Sudden cardiac death in young athletes

Although regular aerobic physical activity increases exercise capacity and plays a role in both primary and secondary prevention of a variety of chronic disorders, competitive physical exercise is associated with a significant increase of risk of sudden death in athletes, especially adolescents and young adults. Several pathogenetic mechanisms have been speculated, including silent cardiovascular conditions, mostly cardiomyopathy, premature coronary artery disease and congenital coronary anomalies. Uneventful events, especially commotio cordis, and abuse of unfair and dangerous performance-enhancing drugs, are also claimed as potential causes. Although identification of athletes at major risk and prevention of adverse events seems the more pervasive strategy, guidelines for screening athletes differ widely on international basis and even among the different Sport federations. The aim of this review was to compile the current knowledge on the prevalence and the most common causes of sudden death in sportsmen, providing an overview of the guidelines for pre-participation screening.     

Sudden cardiac death in young athletes

Most cases of sudden cardiac death in young athletes (<35 years) are caused by inherited cardiomyopathies, notably hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy.     

Sudden cardiac death risk stratification in patients with heart failure

The multiplicity of mechanisms contributing to arrhythmogenesis in patients with heart failure carries obvious implications for risk stratification. If patients having the propensity to develop arrhythmias by these different mechanisms are to be identified, tests must be devised that reveal the substrates or other factors that relate to each mechanism. In the absence of this, efforts to risk stratify patients are likely to be neither cost-effective nor accurate. This article reviews the current knowledge base of risk stratification for sudden death in patients with heart failure, while acknowledging several limitations in the studies examined.     

Sudden cardiac death in adult congenital heart disease

Background Sudden cardiac death(SCD)is a major cause of mortality in adults with congenital heart disease(CHD).The aim of this study was to determine the adult CHD population at risk of SCD and the clinical parameters associated with SCD.Methods and Results We performed a multicenter case-controlled study.Patients who died suddenly due to proven or presumed arrhythmia were included(cases).For each case,two controls matched on diagnosis,type of surgical intervention,age and gender were included.From three databases including 25790 adults with CHD,1189 deaths(5%)were identified,of whom 213 patients(19%)died suddenly.Arrhythmic death occurred in 171 of 1189 patients.The underlying cardiac lesions were mild,moderate and severe CHD in 12%,33% and 55% of the SCD cases,respectively.Clinical variables associated with SCD were supraventricular tachycardia(SVT,OR 3.5,95% CI 1.5-7.9,P = 0.004),moderate to severe systemic ventricular dysfunction(OR 3.4,95% CI 1.1-10.4,P = 0.034),moderate to severe subpulmonary ventricular dysfunction(OR 3.4,95% CI 1.110.2,P = 0.030),increased QRS duration(OR 1.34(per 10 ms increase),95% CI 1.10-1.34,P = 0.008),and QT dispersion(OR 1.22(per 10 ms increase),95% CI 1.22-1.48,P = 0.008).Conclusions The clinical parameters found to be associated with SCD in adults with a broad spectrum of CHD,including systemic right ventricles,are similar to those in ischemic heart disease.Moreover,even those patients with mild cardiac lesions,are potentially at risk for SCD.This highlights the need for further prospective studies as well as vigilant ongoing follow-up of the adult with CHD.     

Sudden cardiac death in the young: Epidemiology and overview

Sudden cardiac death (SCD), particularly in the young athlete, is a rare though devastating event for families, institutions, and communities at large. It can also affect the nonathlete and occur at rest, although most commonly associated with exercise activities and/or sports participation. Common causes of SCD include cardiomyopathies, particularly hypertrophic cardiomyopathy in the United States, congenital coronary artery anomalies, channelopathies, among others. This report will explore an overview of the prevalence and causes of SCD in the young.     

