR) (an "optimal" IO scenario) after 10 minutes of untreated ventricular fibrillation (VF) cardiac arrest would improve outcome in comparison with either IV epinephrine after 8 minutes of CPR (a "realistic" IV scenario) or placebo controls with no epinephrine.</AbstractText>Thirty swine were randomized to IO epinephrine, IV epinephrine, or placebo. Important outcomes included return of spontaneous circulation (ROSC), 24-hour survival, and 24-hour survival with good neurological outcome (cerebral performance category 1).</AbstractText>ROSC after 10 minutes of untreated VF was uncommon without administration of epinephrine (1 of 10), whereas ROSC was nearly universal with IO epinephrine or delayed IV epinephrine (10 of 10 and 9 of 10, respectively; P = 0.001 for either versus placebo). Twenty-four hour survival was substantially more likely after IO epinephrine than after delayed IV epinephrine (10 of 10 vs. 4 of 10, P = 0.001). None of the placebo group survived at 24 hours. Survival with good neurological outcome was more likely after IO epinephrine than after placebo (6 of 10 vs. 0 of 10, P = 0.011), and only 3 of 10 survived with good neurological outcome in the delayed IV epinephrine group (not significant versus either IO or placebo).</AbstractText>In this swine model of prolonged VF cardiac arrest, epinephrine administration during CPR improved outcomes. In addition, early IO epinephrine improved outcomes in comparison with delayed IV epinephrine.</AbstractText> |
15,383 | Identification of a novel loss-of-function calcium channel gene mutation in short QT syndrome (SQTS6). | Short QT syndrome (SQTS) is a genetically determined ion-channel disorder, which may cause malignant tachyarrhythmias and sudden cardiac death. Thus far, mutations in five different genes encoding potassium and calcium channel subunits have been reported. We present, for the first time, a novel loss-of-function mutation coding for an L-type calcium channel subunit.</AbstractText>The electrocardiogram of the affected member of a single family revealed a QT interval of 317 ms (QTc 329 ms) with tall, narrow, and symmetrical T-waves. Invasive electrophysiological testing showed short ventricular refractory periods and increased vulnerability to induce ventricular fibrillation. DNA screening of the patient identified no mutation in previously known SQTS genes; however, a new variant at a heterozygous state was identified in the CACNA2D1 gene (nucleotide c.2264G > C; amino acid p.Ser755Thr), coding for the Ca(v)α(2)δ-1 subunit of the L-type calcium channel. The pathogenic role of the p.Ser755Thr variant of the CACNA2D1 gene was analysed by using co-expression of the two other L-type calcium channel subunits, Ca(v)1.2α1 and Ca(v)β(2b), in HEK-293 cells. Barium currents (I(Ba)) were recorded in these cells under voltage-clamp conditions using the whole-cell configuration. Co-expression of the p.Ser755Thr Ca(v)α(2)δ-1 subunit strongly reduced the I(Ba) by more than 70% when compared with the co-expression of the wild-type (WT) variant. Protein expression of the three subunits was verified by performing western blots of total lysates and cell membrane fractions of HEK-293 cells. The p.Ser755Thr variant of the Ca(v)α(2)δ-1 subunit was expressed at a similar level compared with the WT subunit in both fractions. Since the mutant Ca(v)α(2)δ-1 subunit did not modify the expression of the pore-forming subunit of the L-type calcium channel, Ca(v)1.2α1, it suggests that single channel biophysical properties of the L-type channel are altered by this variant.</AbstractText>In the present study, we report the first pathogenic mutation in the CACNA2D1 gene in humans, which causes a new variant of SQTS. It remains to be determined whether mutations in this gene lead to other manifestations of the J-wave syndrome.</AbstractText> |
15,384 | Novel compound heterozygous mutations T2C and 1149insT in the KCNQ1 gene cause Jervell and Lange-Nielsen syndrome. | Mutations in the KCNQ1 gene account for more than 90% of the individuals with Jervell and Lange-Nielsen syndrome (JLNS). In this study, we identified and characterized two novel KCNQ1 mutations that caused JLNS. A 6-year-old deaf girl suffering from recurrent syncope had a documented electrocardiogram with polymorphic ventricular fibrillation since the age of 4 years. The baseline electrocardiogram showed a significantly prolonged corrected QT interval (524 msec). Genetic analysis revealed that the proband carried two heterozygous mutations of T2C and 1149insT in the KCNQ1 gene on separate alleles. Patch-clamp analysis demonstrated that the T2C mutation resulted in significant reduction in the slowly activated delayed rectifier current (IKs). Furthermore, western blot analysis and