Evaluation of platelet activation, fibrinolysis, and hemostatic activation during high dose dobutamine stress echocardiography

Abstract

Acute myocardial infarction during high-dose dobutamine stress echocardiography (DSE) has been reported in patients with no indication of severe obstructive coronary artery disease, but the mechanism of thrombosis remains unclear. We hypothesized that an increase in platelet and hemostatic activation secondary to high dose dobutamine might be a contributing factor. Twelve patients undergoing outpatient DSE and with either a normal DSE results (n = 11) or normal coronaries by follow-up angiography (n = 1) were included. Patients with documented ischemia were excluded to eliminate the possibility of ischemia-induced platelet activation. Three separate samples of blood were drawn at baseline, peak dobutamine infusion and 30 minutes after the end of infusion. Blood was assayed for beta-thromboglobulin (BTG) as a platelet activation marker, D-Dimer as a fibrinolytic marker, and prothrombin fragment 1.2 (F1.2) as a marker of thrombin formation. Using ANOVA analysis, there were no significant differences between BTG, D-Dimer or F1.2 at baseline, peak dobutamine and half-hour into recovery. In this study, high dose DSE did not result in a significant increase in platelet, hemostatic or fibrinolytic activation in patients with low risk for obstructive coronary artery disease.