BACKGROUND: In patients with postinfarction sustained ventricular tachycardia showing one or more antiarrhythmic drug failures, the question is how long to proceed with new drug trials before deciding to perform map-guided arrhythmia surgery. Although the techniques of this surgery developed rapidly in the early 1980s, this therapy may be offset by damage to residual left ventricular function. However, surgery has been shown to be very effective in selected groups of patients. METHODS: A randomized study was carried out in patients with postinfarction ventricular tachycardia and eligible for arrhythmia surgery based on residual left ventricular function. Therapy failure was defined by the occurrence of the following events: spontaneous recurrence of ventricular tachycardia or ventricular fibrillation, sudden cardiac death, inducibility of sustained ventricular tachycardia or ventricular fibrillation with programmed stimulation of the heart, symptomatic non-sustained ventricular tachycardia requiring therapy or side-effects of antiarrhythmic drugs requiring withdrawal. In the drug limb, failure of the first antiarrhythmic drug was accepted but failure of a second and different drug was regarded as true therapy failure. RESULTS: After randomization, antiarrhythmic drug therapy was administered in 33 patients, and 30 patients underwent surgery. Neither group differed in baseline characteristics, and the mean number of drug failures before randomization was 2.7. The Kaplan-Meier therapeutic failure of antiarrhythmic drugs was 39 +/- 11%, 42 +/- 11% and 51 +/- 18% at 0.5-, 1- and 4-year follow-up, respectively, whereas the therapeutic failure of cardiac surgery was 37 +/- 11%, 37 +/- 11% and 50 +/- 20% at 0.5, 1 and 4 years, respectively, showing no statistical difference. The 1- and 4-year Kaplan-Meier survival of the antiarrhythmic drug-treated group was 91 +/- 6% and 78 +/- 15%, respectively, and of the surgical group 92 +/- 6% and 59 +/- 20%, respectively, and did not differ between either group. However, the relative risk for total cardiac death was higher in the surgical limb than in the drug limb (relative risk 2.2, CI 0.68-7.48). CONCLUSION: This study demonstrated no difference between the therapeutic result of continuation of two different antiarrhythmic drugs and that of arrhythmia surgery. Despite the small number of patients studied, it is recommended that drug therapy should continue as long as this regimen is tolerated by the patient. When true drug refractoriness or side-effects of drugs arise, arrhythmia surgery offers a valuable alternative. However, when additional reasons for cardiac surgery exist, arrhythmia surgery should be undertaken earlier and may become the first choice of treatment of postinfarction ventricular tachycardia.
RCT Entities:
BACKGROUND: In patients with postinfarction sustained ventricular tachycardia showing one or more antiarrhythmic drug failures, the question is how long to proceed with new drug trials before deciding to perform map-guided arrhythmia surgery. Although the techniques of this surgery developed rapidly in the early 1980s, this therapy may be offset by damage to residual left ventricular function. However, surgery has been shown to be very effective in selected groups of patients. METHODS: A randomized study was carried out in patients with postinfarction ventricular tachycardia and eligible for arrhythmia surgery based on residual left ventricular function. Therapy failure was defined by the occurrence of the following events: spontaneous recurrence of ventricular tachycardia or ventricular fibrillation, sudden cardiac death, inducibility of sustained ventricular tachycardia or ventricular fibrillation with programmed stimulation of the heart, symptomatic non-sustained ventricular tachycardia requiring therapy or side-effects of antiarrhythmic drugs requiring withdrawal. In the drug limb, failure of the first antiarrhythmic drug was accepted but failure of a second and different drug was regarded as true therapy failure. RESULTS: After randomization, antiarrhythmic drug therapy was administered in 33 patients, and 30 patients underwent surgery. Neither group differed in baseline characteristics, and the mean number of drug failures before randomization was 2.7. The Kaplan-Meier therapeutic failure of antiarrhythmic drugs was 39 +/- 11%, 42 +/- 11% and 51 +/- 18% at 0.5-, 1- and 4-year follow-up, respectively, whereas the therapeutic failure of cardiac surgery was 37 +/- 11%, 37 +/- 11% and 50 +/- 20% at 0.5, 1 and 4 years, respectively, showing no statistical difference. The 1- and 4-year Kaplan-Meier survival of the antiarrhythmic drug-treated group was 91 +/- 6% and 78 +/- 15%, respectively, and of the surgical group 92 +/- 6% and 59 +/- 20%, respectively, and did not differ between either group. However, the relative risk for total cardiac death was higher in the surgical limb than in the drug limb (relative risk 2.2, CI 0.68-7.48). CONCLUSION: This study demonstrated no difference between the therapeutic result of continuation of two different antiarrhythmic drugs and that of arrhythmia surgery. Despite the small number of patients studied, it is recommended that drug therapy should continue as long as this regimen is tolerated by the patient. When true drug refractoriness or side-effects of drugs arise, arrhythmia surgery offers a valuable alternative. However, when additional reasons for cardiac surgery exist, arrhythmia surgery should be undertaken earlier and may become the first choice of treatment of postinfarction ventricular tachycardia.