Is coronary thrombolysis associated with side effects that significantly compromise clinical benefits?

Abstract

R apid restoration of coronary artery patency is a ational treatment objective in acute myocardial infarction, which has now been well established to be of clinical benefit. Currently, this objective can be approached by thrombolytic therapy with intravenous streptokinase (SK) or tissue plasminogen activator (t-PA), and by percutaneous transluminal coronary angioplasty (PTCA) . Curiously, despite its more traumatic aspects, immediate PTCA in acute myocardial infarction is associated with an unexpectedly low in-hospital mortality.‘-5 A collective mortality of 2.2% has been reported,5 and in a 395 patient-prospective randomized trial of PTCA versus t-PA, reinfarction or death in the hospital was 5.1% and 12.0% for PTCA and t-PA, respectively (p = 0.02) .l Not surprisingly, intracranial bleeding also occurred more frequently in patients treated with t-PA. This significant difference between the clinical results obtained with PTCA and thrombolysis in acute myocardial infarction may simply be related to the fact that PTCA induces a higher rate and extent of coronary artery patency than thrombolysis. Such a conclusion is supported by the findings from 1 study, that both patency and ejection fraction were significantly better after PTCA than after SK.2 By contrast, ejection fraction, both at rest and during exercise, and measured at 6 weeks, was identical in another study in which a significantly lower mortality was found after PTCA than after t-PA.’ This suggests that the mortality difference found may not have been exclusively related to a difference in reperfusion since reperfusion has been shown to correlate with ejection fraction.6 Moreover, in studies in which PTCA was performed to correct residual coronary stenosis immediately after tbrombolytic therapy, no improvement in clinical outcome was obtained.778 Therefore, differences in patency induced by coronary tbrombolysis compared with PTCA may not be the only explanation for significant differences in major clinical end points. An additional explanation may be that adverse effects associated with current thrombolytic regimens undermine their effect on coronary reperfu-