Sudden cardiac death

Opinion statement  

Sudden cardiac death

Opinion statement Sudden cardiac death is often due to a ventricular arrhythmia. When a patient presents with a malignant arrhythmia unrelated to a transient reversible cause, there is a high probability of recurrent arrhythmia and sudden death. Clinical trials have shown a uniform survival benefit from implantable cardioverter-defibrillator (ICD) therapy in survivors of a malignant arrhythmia when compared with drug therapy. However, only 1% to 5% of patients survive an out-of-hospital cardiac arrest, emphasizing the need for primary prevention of sudden death. Clinical trial data available in this regard are largely limited to patients with coronary artery disease (CAD). Mortality can be reduced by the ICD in patients with CAD and depressed left ventricular ejection fraction (LVEF) less than 30%. If left ventricular function is only moderately depressed (LVEF between 30% and 40%), the presence of nonsustained ventricular tachycardia with inducible ventricular arrhythmia at electrophysiologic testing identifies patients who benefit from an ICD. The role of the ICD in primary prevention of sudden death in patients with nonischemic dilated cardiomyopathy is less clear at this time. Preliminary data indicate that the presence of heart failure symptoms in this population increases risk of sudden death that can be prevented by an ICD. Antiarrhythmic drugs have little role in prevention of sudden death; however, drugs that block the effects of β-adrenergic stimulation, angiotensin, and aldosterone reduce mortality partly through their salutary effects on sudden death. Finally, a number of inherited defects of genes coding for ion channels, contractile sarcomeric proteins, and cell-to-cell junction proteins can result in primary electrical abnormalities and sudden death. The ICD is effective for secondary prevention, but its role in primary prevention is controversial and should be based on individual risk factors.     

Sudden cardiac death

SCD continues to be an important cause of death and morbidity. Despite expanding insight into the mechanisms causing SCD, the population at high risk is not being effectively identified. Although there is still much to do in the management phase of SCD (predicting the efficacy of various therapies), recent clinical trials have helped define the relative risks and benefits of therapies in preventing SCD. Trials are underway to determine whether treating other patient populations, including asymptomatic patients after MI, will improve survival rate. The approach to reducing mortality rate will always be multifaceted; primary prevention of coronary artery disease and prompt salvage of jeopardized myocardium are 2 important aspects of this approach. In addition to interventions for MI, such as myocardial revascularization when indicated, simple and easily administered therapies that are likely to remain the most effective prophylactic interventions are aspirin, ACE inhibitors, beta-blockers, and cholesterol-lowering agents. However, the MADIT and AVID data clearly demonstrate a role for ICD therapy in a subgroup of patients who have VT/VF and are at risk of cardiac arrest. Even though the absolute magnitude of benefit associated with ICDs is still to be determined, the AVID study and other recent reports provide convincing evidence that patients who have VT/VF fare better with ICDs than with antiarrhythmic drug therapy. For the high-risk population described in this article, in addition to aggressive anti-ischemic and heart failure therapy, ICDs are now a mainstay of life-saving treatment. Still to be surmounted is the challenge of identifying patients who have nonischemic substrates and of providing them with the appropriate therapy. Guided by genetic studies and new insight into the mechanisms of such problems as congenital long QT syndrome, life-saving and life-enhancing therapies may soon be available for the management of SCD.     

心脏性猝死

心脏性猝死（sudden cardiac death，SCD）是指由各种心脏原因引起的自然死亡。发病突然、进展迅速，死亡发生在症状出现后1h内。患者发生猝死事件前可以有心脏疾病表现，但猝死的发生具有无法预测的特点。发生心脏骤停的患者能被成功复苏的机会很小，美国约为15％，而大多国家仅为0—5％。因为绝大多数心脏骤停发生在医院外，不能得到有效的快速治疗干预（如初步的紧急心肺复苏术），仅有发生在医院内或有幸经过初步抢救治疗并及时送至急诊室的心脏骤停患者，有机会得到有效治疗而幸存。因此SCD具有突发、迅速、不可预料和病死率高的特征，是直接危及人们生命的一大杀手。     

