TY - JOUR
T1 - Clinical and electrophysiologic determinants, treatment and survival of patients with sustained malignant ventricular tachyarrhythmias occurring late after myocardial infarction
AU - Gomes, J. Anthony
AU - Winters, Stephen L.
AU - Ergin, Arisan
AU - Machac, Joseph
AU - Estioko, Manuel
AU - Alexopoulous, Dimitrious
AU - Pe, Elena
PY - 1991
Y1 - 1991
N2 - To assess the clinical and electrophysiologic determinants, treatment and survival of patients with sustained malignant ventricular tachyarrhythmias late after myocardial infarction, a total of 108 patients (mean age 61 ± 10 years) were studied. Thirty-two patients (Group I) had sustained ventricular tachyarrhythmias 8 to 60 days (mean 13 ± 9) after acute myocardial infarction. The remaining 76 patients (Group II), who served as a control group, had no sustained ventricular tachyarrhythmias ≤60 days after infarction. The most significant independent determinants of sustained ventricular tachyarrhythmias late after infarction were the presence of late potentials (chi square = 16.07, p = 0.0001), defined as an abnormal signal-averaged QRS complex in association with an abnormal root-mean-square voltage in the terminal 40 ms of the QRS complex, and an abnormal ejection fraction of <40% (chi square = 10.09, p = 0.001). Sustained ventricular tachycardia was induced in 27 (96%) of 28 Group I patients. Among the 32 patients in Group I, antitachy-cardia therapy included antiarrhythmic drug therapy as the sole preventive measure in 14 (44%); map-guided surgery or coronary artery bypass surgery, or both, in 14 (44%) and the automatic cardioverter-defibrillator in 4 (12%). The arrhythmias were rendered noninducible in 83% of patients after map-guided surgery and in 41% after drug therapy. During a follow-up period of 20 ± 14 months, five Group I patients (15%) had an arrhythmic event and four (9.3%) had a cardiac-related death. All five patients who had an arrhythmic event were receiving antiarrhythmic drug therapy. None of the patients who had successful map-guided surgery had an arrhythmic event. The long-term 2-year arrhythmia-free survival (0.83 versus 0.92) and total survival (0.87 versus 0.92) were not significantly different between Group I and Group II. Conclusions: 1) Sustained ventricular tachycardia/ventricular fibrillation late (8 to 60 days) after myocardial infarction is usually due to the presence of a well formed substrate rather than the occurrence of acute myocardial ischemia. 2) A marked improvement in survival not significantly different from that of a control group of patients with no sustained ventricular tachyarrhythmias and better left ventricular function was observed with an aggressive approach consisting of electrophysiological!) guided therapy inclusive of map-guided surgery, coronary revascularization, drug therapy and the automatic implantable cardioverter-defibrillator. 3) Patients with more than two episodes of drug-resistant sustained ventricular tachyarrhythmias do better with early surgery than with antiarrhythmic therapy.
AB - To assess the clinical and electrophysiologic determinants, treatment and survival of patients with sustained malignant ventricular tachyarrhythmias late after myocardial infarction, a total of 108 patients (mean age 61 ± 10 years) were studied. Thirty-two patients (Group I) had sustained ventricular tachyarrhythmias 8 to 60 days (mean 13 ± 9) after acute myocardial infarction. The remaining 76 patients (Group II), who served as a control group, had no sustained ventricular tachyarrhythmias ≤60 days after infarction. The most significant independent determinants of sustained ventricular tachyarrhythmias late after infarction were the presence of late potentials (chi square = 16.07, p = 0.0001), defined as an abnormal signal-averaged QRS complex in association with an abnormal root-mean-square voltage in the terminal 40 ms of the QRS complex, and an abnormal ejection fraction of <40% (chi square = 10.09, p = 0.001). Sustained ventricular tachycardia was induced in 27 (96%) of 28 Group I patients. Among the 32 patients in Group I, antitachy-cardia therapy included antiarrhythmic drug therapy as the sole preventive measure in 14 (44%); map-guided surgery or coronary artery bypass surgery, or both, in 14 (44%) and the automatic cardioverter-defibrillator in 4 (12%). The arrhythmias were rendered noninducible in 83% of patients after map-guided surgery and in 41% after drug therapy. During a follow-up period of 20 ± 14 months, five Group I patients (15%) had an arrhythmic event and four (9.3%) had a cardiac-related death. All five patients who had an arrhythmic event were receiving antiarrhythmic drug therapy. None of the patients who had successful map-guided surgery had an arrhythmic event. The long-term 2-year arrhythmia-free survival (0.83 versus 0.92) and total survival (0.87 versus 0.92) were not significantly different between Group I and Group II. Conclusions: 1) Sustained ventricular tachycardia/ventricular fibrillation late (8 to 60 days) after myocardial infarction is usually due to the presence of a well formed substrate rather than the occurrence of acute myocardial ischemia. 2) A marked improvement in survival not significantly different from that of a control group of patients with no sustained ventricular tachyarrhythmias and better left ventricular function was observed with an aggressive approach consisting of electrophysiological!) guided therapy inclusive of map-guided surgery, coronary revascularization, drug therapy and the automatic implantable cardioverter-defibrillator. 3) Patients with more than two episodes of drug-resistant sustained ventricular tachyarrhythmias do better with early surgery than with antiarrhythmic therapy.
UR - http://www.scopus.com/inward/record.url?scp=0025733164&partnerID=8YFLogxK
U2 - 10.1016/S0735-1097(10)80093-2
DO - 10.1016/S0735-1097(10)80093-2
M3 - Article
C2 - 1991887
AN - SCOPUS:0025733164
SN - 0735-1097
VL - 17
SP - 320
EP - 326
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 2
ER -