confocal imaging revealed that the T2C mutation produced a truncated protein with trafficking defects. In contrast, the 1149insT mutation failed to generate any measurable current, consistent with no protein expression in both the cell membrane and cytoplasm. Moreover, co-expression of the T2C and 1149insT mutations significantly reduced the peak tail current density to 8.27% of the wild-type (WT) current value, while co-transfected WT channels with either T2C or 1149insT mutant channels produced comparable current and channel kinetics to that of WT channels. Our study demonstrates that the compound heterozygous mutations T2C and 1149insT cause the 'loss-of-function' of the IKs that may account for the clinical phenotype of the proband. Multiple mechanisms have been involved in the pathogenesis of 'loss-of-function' of IKs. |
15,385 | HeartSaver: a mobile cardiac monitoring system for auto-detection of atrial fibrillation, myocardial infarction, and atrio-ventricular block. | A mobile medical device, dubbed HeartSaver, is developed for real-time monitoring of a patient's electrocardiogram (ECG) and automatic detection of several cardiac pathologies, including atrial fibrillation, myocardial infarction and atrio-ventricular block. HeartSaver is based on adroit integration of four different modern technologies: electronics, wireless communication, computer, and information technologies in the service of medicine. The physical device consists of four modules: sensor and ECG processing unit, a microcontroller, a link between the microcontroller and the cell phone, and mobile software associated with the system. HeartSaver includes automated cardiac pathology detection algorithms. These algorithms are simple enough to be implemented on a low-cost, limited-power microcontroller but powerful enough to detect the relevant cardiac pathologies. When an abnormality is detected, the microcontroller sends a signal to a cell phone. This operation triggers an application software on the cell phone that sends a text message transmitting information about patient's physiological condition and location promptly to a physician or a guardian. HeartSaver can be used by millions of cardiac patients with the potential to transform the cardiac diagnosis, care, and treatment and save thousands of lives. |
15,386 | Increased left ventricular mass and decreased left ventricular systolic function have independent pathways to ventricular arrhythmogenesis in coronary artery disease. | Following myocardial infarction, individual patients can have wide variations in the extent of left ventricular systolic dysfunction (LVSD) and increased left ventricular (LV) mass. Both affect the risk for sudden cardiac death, but only LV ejection fraction is used for risk prediction.</AbstractText>The purpose of this study was to evaluate the independent as well as the additive contributions of increased LV mass and decreased LV ejection fraction to sudden cardiac death in the general population.</AbstractText>In the ongoing Oregon Sudden Unexpected Death Study, we studied consecutive SCD cases (n = 191) and coronary artery disease controls (n = 203) from the Portland, Oregon, metropolitan area (population approximately 1,000,000; 2002-2008). Comparisons of echocardiographic LV mass obtained prior and unrelated to sudden cardiac death (SCD) were conducted, and a logistic regression model was used to evaluate the relationship between SCD, severe LVSD, LV mass, and other relevant clinical variables.</AbstractText>In a multivariate model, both severe LVSD and left ventricular hypertrophy (LVH) were associated with increased SCD risk (odds ratio [OR] 1.9, 95% confidence interval [CI] 1.1-3.2 for severe LVSD; OR 1.8, 95% CI 1.1-2.9 for LVH). In patients with coexisting severe LVSD and LVH, risk of SCD was additive (OR 3.5, 95% CI 1.7-7.2). In the same model, increased age, atrial fibrillation/flutter, elevated creatinine, and diabetes independently increased risk, and use of angiotensin receptor blockers attenuated risk.</AbstractText>Reduced LV ejection fraction and increased LV mass had independent and additive effects on risk of sudden death. Despite the significant overlap between the two conditions, these findings point toward the existence of independent mechanistic pathways for ventricular arrhythmias that occur due to LVSD and LVH.</AbstractText>Copyright © 2011 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
