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Thrombolytic therapy for unstable angina
S Borzak1, J Verter, H S Bajwa
1Henry Ford Heart & Vascular Institute, Division of Cardiovascular Medicine, Henry Ford Hospital, Detroit, MI 48202.
Insights
Thrombolytic therapy for unstable angina (UA) shows a trend toward fewer clinical events but increases bleeding complications. Larger trials are needed to determine its net clinical value in treating UA.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Unstable angina (UA) pathogenesis involves intracoronary thrombus formation.
- Thrombolytic therapy is standard for myocardial infarction but not widely accepted for UA.
Purpose of the Study:
- To review the clinical value of thrombolytic therapy for unstable angina.
- To assess the efficacy and safety of thrombolytic agents in UA patients.
Main Methods:
- Review of evidence supporting thrombus formation in UA.
- Analysis of studies on thrombolytic therapy's angiographic and clinical endpoints.
- Synthesis of data from twelve randomized controlled trials in 611 UA patients.
Main Results:
- Thrombolytic therapy reduced angiographically detected thrombus but had minimal effect on luminal narrowing.
- A trend towards fewer clinical events (death, infarction, revascularization) was observed in treated patients.
- Increased bleeding complications were noted in patients receiving thrombolytic therapy.
Conclusions:
- The clinical efficacy of thrombolytic therapy for UA cannot be definitively excluded.
- Insufficient patient numbers in existing trials may limit definitive conclusions.
- Larger, more definitive trials are required to establish the net clinical value of thrombolytic therapy for unstable angina.
Abstract:
Thrombolytic therapy for unstable angina has not gained acceptance as a primary treatment for unstable angina (UA) despite the evidence showing a reduction in mortality when these agents are given for myocardial infarction. The purpose of this review is to examine the clinical value of thrombolytic therapy for UA. The multiple lines of evidence supporting intracoronary thrombus formation as a key mechanism in the pathogenesis of UA are reviewed. Studies examining the effect of thrombolytic therapy on angiographic endpoints have shown little effect on the extent of luminal narrowing, but do reveal a decrease in angiographically detected thrombus. Twelve randomized, controlled trials of thrombolytic agents in 611 UA patients with predefined clinical endpoints have been published. These trials varied widely in design and adjunctive therapy both in treated and control grops. Review of these trials show a tendency to fewer clinical events such as death, infarction, and need for revascularization in treated patients, with a corresponding increase in bleeding complications. Clinical efficacy of thrombolytic therapy cannot be excluded by the available data, perhaps in part because of insufficient numbers of patients treated. Determination of the net clinical value of thrombolytic therapy must await larger and more definitive trials.