Background-Arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) is a condition associated with the risk of sudden death (SD). Methods and Results-We conducted a multicenter study of the impact of the implantable cardioverter-defibrillator (ICD) for prevention of SD in 132 patients (93 males and 39 females, age 40Ϯ15 years) with ARVC/D. Implant indications were a history of cardiac arrest in 13 patients (10%), sustained ventricular tachycardia in 82 (62%), syncope in 21 (16%), and other in 16 (12%). During a mean follow-up of 39Ϯ25 months, 64 patients (48%) had appropriate ICD interventions, 21 (16%) had inappropriate interventions, and 19 (14%) had ICD-related complications. Fifty-three (83%) of the 64 patients with appropriate interventions received antiarrhythmic drug therapy at the time of first ICD discharge. Programmed ventricular stimulation was of limited value in identifying patients at risk of tachyarrhythmias during the follow-up (positive predictive value 49%, negative predictive value 54%). Four patients (3%) died, and 32 (24%) experienced ventricular fibrillation/flutter that in all likelihood would have been fatal in the absence of the device. At 36 months, the actual patient survival rate was 96% compared with the ventricular fibrillation/flutter-free survival rate of 72% (PϽ0.001). Patients who received implants because of ventricular tachycardia without hemodynamic compromise had a significantly lower incidence of ventricular fibrillation/flutter (log rankϭ0.01). History of cardiac arrest or ventricular tachycardia with hemodynamic compromise, younger age, and left ventricular involvement were independent predictors of ventricular fibrillation/flutter. Conclusions-In

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Post-myocardial infarction risk stratification, especially arrhythmic risk stratification, is an issue that has still not been wholly addressed in modern clinical cardiology. In the past 10 years, arrhythmic risk stratification has been approached mainly by evaluating frequency and complexity of premature ventricular contractions, detected on Holter monitoring, often in association with determination of percent ejection fraction. This methodology has been proven to be limited and fallacious according to the Cardiac Arrhythmia Suppression Trial I and II (CAST I,II) results, in which suppression of premature ventricular contractions or premature ventricular beats throughout by antiarrhythmic drugs resulted in an increase in both cardiac and arrhythmic mortality. Only amiodarone as an antiarrhythmic drug, as proven in the recent European Myocardial Infarct Amiodarone Trial (EMIAT) and Canadian Amiodarone Myocardial Infarction Trial (CAMIAT), was effective in reducing arrhythmic mortality without affecting cardiac mortality, in patients selected mainly because of a reduced ejection fraction, with and without premature ventricular contractions. Conversely, it is well known that beta-blockers are effective in preventing sudden death in post-acute myocardial infarction (AMI) patients, thus reducing cardiac and arrhythmic mortality. Conversely, in other institutions, risk stratification in post-AMI patients has been performed by electrophysiologic study obtained, without any previous noninvasive arrhythmic risk stratification, in all post-AMI patients. In recent years, many other noninvasive electrocardiology parameters, such as late potentials (signal-averaged electrocardiography), heart rate variability, baroreflex sensitivity, and, more recently, T-wave alternance, have been shown to be useful, but they are associated with a low specificity in the noninvasive identification of patients at high risk for arrhythmic mortality. Conversely, in the Multicenter Automatic Defibrillation Implantation Trial (MADIT), electrophysiology confirmed that inducibility of ventricular tachycardia shows high specificity and a high predictive value for arrhythmic events. Nevertheless, the MADIT study population is not comparable to a cohort of consecutive patients who have recently had a myocardial infarction. In this setting, the highest risk of arrhythmic events can be observed in patients with depressed percent ejection fraction (< 35%) and in the first 6 months after AMI. Today, the most convincing approach seems to be the one combining both noninvasive risk stratification parameters (e.g., premature ventricular beats > 10/h or reduced heart rate variability < 70 ms or a positive signal-averaged electrocardiogram) followed by a further arrhythmic risk stratification, obtained through electrophysiologic study. Several published and ongoing trials that utilize various arrhythmic risk stratification techniques as part of their protocol are reviewed.

To develop a quantitative relation between the overall severity of acute ischemia and left ventricular global and regional function, two minor axis internal diameters and myocardial wall thickness were determined using ultrasonic crystals in 10 open chest dogs with carotid-left anterior descending artery cannulation. The overall extent of ischemia produced by graded stenosis of the cannulation system was estimated by total myocardial blood flow deficit, calculated using radioactive microspheres and a balloon-reservoir perfusion technique permitting precise separation of ischemic from nonischemic tissue. Although cardiac output and left ventricular stroke work were maintained through chamber enlargement until total myocardial blood flow deficit was about 10%, ejection indexes of left ventricular function decreased progressively with increasing ischemia and correlated inversely with total myocardial blood flow deficit (r = -0.55 to -0.73). Ejection indexes of left ventricular global function correlated directly with regional function in the ischemic zone (r = 0.67 to 0.83), although global function decreased at a far slower rate than regional contraction during progressive coronary stenosis with an ischemic region comprising about 25% of total left ventricular weight. During myocardial ischemia, regional dysfunction resulted in progressive global contractile dysfunction; left ventricular hemodynamic status was maintained until ischemia was severe.