15,387 | Mild hypothermia delays the development of stone heart from untreated sustained ventricular fibrillation--a cardiovascular magnetic resonance study. | 'Stone heart' resulting from ischemic contracture of the myocardium, precludes successful resuscitation from ventricular fibrillation (VF). We hypothesized that mild hypothermia might slow the progression to stone heart.</AbstractText>Fourteen swine (27 ± 1 kg) were randomized to normothermia (group I; n=6) or hypothermia groups (group II; n=8). Mild hypothermia (34 ± 2 °C) was induced with ice packs prior to VF induction. The LV and right ventricular (RV) cross-sectional areas were followed by cardiovascular magnetic resonance until the development of stone heart. A commercial 1.5T GE Signa NV-CV/i scanner was used. Complete anatomic coverage of the heart was acquired using a steady-state free precession (SSFP) pulse sequence gated at baseline prior to VF onset. Un-gated SSFP images were obtained serially after VF induction. The ventricular endocardium was manually traced and LV and RV volumes were calculated at each time point.</AbstractText>In group I, the LV was dilated compared to baseline at 5 minutes after VF and this remained for 20 minutes. Stone heart, arbitrarily defined as LV volume <1/3 of baseline at the onset of VF, occurred at 29 ± 3 minutes. In group II, there was less early dilation of the LV (p<0.05) and the development of stone heart was delayed to 52 ± 4 minutes after onset of VF (P<0.001).</AbstractText>In this closed-chest swine model of prolonged untreated VF, hypothermia reduced the early LV dilatation and importantly, delayed the onset of stone heart thereby extending a known, morphologic limit of resuscitability.</AbstractText>© 2011 Sorrell et al; licensee BioMed Central Ltd.</CopyrightInformation> |
15,388 | Ventricular arrhythmia in X-linked Emery-Dreifuss muscular dystrophy: a lesson from an autopsy case. | Emery-Dreifuss muscular dystrophy (EDMD) is a distinctive form of muscular dystrophy which is often associated with cardiac abnormalities. Conduction disturbances are frequently observed, and may necessitate pacemaker implantation to prevent sudden death. In this case report, we present an autopsy of a 31-year-old man with X-linked EDMD who developed only minimal skeletal muscle symptoms, and who died from ventricular arrhythmia despite undergoing a previous pacemaker implantation. Ventricular arrhythmias in X-linked EDMD patients are also discussed. |
15,389 | Baseline B-type natriuretic peptide: a gender-specific predictor of procedure-outcome in atrial fibrillation patients undergoing catheter ablation. | Close association between atrial fibrillation (AF) and brain natriuretic peptide (BNP) has been demonstrated by several studies. Important gender differences exist in AF patients including a higher plasma BNP level in women. Therefore, it is imperative to evaluate the relationship between AF and BNP separately in men and women.</AbstractText>This study examined possible gender-specific role of BNP in predicting procedure outcome in AF patients undergoing catheter ablation.</AbstractText>The study population included 568 consecutive patients (age 62 ± 10, male 73%, paroxysmal 25%, persistent 38%, and long-standing persistent AF 37%) undergoing AF ablation, who had structurally normal heart and left ventricular ejection fraction ≥45%. Baseline BNP was measured in all. Patients were grouped into "normal" and "high" BNP based on gender-specific cut-off values (<50 and ≥50 pg/mL in males, <100 and ≥ 100 pg/mL in females).</AbstractText>Baseline BNP was significantly higher among women than men (126 ± 112 versus 87 ± 99, P = 0.009). At 12 ± 6 month follow-up, 304 of 414 (73%) males and 98 of 154 (64%) females were AF/atrial tachycardia-free off antiarrhythmic drugs (log-rank P = 0.018). In multivariable analysis, BNP remained an independent predictor of AF recurrence (BNP ≥ 50: hazard ratio [HR] 2.54, P = 0.006) in males. No such association was observed among females (BNP ≥ 100: HR 0.79, 95% CI 0.43-1.42; P = 0.426).</AbstractText>Baseline BNP was found to be an independent predictor of AF recurrence in male patients undergoing ablation. This correlation between BNP and AF recurrence was not observed in females. Thus, BNP plays a gender-specific prognostic role in AF.</AbstractText>© 2011 Wiley Periodicals, Inc.</CopyrightInformation> |