Sudden cardiac death

Most sudden deaths in industrial nations are the result of underlying coronary artery disease. Longitudinal studies have demonstrated that the percent of all coronary events presenting as sudden death increases with age in both men and women. Relative weight is another important risk factor; the age-adjusted rate of sudden cardiac death for the upper weight tercile in the Framingham study was over 2 times higher for men and 3 times higher for women than the rate for the lower weight tercile. Most patients who die suddenly initially experience ventricular tachycardia that subsequently degenerates into ventricular fibrillation. Patients with a high risk of sudden cardiac death include: survivors of myocardial infarction with left ventricular dysfunction or complex ventricular ectopy, or both; survivors of out-of-hospital cardiac arrest, particularly when the event is not associated with an acute myocardial infarction; patients with recurrent ventricular tachycardia; and patients with dilated congestive cardiomyopathy, particularly when associated with ventricular ectopy. Reducing the risk of sudden death in these patients remains a major challenge.     

Sudden cardiac death risk factors in patients with heart failure treated with carvedilol

BACKGROUND: Chronic heart failure (CHF) is associated with a high risk of sudden cardiac death (SCD). Most frequently SCD occurs in patients with NYHA class II and III. AIM: To evaluate the influence of prolonged carvedilol therapy on SCD risk in CHF patients. METHODS: The study included 86 patients (81 men and 5 women) aged 56.8+/-9.19 (35-70) years with CHF in NYHA class II and III receiving an ACE inhibitor and diuretics but not beta-blockers. At baseline and after 12 months of carvedilol therapy the following risk factors for SCD were analysed: in angiography - occluded infarct-related artery; in echocardiography - left ventricular ejection fraction (LVEF) <30%, volume of the left ventricle (LVEDV) >140 ml; in ECG at rest - sinus heart rate (HRs) >75/min, sustained atrial fibrillation, increased QTc; in 24-hour ECG recording - complex arrhythmia, blunted heart rate variability (SDNN <100 ms) and abnormal turbulence parameters (TO and TS or one of them); in signal-averaged ECG - late ventricular potentials and prolonged fQRS >114 ms. The analysis of SCD risk factors in basic examination in patients who suddenly died was also performed. RESULTS: During one-year carvedilol therapy heart transplantation was performed in 2 patients; 5 patients died. At 12 months the following risk factors for SCD were significantly changed: HRs >75/min (50 vs. 16 patients, p=0.006), LVEF <30% (37 vs. 14 patients, p=0.01), SDNN <100 ms (19 vs. 9 patients, p=0.04). At 12 months the number of risk factors for SCD in each patient was significantly reduced (p=0.001). In patients who suddenly died we found a greater amount of SCD risk factors in basic examination (7 vs. 5) as compared to alive patients. CONCLUSIONS: Prolonged beta-adrenergic blockade reduces risk of sudden cardiac death through significant LVEF increase, reduction of HR at rest and improvement of HRV.     

Sudden cardiac death in the young: a clinical genetic approach

The sudden death of a young person is a devastating event for both the family and community. Over the last decade, significant advances have been made in understanding both the clinical and genetic basis of sudden cardiac death in the young. Many of the causes of sudden death in the young are due to genetic heart disorders, which can lead to both structural (e.g. hypertrophic cardiomyopathy) and arrhythmogenic (e.g. familial long QT syndrome) abnormalities. Most commonly, sudden cardiac death in the young can be the first presentation of an underlying heart problem, leaving the family at a loss as to why an otherwise healthy young person has died. Not only is this a tragic event for those involved, but it also presents a medical challenge to the clinician involved in the management of the surviving family members. Evaluation of families requires a multidisciplinary approach, which should include cardiologists, a clinical geneticist, a genetic counsellor and the forensic pathologist directly involved in the sudden death case. This multifaceted cardiac genetic service is crucial in the evaluation and management of the clinical, genetic, psychological and social complexities observed in families in which there has been a young sudden cardiac death.