Thrombolysis in postinfarction angina

Postinfarction angina carries a poor prognosis, with a 20-70% incidence of recurrent myocardial infarction (MI) or death within the subsequent 3-6 months. The pathophysiologic mechanisms causing postinfarction angina may include thrombus, complex coronary arterial lesions that form a nidus for thrombus formation, inadequate collateral supply following acute MI, or intimal endothelial dysfunction. The role of thrombus has been established in the pathophysiology of Q-wave MI, and thrombolytic treatment of patients presenting with acute transmural MI has been shown to salvage left ventricular function and to reduce mortality. However, thrombolytic therapy for the acute MI does not reduce the incidence of recurrent ischemia or infarction, as is evident from the 18-26% incidence of recurrent ischemia reported in the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) and Thrombolysis in Myocardial Infarction (TIMI) trials. In the Gruppo Itaiiano per lo Studio della Streptochinasi nell Infarto Miocardico (GISSI) study the incidence of reinfarction was documented as 4% in the streptokinase group, which was actually significantly greater than in the placebo group (2%). In a randomized placebo-controlled study of thrombolysis for postinfarction angina, 29 patients were randomized to placebo (P group, n = 17) or to thrombolytic therapy (T group, n = 12). Patient groups were similar with respect to age, location of MI, ejection fraction, severity of coronary artery disease, and antianginal therapy. Patients underwent coronary angtography 6 ± 1 days postinfarction. Filling defects consistent with intracoronary thrombus was seen in 11 of 12 T group patients and in 11 of 17 P group patients prior to treatment. Lysis occurred in 7 of 11 T patients and 1 of 11P (p < 0.02). Holter-detected silent ischemia was compared pre- and posttherapy. Of patients with pretherapy Holter studies, silent ischemia occurred in 8 of 15 P patients (1.7 ± 0.33 episodes/24 hr, lasting 27.9 ± 12.1 min/24 hr) and in 2 of 9 T patients (0.6 ± 0.4 episodes/24 hr lasting 9.4 ± 3.1 min/24 hr). There was no significant change in the amount of silent ischemia following therapy in either group. Clinical ischemic events occurred in 3 of 12 T patients and in 5 of 17 P patients (no difference between the 2 groups). This study showed that thrombus was commonly seen in patients with postinfarction angina, and thrombolytic therapy could successfully lyse the clot 6 days postinfarction. However, despite achieving successful thrombolysis, in patients who were already receiving an intensive antianginal regimen for postinfarction angina, thrombolytic therapy did not result in an improvement in Holter-detected or clinical ischemia.