Electrophysiologic effects of thrombolytic therapy in patients with a transmural anterior myocardial infarction complicated by left ventricular aneurysm formation

AbstractTo assess the effects of early thrombolytic therapy on the incidence of clinical and induced ventricular arrhythmias in high risk postmyocardial infarction patients, 32 patients with a transmural anterior myocardial infarction complicated by left ventricular aneurysm formation were prospectively evaluated. Sixteen patients (Group A) received routine care because of contraindication to thrombolytic therapy or other factors and 16 (Group B) received either tissue plasminogen activator or streptokinase within 6 h of the onset of chest pain. The two groups were similar in left ventricular ejection fraction (mean ± SD, 28 ± 9% [Group A] versus 30 ± 8% [Group B]) and occurrence of spontaneous nonsustained ventricular tachycardia, new bundle branch block and congestive heart failure. Group B patients had higher peak creatine kinase MB levels (446 ± 336 versus 205 ± 120 IU; p = 0.017) and earlier time to peak creatine kinase values (13.4 ± 6.6 versus 19.1 ± 6.1 h; p = 0.006).Twenty patients who had no clinical sustained ventricular arrhythmias underwent electrophysiologic study 13 ± 6 days after infarction. Ventricular tachycardia was induced during the study in 7 (88%) of 8 Group A patients, but in only 1 (8%) of 12 Group B patients given thrombolytic therapy (p = 0.0008).During a mean follow-up period of 11 ± 8 months, eight Group A patients (50%) died suddenly or were resuscitated from sustained ventricular tachycardia; all Group B patients are alive and have had no clinical arrhythmic events (p = 0.002). Four of the 8 patients with inducible ventricular tachycardia at electrophysiologic study have had a clinical arrhythmic event, whereas the 12 patients without inducible tachycardia are arrhythmia free (p = 0.020).Thus, patients with a transmural anterior myocardial infarction and subsequent left ventricular aneurysm formation had an improved arrhythmic outcome if they received early thrombolytic therapy. Furthermore, thrombolytic therapy dramatically improved electrical stability as elucidated by electrophysiologic study. These results were observed despite the failure of thrombolytic therapy to significantly improve global left ventricular ejection fraction or affect clinical variables normally associated with a poor prognosis