15,390 | The increased mortality from witnessed out-of-hospital cardiac arrest in the home. | Research in 2008 demonstrated that the majority of out-of-hospital cardiac arrests (OHCAs) occur in the home, and many important characteristics differ between private and public locations. However, the influence of the location of collapse on survival from OHCA is not well understood. Furthermore, most of the reports have been from Western countries; there is little research from Asia that differentiates the conditions of OHCA.</AbstractText>To investigate the influence of the location of collapse on being discharged alive from OHCA and whether the location of collapse is also an independent predictor of survival from OHCA in Japan.</AbstractText>We analyzed 463 consecutive cases of witnessed OHCA with cardiac etiology that occurred between October 2004 and September 2008 in Japan. We investigated the characteristics of OHCA patients who collapsed in private and public locations, and assessed the influence of the location of collapse on survival from OHCA.</AbstractText>Patients who collapsed outside the home were younger, more likely to be male, more likely to receive bystander cardiopulmonary resuscitation (CPR), and more likely to have ventricular fibrillation (VF)/pulseless ventricular tachycardia (VT) and had a shorter time interval between collapse and 9-1-1 call than patients who collapsed in the home. Mortality was significantly higher in the group who collapsed in the home. The independent influence of the location of collapse was eliminated by additional adjustment for time interval from collapse to 9-1-1 call, age, bystander CPR, and initial cardiac rhythm. Finally, VF/pulseless VT as the initial rhythm and bystander CPR were independently associated with the patient's being discharged alive; the location of collapse was not an independently associated variable.</AbstractText>The present analysis demonstrated that there were significant differences in survival between groups of patients who suffered from cardiac arrest inside and outside the home in Japan. The outside-the-home group had a higher rate of survival from OHCA; however, the location of collapse was not an independent predictor of survival from OHCA. Education of the families of high-risk patients in placing a rapid emergency call and performing effective CPR might be needed to improve survival from cardiac arrest in the home.</AbstractText> |
15,391 | Mild hypothermia treatment in patients resuscitated from non-shockable cardiac arrest. | Therapeutic hypothermia has proved effective in improving outcome in patients after cardiac arrest due to ventricular fibrillation (VF). The benefit in patients with non-VF cardiac arrest is still not defined.</AbstractText>This prospective observational study was conducted in a university hospital setting with historical controls. Between 2002 and 2010 387 consecutive patients have been admitted to the intensive care unit (ICU) after cardiac arrest (control n=186; hypothermia n=201). Of those, in 175 patients the initial rhythm was identified as non-shockable (asystole, pulseless electrical activity) rhythm (control n=88; hypothermia n=87). Neurological outcome was assessed at ICU discharge according to the Pittsburgh cerebral performance category (CPC). A follow-up was completed for all patients after 90 days, a Kaplan-Meier analysis and Cox regression was performed.</AbstractText>Hypothermia treatment was not associated with significantly improved neurological outcome in patients resuscitated from non-VF cardiac arrest (CPC 1-2: hypothermia 27.59% vs control 18.20%, p=0.175). 90-Day Kaplan-Meier analysis revealed no significant benefit for the hypothermia group (log rank test p=0.82), and Cox regression showed no statistically significant improvement.</AbstractText>In this cohort patients undergoing hypothermia treatment after non-shockable cardiac arrest do not benefit significantly concerning neurological outcome. Hypothermia treatment needs to be evaluated in a large multicentre trial of cardiac arrest patients found initially to be in non-shockable rhythms to clarify whether cooling may also be beneficial for other rhythms than VF.</AbstractText> |
15,392 | Valve replacement in pediatric patients: a single center experience. | Reconstructive surgery is the primary goal in pediatric patients with valve disease. However, in cases with irreparable valve lesions, valve replacement is the only option. This study aimed to retrospectively analyze the clinical experience of heart valve prosthesis replacement in children.</AbstractText>Between January 1990 and July 2009, 35 pediatric patients (16 boys, 19 girls) underwent mechanical valve replacement in Shandong University Qilu Hospital. The ages ranged from 2.5 to 14 years (mean, (8.8 ± 3.8) years) and body weight varied from 11 to 37 kg (mean, (22.1 ± 5.2) kg). Mechanical valve replacement was performed because of congenital heart disease in 23 patients, rheumatic disease in ten patients and infective endocarditis in two patients. St. Jude bileaflet mechanical valves were implanted in all the 35 patients including mitral valve replacement (MVR) in 18, aortic valve replacement (AVR) in 12, tricuspid valve replacement (TVR) in two, AVR and MVR in two and MVR and TVR in one. The size of the prostheses ranged between 19 and 27 mm. All patients received long-term anticoagulation treatment with sodium warfarin, aiming to maintain an international normalized ratio between 1.5 to 2.0. Follow-up was performed in all the patients with a total follow-up of 119.4 patient-years.