Importance of Myocardial Infarct Artery Patency on the Prevalence of Ventricular Arrhythmia and Late Potentials After Thrombolysis in Acute Myocardial Infarction Frank V. Aguirre, MD, Morton J. Kern, MD, Judith Hsia, MD, Harvey Serota, MD, DeniseJanosik, MD, Terry Greenwalt, BA, Allan M. Ross, MD, and Bernard R. Chaitman, MD Sustained infarct artery patency is an important determinant of survival in patients with acute myocardial infarction. We studied 61 patients with acute myocardial infarction who received intravenous recombinant tissue-type plasmino- gen activator, aspirin or heparin within 6 hours of symptom onset, to determine if infarct artery patency after intravenous thrombolytic therapy influences myocardial electrical stability as mea- sured by the prevalence of spontaneous ventricu- lar ectopy or late potential activity. Infarct artery patency was determined by angiographic evalua- tion 2.5 f 3 days after infarctlon. Forty-eight patients (79%) had a patent infarct-related ar- tery and 13 (21%) patients had an occluded ves- sel. The mean number of ventricular premature complexes (VPCs)/hour (p <O.Ol) and the preva- lence of late potentials (54 vs 19%; p <0.03) were significantly higher in patients with an oc- cluded versus patent-infarct related vessel. Al- though VPC frequency and late potentials were not influenced by the time to thrombolytic treat- ment, patients with a patent infarct-related ar- tery had a lower prevalence of late potentials re- gardless of whether treatment was initiated 52 hours (25% patent vs 50% occluded; p = not sig- nificant) or 2 to 6 hours (16% patent vs 55% oc- cluded; p >0.03) after symptom onset. Thus, successful thrombolysis decreases the frequency of ventricular ectopic activity and late potentials in the early postinfarction phase. The reduction in both markers of electrical instability From the Cardiology Division, St. Louis University Medical Center,St. Louis, Missouri; and the Cardiology Division, George WashingtonUni- versity, Washington,DC. Manuscript received May 20, 1991; revised manuscript receivedand accepted July 9, 199 1. Addressfor reprints: Frank V. Aguirre, MD, Cardiac Catheteriza- tion Laboratory, St. Louis University Medical Center, 3635Vista Ave- nue at Grand Boulevard, St. Louis, Missouri 63110. may help explain why the prognosis after suc- cessful thrombolysis is improved after acute myocardial infarction. (Am J Cardiol 1991;6&1410-1416) T he benefit of thrombolytic therapy on both short- and long-term survival after acute myo- cardial infarction is well established.‘a2 The mechanisms responsible for enhanced survival in pa- tients treated with thrombolytic therapy remain contro- versial, but may be related to properties other than preservation of left ventricular function alone.3Recent studies have determined that early recanalization and sustainedpatency of the infarct-related vessel may en- hance survival in patients after myocardial infarction by contributing to improved ventricular remodeling and healing, establishing collateral blood flow to noninfarct myocardial segmentsand reducing electrical instabili- ty.3 The latter mechanism is particularly important since sudden death secondaryto malignant ventricular arrhythmia may account for up to 40% of total mortali- ty in the first year after the index infarction.4,5 In the present study, we tested the hypothesis that patients with acute myocardial infarction treated within 6 hours of symptom onset with thrombolytic therapy who attain infarct artery patency have a more stable myocardial electrical substrate and reduced prevalence of ventricular arrhythmia and late potential activity in the early postinfarct phase.In addition, the relation be- tween the time from symptom onset to initiation of thrombolytic therapy and infarct artery patency was examined to determine their impact on myocardial electrical stability. METHODS Patients: Data were obtained through a retrospec- tive review of 6 1 patients who presented with 130 min- utes of chest pain, ST-segmentelevation Ll mm in L2 contiguous leads and who received treatment within 6 1410 THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 68 DECEMBER 1, 1991