PLATELET ACTIVATION DURING DOBUTAMINE STRESS ECHOCARDIOGRAPHY

Background Dobutamine stress echocardiography (DSE) is a common, usefu l test for the evaluation of coronary artery disease. Two of 650 patie nts who underwent DSE at our institution sustained nonfatal myocardial infarction either during DSE or shortly thereafter. Although DSE is a ssociated with low morbidity rates, this rate is higher than our exper ience with exercise treadmill testing (ETT). Methods Six individuals w ho did not undergo DSE or rn were enrolled to evaluate direct in vitro effects of dobutamine on platelets. Nine patients undergoing DSE and seven patients undergoing Err were enrolled to evaluate in vivo platel et activation. We used flow cytometry and fluorescent-labeled monoclon al antibodies to activation-dependent platelet antigens to detect dobu tomine-associared platelet activation both in vitro and in vivo. Resul ts In vitro we found a synergistic increase in epinephrine-induced CD6 2 expression in the presence of dobutamine. The response to the combin ation of dobutamine and epinephrine was 151% to 565% of the expected r esponse. In vivo there was a dose-and time-dependent rise in the perce ntage of platelets expressing CD62 in all nine subjects undergoing DSE . The median percentage of platelets expressing CD62 was 1.6% (range 0 .1% to 6.8%), 6.5% (range 0.2% to 11.7%), 11.6% (range 5.9% to 19.1%), and 11.4% (range 7.2% to 25.0%) in the samples obtained at baseline, 20 mu g/kg/min of dobutamine, 40 mu g/kg/min of dobutamine, and during the recovery phase, respectively (repeated measures analysis of varia nce, p = 0.02). There was no increase in CD62 expression on platelets obtained from seven patients at peak Err. The median percentage of CD6 2 at baseline ETT was 1.9% (range 0.2% to 7.3%) and at peak was 2.6% ( range 0.4% to 7.0%) (p = 0.156, Wilcoxon signed rank test). Conclusion We conclude that platelet activation occurs in vivo in patients under going DSE and that this may be caused by a synergistic effect of dobut amine with physiologic platelet agonists.