</AbstractText>The operative mortality was 8.57% (3/35). One patient, who underwent cardiac debridement and AVR, died 2 hours after being admitted to the intensive care unit because of severe low cardiac output syndrome and ventricular fibrillation. Two patients died of cardiogenic shock and renal failure during initial hospitalization after the operation. One patient who received replacement of a tricuspid valve developed complete heart block requiring temporary pacing and recovered sinus rhythm 4 days later. Thirty-two patients survived and their cardiac function was in New York Heart Association (NYHA) class I to class II when discharged. Late events included hemorrhage and endocarditis. Two patients required reoperation. No late deaths occurred during the follow-up.</AbstractText>Mechanical valve replacement remains an acceptable treatment option in children when the valve reparation is impossible or unsuccessful. The operative mortality and incidence of any valve-related events such as endocarditis, reoperation, thromboembolism or anticoagulation-related bleeding are acceptable.</AbstractText> |
15,393 | T-wave alternans: clinical performance, limitations and analysis methodologies. | Accurate recognition of individuals at higher immediate risk of sudden cardiac death (SCD) is still an open question. The fortuitous nature of acute cardiovascular events just does not seem to fit the well-known model of ventricular tachycardia/fibrillation induction in a static arrhythmogenic substrate by a synchronous trigger. On the mechanism of SCD, a dynamical electrical instability would better explain the rarity of the simultaneous association of a correct trigger and an appropriate cardiac substrate. Several studies have been conducted trying to measure this cardiac electrical instability (or any valid surrogate) in an ECG beat stream. Among the current possible candidates we can number QT prolongation, QT dispersion, late potentials, T-wave alternans (TWA), and heart rate turbulence. This article reviews the particular role of TWA in the current cardiac risk stratification scenario. TWA findings are still heterogeneous, ranging from very good to nearly null prognostic performance depending on the clinical population observed and clinical protocol in use. To fill the current gaps in the TWA base of knowledge, practitioners, and researchers should better explore the technical features of the several technologies available for TWA evaluation and pay greater attention to the fact that TWA values are responsive to several factors other than medications. Information about the cellular and subcellular mechanisms of TWA is outside the scope of this article, but the reader is referred to some of the good papers available on this topic whenever this extra information could help the understanding of the concepts and facts covered herein. |
15,394 | Sodium nitroprusside enhanced cardiopulmonary resuscitation improves survival with good neurological function in a porcine model of prolonged cardiac arrest. | To assess the effectiveness of sodium nitroprusside (SNP)-"enhanced" cardiopulmonary resuscitation (SNPeCPR) on 24-hr survival rates compared to standard CPR in animals after cardiac arrest. SNPeCPR consists of large intravenous SNP bolus doses during CPR enhanced by active compression-decompression CPR, an inspiratory impedance threshold device (ITD), and abdominal binding (AB). The combination of active compression-decompression CPR+ITD+AB without SNP will be called "enhanced" or eCPR.</AbstractText>Randomized, blinded, animal study.</AbstractText>Preclinical animal laboratory.</AbstractText>Twenty-four female farm pigs (30 ± 1 kg).</AbstractText>Isoflurane anesthetized and intubated pigs were randomized after 8 mins of untreated ventricular fibrillation to receive either standard CPR (n = 8), SNPeCPR (n = 8), or eCPR (n = 8) for 25 mins followed by defibrillation.</AbstractText>The primary end point was carotid blood flow during CPR and 24-hr survival with good neurologic function defined as an overall performance category score of ≤2 (1 = normal, 5 = brain dead or dead). Secondary end points included hemodynamics and end-tidal CO2. SNPeCPR significantly improved carotid blood flow and 24-hr survival rates with good neurologic function compared to standard CPR or eCPR (six of eight vs. zero of eight vs. one of eight, p < .05). The improved survival rates were associated with higher coronary perfusion pressure and ETco2 during CPR.</AbstractText>In pigs, SNPeCPR significantly improved hemodynamics, resuscitation rates, and 24-hr survival rates with good neurologic function after cardiac arrest when compared with standard CPR or eCPR alone.</AbstractText> |
