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Updated: Jun 30, 2026
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Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
Published on: May 28, 2019
[Unstable angina pectoris: coagulation disorder and its therapy]
1Cardiac Unit, Massachusetts General Hospital, Boston.
Praxis
|February 21, 1995
Summary
Unstable angina begins with plaque rupture, causing blood clots (thrombosis). Aspirin and heparin help, but new antithrombotic drugs show promise for acute coronary syndromes.
Area of Science:
- Cardiology
- Hematology
- Pathophysiology
Background:
- Unstable angina is initiated by atherosclerotic plaque rupture.
- Plaque rupture triggers platelet activation and intracoronary thrombus formation.
- Coronary thrombosis plays a key pathophysiologic role in unstable angina.
Purpose of the Study:
- To review the pathophysiology of unstable angina.
- To discuss diagnostic methods for coronary thrombosis.
- To evaluate current and emerging therapeutic strategies.
Main Methods:
- Review of existing literature on unstable angina and coronary thrombosis.
- Analysis of diagnostic techniques including autopsy, angiography, and angioscopy.
- Evaluation of clinical trial data for antithrombotic therapies.
Main Results:
- Coronary thrombosis is a hallmark of unstable angina, detectable via multiple methods.
- Biochemical markers confirm increased platelet and thrombin activity.
- Aspirin and heparin demonstrate efficacy; thrombolytic therapy is ineffective.
- Novel antithrombotic agents and GPIIb/IIIa inhibitors are under investigation.
Conclusions:
- Coronary thrombosis is central to unstable angina pathophysiology.
- Effective treatments focus on antithrombotic and antiplatelet strategies.
- Emerging therapies offer new avenues for managing acute coronary syndromes.
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