SUDDEN CARDIAC DEATH



The most commonly used definition of sudden death is unexpected, nontraumatic death occur­ring within an hour after the onset of symptoms; some studies have included death occurring within 24 hours of the onset of symptoms. Sudden cardiac death claims approximately 1200 lives daily in the United States and is the leading cause of death among men between the ages of 20 and 60. By far the most common cause of sudden death is cardiac, and within that group, the most com­mon cause is ventricular tachyarrhythmias.

Nonarrhythmic causes of sudden death are listed in.
Ventricular tachyarrhythmias, generally related to ischemic heart disease, are the most common cause of sudden cardiac death. Although 75 per cent of patients resuscitated from ventricular fi­brillation have extensive coronary artery disease, only 20 per cent have evidence of acute trans­mural myocardial infarction. Approximately 75 per cent of patients have a previous history of car­diac disease; sudden death is the first manifes­tation of cardiac disease in the remainder. The difference in recurrence of sudden death in pa­tients with (2 per cent at one year) and without (22 per cent at one year) acute myocardial infarction may be due to different arrhythmia mecha­nisms. Patients with ventricular fibrillation at the time of an acute myocardial infarction probably do not need long-term antiarrhythmic therapy un­less chronic late ventricular tachycardia is doc­umented. The risk of recurrent ventricular fibril­lation is higher if there is evidence of left ventricular dysfunction or evidence of previous myocardial infarction.

Nonatherosclerotic etiol­ogies of ventricular tachyarrhythmias associated with sudden death are mitral valve prolapse, hy­pertrophic or other cardiomyopathies, antiar­rhythmic drugs, myocarditis, prolonged QT syn­drome, and Wolff-Parkinson-White syndrome with rapid antegrade conduction over an acces­sory pathway.

The identification of patients at high risk for sudden cardiac death can be difficult. The occur­rence of complex ventricular ectopy including multiform PVC’s, pairs, and ventricular tachycar­dia in survivors of myocardial infarction is as­sociated with a two- to three-fold increase in sub­sequent sudden death; however, suppression of ventricular ectopy with antiarrhythmic agents has not been proven to decrease the incidence of sud­den death, and the necessity of suppressing less complex forms of ventricular ectopy is unclear. The risk of sudden cardiac death and the inci­dence of complex ectopy is greater in patients with poor left ventricular function.

The patient who has suffered sudden cardiac arrest in the absence of acute myocardial infarc­tion and the patient with recurrent symptomatic ventricular tachyarrhythmias must be treated with antiarrhythmic therapy. The end point of an­tiarrhythmic therapy to be used to judge efficacy is often unclear. The mere attainment of “thera­peutic” serum levels of an antiarrhythmic agent is not usually sufficient to guard against recurrent ventricular tachyarrhythmias. Prolonged electro­cardiographic monitoring is noninvasive, simple, and widely available. However, many patients with sudden death demonstrate very little spon­taneous ectopy between episodes; therefore, suppression of spontaneous ectopy cannot be used as an end point in these patients. In addition, even in patients with spontaneous ectopy, it is not clear whether an appropriate end point would be elimination of all ventricular tachycardia, all complex ectopy, or all PVC’s. Drug evaluation using exercise testing and prolonged ambulatory recording to judge efficacy has been reported to decrease the incidence of recurrent malignant tachyarrhythmias but can only be used in patients with spontaneous high-grade ventricular ectopy between episodes of sustained tachyarrhythmia. Most investigators feel that patients experiencing sudden cardiac arrest in the absence of acute my­ocardial infarction should undergo serial electro­physiological testing to guide antiarrhythmic therapy. The suppression with a drug of ventric­ular tachycardia inducible by electrical stimula­tion appears to provide a better indicator of drug success than suppression of spontaneous ectopy and can be used in patients with little or no spon­taneous ectopy. If arrhythmias cannot be con­trolled with drugs, the implantable cardioverter defibrillator and/or cardiac surgery are options. Coronary artery revascularization alone is usually not sufficient to prevent recurrent ventricular tachyarrhythmias.

Antiarrhythmic therapy in patients after my­ocardial infarction as prophylaxis for malignant cardiac arrhythmias has not been proven effec­tive. However, in certain highrisk patients an­tiarrhythmic therapy may be warranted, for ex­ample, those with nonsustained ventricular tachycardia after infarction. Several large multi-center studies have demonstrated a decrease in the incidence of sudden death in patients treated with beta-adrenergic receptor blocking agents after myocardial infarction, and these drugs prob­ably should be considered if no contraindication to their administration exists.