15,395 | Permanent atrial standstill with irregular junctional ectopic rhythm mimicking atrial fibrillation. | We present an interesting case of 'pseudo' atrial fibrillation which was further diagnosed as atrial standstill with irregular junctional ectopic rhythm during electrophysiologic study. A 56-year-old woman presented to a health facility with symptoms of palpitation, lightheadedness, and shortness of breath. Upon detection of irregular rhythm with narrow QRS complexes and no visible P waves on the electrocardiogram, newly developed atrial fibrillation was considered and a direct current cardioversion was performed, during which cardiac asystole developed necessitating cardiopulmonary resuscitation. The patient was then transferred to our institution. Echocardiographic examination showed biatrial dilatation, normal left ventricular systolic function, marked left ventricular hypertrophy, severe aortic stenosis, moderate mitral regurgitation, and severe tricuspid regurgitation. The electrocardiogram showed an irregular rhythm with narrow QRS complexes without any fibrillatory f waves and 24-hour Holter monitoring revealed three episodes of ventricular asystole lasting for more than 3.5 seconds. During the electrophysiologic study, no electrical activity was observed at the high and low levels of the right atrial lateral free wall and septal wall. The final diagnosis was established as atrial standstill and irregular junctional ectopic rhythm. The patient refused aortic valve replacement and died due to progression of the underlying disease one year following permanent pacemaker implantation.. |
15,396 | [Closure of secundum atrial septal defects by the Amplatzer occluder device]. | Percutaneous closure of secundum atrial septal defects (ASD) has become an important alternative treatment to surgery. We evaluated our clinical experience with, and short-term results of transcatheter closure of ASDs with the Amplatzer septal occluder in adult patients.</AbstractText>The study included 52 patients (36 women, 16 men; mean age 33±14 years; range 14 to 69 years) who underwent transcatheter ASD closure with the Amplatzer occluder device. The mean ASD diameter measured by transesophageal echocardiography was 19.5±5.7 mm and the mean device diameter was 24.5±5.7 mm. All the patients were assessed clinically and echocardiographically one month after the procedure.</AbstractText>Transcatheter ASD closure was successfully performed in 48 patients (92.3%) and failed in four patients (7.7%). Echocardiographic controls showed significant decreases in tricuspid regurgitation, right ventricular dilatation, and pulmonary artery pressure (p=0.003, p=0.026, and p=0.0001, respectively). Functional capacity of the patients also showed significant improvements (p=0.0001). After implantation, residual shunts were detected in four patients, all of which disappeared one month after the procedure. Major complications were seen in two patients. One patient developed ventricular fibrillation immediately after the procedure due to device embolization. One patient with left ventricular dysfunction developed device thrombosis due to cessation of dual antiplatelet therapy, which was successfully treated by anticoagulation therapy. Arrhythmia was not observed in any patient.</AbstractText>Percutaneous closure of secundum ASDs with the Amplatzer occluder device is a safe and effective procedure with a high success rate.</AbstractText> |
15,397 | Intracardiac electrogram T-wave alternans/variability increases before spontaneous ventricular tachyarrhythmias in implantable cardioverter-defibrillator patients: a prospective, multi-center study. | T-wave alternans (TWA) increases before ventricular tachycardia (VT) or fibrillation (VF), suggesting that it may warn of VT/VF in implantable cardioverter-defibrillator patients. Recently, we described a method for measuring alternans and nonalternans variability (TWA/V) from electrograms (EGMs) stored in implantable cardioverter-defibrillators before VT/VF. The goal of this prospective, multicenter study was to determine whether EGM TWA/V was greater before VT/VF than at baseline.</AbstractText>We enrolled 63 implantable cardioverter-defibrillator patients. TWA/V was computed from stored EGMs before spontaneous VT/VF and from sequential windows of 8 pairs of beats using 4 different control recordings: baseline rhythm, rapid pacing at 105 bpm, segments of ambulatory Holter EGMs matched to the time of VT/VF episodes, and EGMs before spontaneous supraventricular tachycardia. During follow-up, 28 patients had 166 episodes of VT/VF. TWA/V was greater before VT/VF (62.9 ± 3.1 μV; n = 28) than during baseline rhythm (12.8 ± 1.8 μV; P < 0.0001; n = 62), during rapid pacing (14.5 ± 2.0 μV; P < 0.0001; n = 52), before supraventricular tachycardia (27.5 ± 6.1 μV; P < 0.0001; n = 9), or during time-matched ambulatory controls (12.3 ± 3.5 μV; P < 0.0001; n = 16). By logistic regression, the odds of VT/VF increased by a factor of 2.2 for each 10-μV increment in TWA/V (P < 0.0001).</AbstractText>In implantable cardioverter-defibrillator patients, EGM TWA/V is greater before spontaneous VT/VF than in control recordings. Future implantable cardioverter-defibrillators that measure EGM TWA/V continuously may warn patients and initiate pacing therapies to prevent VT/VF.</AbstractText> |
