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Peripheral Venous Platelet Aggregates in Patients With Unstable Angina Pectoris and Acute Myocardial Infarction

Department of Internal Medicine, Cardiac Unit, University of Texas Southwestern ; Medical School, Dallas, Texas.

James T. Willerson

Ischemic Heart Center, L5.134 University of Texas Southwestern Medical School 5323 Harry Hines Boulevard Dallas, Texas 75235

In vivo peripheral venous platelet aggregates (PVPA) have been demon strated in patients with myocardial infarction (MI), transient cerebral ischemic attacks (TIAs), and acute arterial insufficiency by the platelet count ratio (PCR) method. But PVPA determinations have not been reported in patients with unstable angina pectoris (UA), controls have not been specified as acutely ill in earlier studies using this technique, and variability of the method has not been presented in detail. Because platelet aggregation has been mentioned as a possible mechanism for perpetuating myocardial ischemia, we studied 21 acutely ill noncardiac control (NC) patients, 17 UA patients, and 13 MI patients for PVPA.

PCR represents ratio of platelet counts obtained when identical aliquots of blood were drawn into two syringes containing formalin-EDTA and EDTA respectively. Free flow was demonstrated before blood was drawn. Mean PCR was 0.90 ± 0.01 (SE) in NC, 0.85 ± 0.02 in UA, and 0.85 ± 0.02 in MI. In the subset of 7 patients with acute transmural MI, PCR was 0.83 ± 0.02. Only this subset was significantly different from NC (P < 0.001). PCR did not vary significantly with age or sex. Aspirin history was positive in 25-30% of the patients in each group and raised PCR by an average of 0.04 units. When PCR was repeated after 45 minutes in 6 patients, moderate variability with a mean absolute change in PCR of 0.08 was noted.

Our data fail to support an etiologic role for circulating platelet aggre gates in initiating UA. Clinical trials of platelet inhibitors and experimen tal models of arterial insufficiency probably offer the greatest chance of further defining the potential etiologic role of platelet aggregation in initiating or perpetuating myocardial ischemic phenomena.

Angiology, Vol. 28, No. 10, 695-701 (1977)
DOI: 10.1177/000331977702801006


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