Elevated beta thromboglobulin in peripheral venous blood of patients with acute myocardial ischemia: Direct evidence for enhanced platelet reactivity in vivo

Levels of beta thromboglobulin, a platelet-specific protein, in platelet-poor plasma from peripheral venous samples of patients with acute myocardial ischemia were measured in order to obtain direct evidence for enhanced platelet reactivity in vivo in these patients and to determine the value of beta thromboglobulin assay in studying platelet reactivity in patients with ischemic heart disease. The normal beta thromboglobulin concentration in peripheral venous plasma, determined from normal volunteers and patients without known ischemic heart disease or disorders associated with enhanced platelet destruction (control group without platelet destruction), was 30.0 ± 12.6 ng/ml (mean ± standard deviation) (range 10 to 59). The mean beta thromboglobulin level in hospitalized patients with chest pain judged not to be due to acute myocardial ischemia was 33.7 ± 12.0 (range 11 to 65). Patients with deep venous thrombosis, disseminated intravascular coagulation, thrombotic thrombocytopenic purpura and idiopathic thrombocytopenic purpura provided a control group of patients with enhanced platelet destruction; the beta thromboglobulin level in this group was 131.0 ± 12.6 ng/ml (range 38 to 250). Elevated beta thromboglobulin levels were observed in 4 (16 percent) of 25 patients with stable angina pectoris (mean 45.0 ± 22.6 ng/ml, range 22 to 125), in 23 (59 percent) of 39 patients with unstable angina pectoris (mean 83.2 ± 73.7 ng/ml, range 14 to 910) and in 12 (80 percent) of 15 patients with acute myocardial Infarction (mean 118.5 ± 66.2 ng/ml, range 30 to 420) on one or more occasions during hospitalization. The mean values of patients with platelet destruction in the control group (p <0.001), patients with acute myocardial infarction (p <0.005) and patients with unstable angina pectoris (p <0.025) were significantly elevated with respect to values in patients without platelet destruction in the control group. The beta thromboglobulin levels of patients with acute myocardial infarction generally remained elevated during the first 3 to 4 hospital days. Elevation of beta thromboglobulin levels in patients with acute myocardial ischemia provides direct evidence for enhanced platelet reactivity in these patients. However, the temporal relation of the elevated beta thromboglobulin values with clinical deterioration was imprecise, so that it can not be determined from this study whether the enhanced platelet reactivity was a cause or an effect of the acute myocardial ischemia in these patients. Assay of beta thromboglobulin appears to be suitable as an indicator of enhanced platelet reactivity in patients with ischemic heart disease. Its use obviates many of the difficulties in interpretation of the various in vitro analyses of platelet function and platelet survival studies.