Clinical and electrophysiologic determinants, treatment and survival of patients with sustained malignant ventricular tachyarrhythmias occurring late after myocardial infarction

J. Anthony Gomes, Stephen L. Winters, Arisan Ergin, Joseph Machac, Manuel Estioko, Dimitrious Alexopoulous, Elena Pe

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)320-326
Number of pages7
JournalJournal of the American College of Cardiology
Volume17
Issue number2
DOIs
StatePublished - Jan 1 1991

Fingerprint

Tachycardia
Myocardial Infarction
Survival
Therapeutics
Drug Therapy
Anti-Arrhythmia Agents
Ventricular Tachycardia
Infarction
Cardiac Arrhythmias
Control Groups
Cardia
Defibrillators
Implantable Defibrillators
Ventricular Fibrillation
Left Ventricular Function
Coronary Artery Bypass
Myocardial Ischemia

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

@article{20daa13c3a004f9d9c00d25c60904713,
title = "Clinical and electrophysiologic determinants, treatment and survival of patients with sustained malignant ventricular tachyarrhythmias occurring late after myocardial infarction",
abstract = "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.",
author = "Gomes, {J. Anthony} and Winters, {Stephen L.} and Arisan Ergin and Joseph Machac and Manuel Estioko and Dimitrious Alexopoulous and Elena Pe",
year = "1991",
month = "1",
day = "1",
doi = "10.1016/S0735-1097(10)80093-2",
language = "English (US)",
volume = "17",
pages = "320--326",
journal = "Journal of the American College of Cardiology",
issn = "0735-1097",
publisher = "Elsevier USA",
number = "2",

}

Clinical and electrophysiologic determinants, treatment and survival of patients with sustained malignant ventricular tachyarrhythmias occurring late after myocardial infarction. / Gomes, J. Anthony; Winters, Stephen L.; Ergin, Arisan; Machac, Joseph; Estioko, Manuel; Alexopoulous, Dimitrious; Pe, Elena.

In: Journal of the American College of Cardiology, Vol. 17, No. 2, 01.01.1991, p. 320-326.

Research output: Contribution to journalArticle

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 - 1991/1/1

Y1 - 1991/1/1

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

UR - http://www.scopus.com/inward/citedby.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

VL - 17

SP - 320

EP - 326

JO - Journal of the American College of Cardiology

JF - Journal of the American College of Cardiology

SN - 0735-1097

IS - 2

ER -