Mechanisms of sudden cardiac death

Worldwide, sudden cardiac death (SCD) is a major problem. It is most frequently caused by ventricular tachyarrhythmias: Monomorphic and polymorphic ventricular tachycardia (VT), torsade de pointes (TdP), and ventricular fibrillation (VF). Beta blockade, ACE inhibition, coronary reperfusion and other treatments have reduced the incidence of VT but pulseless electrical activity (PEA) is increasingly seen, particularly in patients with advanced chronic heart disease. From existing data, bradyarrhythmia in the form of asystole (usually complete heart block without escape rhythm) causes only a minor proportion (10–15%) of SCD. In patients aged 50 years and more, coronary artery disease plays a dominant role causing more than 75% of SCD cases, either by acute ischemia and ventricular fibrillation or by chronic scar formation and reentrant VT. In younger patients, SCD may occur in patients with structurally normal hearts. A number of arrhythmogenic disorders with an increased risk of SCD have been detected and better understood recently, such as long and short QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, and the early repolarization syndrome. Most importantly, ECG signs and clinical features indicating high risk for SCD have been identified. Knowledge of the exact electrophysiologic mechanisms of ventricular tachyarrhythmias at the cellular level has been improved and mechanisms such as phase 2 reentry and reflection proposed to better understand why and how SCD occurs.     

Tools for risk stratification of sudden cardiac death: A review of the literature in different patient populations

While various modalities to determine risk of sudden cardiac death (SCD) have been reported in clinical studies, currently reduced left ventricular ejection fraction remains the cornerstone of SCD risk stratification. However, the absolute burden of SCD is greatest amongst populations without known cardiac disease. In this review, we summarize the evidence behind current guidelines for implantable cardioverter defibrillator (ICD) use for the prevention of SCD in patients with ischemic heart disease (IHD). We also evaluate the evidence for risk stratification tools beyond clinical guidelines in the general population, patients with IHD, and patients with other known or suspected medical conditions.     

Novel mutation in the SCN5A gene associated with arrhythmic storm development during acute myocardial infarction

BACKGROUND: Ventricular tachycardia (VT) and ventricular fibrillation (VF) complicating Brugada syndrome, a genetic disorder linked to SCN5A mutations, and VF complicating acute myocardial infarction (AMI) both have been linked to phase 2 reentry. OBJECTIVE: Given the mechanistic similarities in arrhythmogenesis, the purpose of this study was to examine the contribution of SCN5A mutations to VT/VF complicating AMI. METHODS: Nineteen consecutive patients developing VF during AMI were enrolled in the study. Wild-type (WT) and mutant SCN5A genes were coexpressed with SCN1B in TSA201 cells and studied using whole-cell patch clamp techniques. RESULTS: Among the cohort of 19 patients, one missense mutation (G400A) in SCN5A was detected in a conserved region. An H558R polymorphism was detected on the same allele. Unlike the other 18 patients, who each developed 1-2 VF episodes during AMI, the mutation carrier developed six episodes of VT/VF within the first 12 hours. All VT/VF episodes were associated with ST-segment changes and were initiated by short-coupled extrasystoles. Flecainide and adenosine challenge performed to unmask Brugada and long QT syndromes both were negative. Peak G400A and G400A+H558R current were 70.7% and 88.4% less than WT current at -35 mV (P 相似文献   

Exploring QT interval changes as a precursor to the onset of ventricular fibrillation/tachycardia

In the present study, we have retrospectively analyzed the corrected QT (QTc) interval before spontaneous episodes of sudden cardiac arrest in patients with a wearable cardioverter defibrillator. Corrected QT interval was measured for all normal beats from 32 recordings of baseline rhythm and compared to normal rhythm before a paired spontaneous cardiac arrhythmia. Before arrhythmia, the QTc (505 ± 73 ms) was not significantly longer than the baseline rhythm (497 ± 73 ms) (P = .23). Considering ventricular tachycardia (VT) events only (12 patients), event QTc (526 ± 75 ms) was not significantly longer than baseline QTc (520 ± 74 ms) (P = .41). Considering fast VT/ventricular fibrillation (VF) events only (20 patients), event QTc (494 ± 70 ms) was not significantly longer than baseline QTc (483 ± 71 ms) (P = .26). The influence of QTc as a measure to indicate an impending VT event in a variety of VT/VF patients remains unclear.     

