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Thrombolysis in postinfarction angina
P Ouyang1, E P Shapiro, S O Gottlieb
1Division of Cardiology, Francis Scott Key Medical Center, Baltimore, Maryland 21224.
Insights
Postinfarction angina often leads to recurrent myocardial infarction (MI). This study investigated thrombolytic therapy
Area of Science:
- Cardiology
- Vascular Medicine
- Interventional Cardiology
Background:
- Postinfarction angina is associated with a high risk of recurrent myocardial infarction (MI) or death within months.
- Pathophysiological mechanisms include thrombus formation, complex coronary lesions, inadequate collateral circulation, and endothelial dysfunction.
- While thrombolytic therapy improves outcomes in acute MI, its effect on reducing recurrent ischemia post-MI is unclear.
Purpose of the Study:
- To evaluate the efficacy of thrombolytic therapy in treating postinfarction angina.
- To assess the impact of thrombolysis on intracoronary thrombus and silent ischemia in patients with postinfarction angina.
Main Methods:
- A randomized placebo-controlled trial involving 29 patients with postinfarction angina.
- Patients were randomized to receive either thrombolytic therapy (T group, n=12) or placebo (P group, n=17).
- Coronary angiography was performed post-MI, and Holter monitoring assessed silent ischemia before and after treatment.
Main Results:
- Intracoronary thrombus was present in most patients in both groups before treatment.
- Thrombolytic therapy resulted in lysis of intracoronary thrombus in a significantly higher proportion of patients in the T group compared to the P group (p < 0.02).
- Data on silent ischemia changes were collected but not detailed in the truncated abstract.
Conclusions:
- Thrombolytic therapy can effectively lyse intracoronary thrombus in patients with postinfarction angina.
- Further research is needed to determine the clinical impact of thrombolysis on recurrent ischemia and long-term outcomes in this patient population.
Abstract:
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 Italiano 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 angiography 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 11 P (p less than 0.02). Holter-detected silent ischemia was compared pre- and posttherapy.(ABSTRACT TRUNCATED AT 250 WORDS)