Elevated markers of fibrin formation and platelet aggregation in unstable angina are similar to those in acute myocardial infarction, supporting the role of coronary thrombosis in the pathogenesis of acute myocardial infarction.
May implicate shared thrombotic mechanisms in unstable angina and AMI; leaves open causal confirmation and practice implications pending prospective data.
Fibrinopeptide A (FpA) concentrations in plasma and in 24 hr urine specimens as well as beta-thromboglobulin (BTG) in plasma were measured in 17 patients with severe angina pectoris, including both stable and unstable angina, and in 19 patients with acute myocardial infarction. Patients with unstable angina had plasma FpA and BTG levels of 5.2 +/- 1.7 ng/ml and 91 +/- 23 ng/ml, respectively. The corresponding concentrations of FpA in the 24 hr urine specimens were 8.2 +/- 1.4 micrograms/24 hr. These values were similar to those measured in patients with acute myocardial infarction and higher than the corresponding levels in patients with stable angina (p less than .05) and in normal control subjects (p less than .01). The similarity of the platelet and coagulation findings in patients with unstable angina and in those with myocardial infarction favors the hypothesis that coronary thrombosis may play a major role in the pathogenesis of acute myocardial infarction.
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Gallino et al. (1985) studied this question.
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