Severe hypercalcemia from multiple myeloma as an acquired cause of short QT

An otherwise healthy 64-year-old man with recently diagnosed multiple myeloma was admitted to hospital with hypercalcemia and renal failure. Despite his electrocardiogram showing short QT/QTc intervals, he was admitted without cardiac monitoring. He died suddenly a few hours later, likely from a fatal arrhythmia. This case illustrates that pronounced QT shortening from hypercalcemia is an underappreciated malignant finding that can portend a significant risk for arrhythmia and sudden cardiac death. In addition, we also discuss the causes of hypercalcemia associated short QT/QTc intervals and its ECG features.     

58例心室颤动病人临床分析

为探讨住院病人心室颤动（简称室颤）的病因和存活出院者的远期生存率,对连续58例经心电监测或心电图证实的重颤住院者进行回顾分析和随访。心功能评价采用NYHA4级分类法。男37例（68±19岁）、女11例（64±17岁）。35例室颤发生于CCU病房、15例发生于心导管室、3例发生于抢救室、5例发生于普通病房。58例中复苏失败死亡者16例,除颤成功后72h内死亡4例,存活出院38例。室颤发生于心肌梗死（简称心梗）急性期7例（12％）,复苏成功6例（86％）。发生于非急性心便51例（88％）,其中陈旧性心梗25例（复苏成功72％）、冠心病12例（复苏成功100％）。其他病因11例,多为晚期慢性心功能不全者（复苏成功14％）。20例住院期间死亡者和38例存活出院者中分别有90％和12％心功能异常。失访3例（8％）,其余35例随访6±3（1～9）年,其中5例死亡（1％）,2例为猝死（6％）,长期服用抗心律失常药物者4例（11％）。结论：急性心梗和心导管操作引起的室颤抢救成功率高（86％～100％）,晚期心脏病室颤抢救成功率低（14％）,除颤早晚和心功能损害程度明显影响抢救成功率和远期存活率。     

Preshock phase singularity and the outcome of ventricular defibrillation

BACKGROUND: Phase singularity (PS) is a topological defect that serves as a source of ventricular fibrillation (VF). Whether or not the quantity of preshock PS determines defibrillation outcome is unclear. OBJECTIVE: The purpose of this study was to test the hypothesis that the number of PSs at the time of shock is an important factor that determines the shock outcome. METHODS: Isolated, perfused rabbit hearts (n = 7) were optically mapped with a potentiometric dye (di-4-ANNEPS). Shocks were delivered during short (10 seconds) and long (1 minute) VF, and the outcome was classified as successful type A (immediate termination), type B (postshock repetitive responses before termination), and unsuccessful. RESULTS: When shock strengths of 50% probability of successful defibrillation (DFT50) +/- 50 V were given in short VF, the types A and B and unsuccessful shocks were associated with a preshock PS number of 0.3 +/- 0.4, 1.4 +/- 0.3, and 1.5 +/- 0.4 (P <.01 by analysis of variance) and shock strengths of 205 +/- 77, 207 +/- 65, and 173 +/- 74 V (P <.01), respectively. When the same shocks were applied during long VF, the PS numbers were 1.7 +/- 0.5, 3.0 +/- 0.5, and 3.5 +/- 0.6, respectively (P <.01), and the shock strengths were 282 +/- 100, 283 +/- 135, and 256 +/- 126 V, respectively (P <.01). If we only analyze shocks with strength at DFT(50), the preshock PS number was still significantly different for short VF (0.6 +/- 0.5, 1.6 +/- 0.9, and 1.5 +/- 0.8; P <.05) and for long VF (1.4 +/- 0.5, 2.7 +/- 0.6, and 2.7+/-1.3; P <.05), respectively. All preshock PSs were eliminated by shocks. However, rapid repetitive activity was then reinitiated in unsuccessful and type B successful shocks but not in type A successful shocks. CONCLUSIONS: A low number or an absence of preshock PS was associated with type A successful defibrillation. There was no difference in preshock PS numbers between unsuccessful and type B successful defibrillation.