A new animal model to study sudden cardiac death.

Sudden cardiac death (SCD) is the most common cause of cardiovascular-related death, accounting for more than 50% of all cardiovascular mortality worldwide. SCD is often the first manifestation of unrecognized cardiac disease. Ventricular tachyarrhythmias, mainly ventricular fibrillation, are primarily responsible for the mechanism underlying most SCD episodes. Ventricular tachyarrhythmias occur frequently in the setting of coronary artery disease with or without the presence of myocardial infarction. In spite of the prevalence of defibrillation programs, and frequent attempts made to resuscitate patients experiencing SCD, the survival rate after SCD was substantially unsatisfactory. Most SCD episodes occur in individuals without previously known cardiac disease, further making the inability to successfully identify and properly treat this disease a critical public health problem. Ventricular fibrillation accounts for most of the deaths occurring in the acute phase of ischemia (within hours to days), whereas sustained, monomorphic ventricular tachycardia due to reentry generated in the scar tissue usually develops in the setting of a healed myocardial infarction (typically weeks to months). There is a distinction in arrhythmias occurring in the subacute phase of myocardial infarction and in the chronic phase. The electrophysiological mechanisms involved with arrhythmia generation and electrical remodeling have been extensively studied. In addition, SCD as the result of ventricular tachyarrhythmias is the most ominous presentation of myocardial infarction. SCD in the immediate period after myocardial infarction represents a clinical challenge, particularly in patients with left ventricular dysfunction or heart failure. It is now well established that ventricular tachyarrhythmia in the setting of infarction is a reentrant arrhythmia where cells in the infarct border have normal action potentials but display slow and discontinuous conduction, which is associated with abnormal connexin expression. Furthermore, it has been noticed that only a minority of patients who have been successfully resuscitated from SCD associated with coronary artery disease subsequently developed a myocardial infarction. The pathophysiology and electrophysiology involved with reperfusion arrhythmia and SCD are distinct from those in the setting of ischemia and infarction. Beyond ischemia-reperfusion etiology, ventricular tachyarrhythmia and SCD are attributed to genetic arrhythmia syndromes and cardiomyopathies. Because such events are