This review summarizes the pathophysiological mechanisms of unstable angina and the evolution of its medical and interventional management.
Summarizes unstable angina mechanisms and therapies; leaves open questions on integrating newer interventions into practice.
Unstable angina is a major cause of morbidity in the United States. In recent years, researchers have identified plaque rupture with subsequent vessel thrombosis as the initial events in the development of ischemic coronary disease. Furthermore, the role of platelet aggregation in thrombogenesis is well characterized. Traditional treatment modalities for unstable angina include pharmacologic agents such as heparin, aspirin, nitroglycerin, calcium channel antagonists, and ß-adrenergic antagonists. Improved medical technology has expanded the management of unstable angina to include use of percutaneous transluminal coronary angioplasty. Recently, advances in molecular biology have provided the opportunity to develop antithrombin-III independent anticoagulants and platelet receptor antibodies to inhibit vessel thrombosis.
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Johnson et al. (1995) studied this question.
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