15,398 | Effectiveness of Cardiac Resynchronization Therapy by QRS Morphology in the Multicenter Automatic Defibrillator Implantation Trial-Cardiac Resynchronization Therapy (MADIT-CRT). | This study aimed to determine whether QRS morphology identifies patients who benefit from cardiac resynchronization therapy with a defibrillator (CRT-D) and whether it influences the risk of primary and secondary end points in patients enrolled in the Multicenter Automatic Defibrillator Implantation Trial-Cardiac Resynchronization Therapy (MADIT-CRT) trial.</AbstractText>Baseline 12-lead ECGs were evaluated with regard to QRS morphology. Heart failure event or death was the primary end point of the trial. Death, heart failure event, ventricular tachycardia, and ventricular fibrillation were secondary end points. Among 1817 patients with available sinus rhythm ECGs at baseline, there were 1281 (70%) with left bundle-branch block (LBBB), 228 (13%) with right bundle-branch block, and 308 (17%) with nonspecific intraventricular conduction disturbances. The latter 2 groups were defined as non-LBBB groups. Hazard ratios for the primary end point for comparisons of CRT-D patients versus patients who only received an implantable cardioverter defibrillator (ICD) were significantly (P < 0.001) lower in LBBB patients (0.47; P < 0.001) than in non-LBBB patients (1.24; P = 0.257). The risk of ventricular tachycardia, ventricular fibrillation, or death was decreased significantly in CRT-D patients with LBBB but not in non-LBBB patients. Echocardiographic parameters showed significantly (P < 0.001) greater reduction in left ventricular volumes and increase in ejection fraction with CRT-D in LBBB than in non-LBBB patients.</AbstractText>Heart failure patients with New York Heart Association class I or II and ejection fraction ≤ 30% and LBBB derive substantial clinical benefit from CRT-D: a reduction in heart failure progression and a reduction in the risk of ventricular tachyarrhythmias. No clinical benefit was observed in patients with a non-LBBB QRS pattern (right bundle-branch block or intraventricular conduction disturbances).</AbstractText>URL: http://www.clinicaltrials.gov. Unique identifier: NCT00180271.</AbstractText> |
15,399 | Initial salivary α-amylase activity predicts malignant ventricular arrhythmias and short-term prognosis after ST-segment elevation myocardial infarction. | Ventricular arrhythmias (VA), including ventricular tachycardia and ventricular fibrillation, are the most common remediable cause of death in patients with acute myocardial infarction. Augmented sympathetic neural activity to the heart and myocardial catecholamine release may be the primary factors in the generation of VA. The aim of this study was to assess the predictive value of salivary α-amylase (sAA) activity, an indicator of sympathetic activity, for malignant VA occurrence and for short-term outcome in patients with ST-segment elevation myocardial infarction (STEMI).</AbstractText>Patients with STEMI (n=91) were recruited from the Emergency Department during the period 1 December 2008 to 31 April 2010. Correlations of initial sAA activity at presentation with VA, as well as 1-month prognosis were analysed.</AbstractText>sAA activity was significantly increased in the VA group (395±173.7; n=9) as compared with the non-VA group (283±89.3; n=82) (p=0.014). The adjusted OR for malignant ventricular arrhythmia occurrence was 1.010 (95% CI 1.001 to 1.018). Eight patients (8.8%) died and 24 (26.4%) had at least one short-term adverse event within the first month after STEMI. Simple logistic regression analysis showed that sAA is an independent predictor for short-term prognosis (p=0.049, OR 1.005, 95% CI 1.000 to 1.009).</AbstractText>Although a prospective study with a large cohort is required, the present results suggest that high initial sAA activity is associated with increased risk of malignant VA and predicts short-term prognosis in patients with STEMI.</AbstractText> |
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