Treatment

1. Most patients with acute myocardial disease and PVCs will respond to intravenous lidocaine, although some patients may require procainamide. In the setting of acute myocardial ischemia (unstable angina or acute MI), many physicians would treat frequent or multiform PVCs with the goal of reducing deaths due to sudden ventricular tachycardia or fibrillation. While single studies have suggested benefit, pooled data and metanalyses find no reduction in mortality from either suppressive or prophylactic treatment of PVCs.

2. In patients with chronic PVCs, there is no evidence that oral antiarrthymics enhance survival. To the contrary, large, randomized studies of postinfarction patients found that treatment with encainide, flecainide, or moricizine increased the incidence of cardiac arrest or arrhythmic death, probably related to their proarrthymic effects. Before treating chronic PVCs, the physician should consider several factors:

a. Underlying heart disease b. The nature of the ectopy c. The presence or absence of symptoms d. The potential side effects of oral antiarrhythmic therapy e. Which technique will be used to judge efficacy of therapy (continuous monitoring versus EP studies)? Oral antiarrhythmic therapy requires careful monitoring. In some patients at risk of sudden cardiac death, automatic internal cardiac defibrillators (AICDs) are used in conjunction with antiarrthymics.

VENTRICULAR PARASYSTOLE Parasystole occurs when an independent ectopic pacemaker is protected from the influence of outside impulses (entrance block) and competes with the dominant pacemaker to produce myocardial depolarizations. A parasystolic pacemaker can arise anywhere in the heart but is most often located in the ventricles, where it produces a rhythm that operates in competition with the sinus node. This ectopic pacemaker has an innate rate; however, not all beats depolarize the ventricle (exit block).

The ECG characteristics of ventricular parasystole are (1) variation in the coupling interval between the preceding sinus beat and the ectopic beat, (2) common relation between the interectopic beat intervals, and (3) occurrence of fusion beats ( Fig 24-17). Usually, long rhythm strips are necessary to establish that the interectopic intervals are multiples of a common parasystolic pacemaker. Because of the difference in response to antiarrthymics, it is important to recognize and differentiate parasystolic beats from PVCs.

FIG. 24-17. The fifth and eighth ventricular complexes are premature and of similar morphology but have different coupling intervals. The second complex (marked "F") represents a fusion beat. The interectopic interval is 2.36 s. (From Heger JW, Niemann JT, Boman KG, et al: Cardiology for the House Officer. Baltimore, Williams & Wilkins, 1982. Used by permission.)

Clinical Significance Ventricular parasystole is most often associated with severe ischemic heart disease, acute MI, hypertensive heart disease, or electrolyte imbalance. Parasystole is often self-limited and benign but infrequently may lead to ventricular tachycardia or fibrillation.

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