Thrombin induced platelet–fibrin clot strength measured by thrombelastography is a novel marker of platelet activation in acute myocardial infarction

Abstract

After disruption of coronary arteriosclerotic plaques, platelet activation plays a causal role in the subsequent thrombus formation, leading to acute myocardial infarction (AMI) [ [1] Trip M.D. Cats V.K. van Capelle F.J.L. et al. Platelet hyperreactivity and prognosis in survivors of myocardial infarction. N Engl J Med. 1990; 322: 1549-1554 Crossref PubMed Scopus (536) Google Scholar ]. Although many attempts have been made to monitor platelet activity to detect atherothrombotic process, thus far an easy, useful and specific assay has not been discovered. As a point-of-care testing, thrombelastography (TEG) specifically evaluates the contribution of platelet to thrombosis. Of the TEG parameters, thrombin-induced platelet–fibrin clot strength (MAthrombin) has been shown to reflect the maximal potential platelet reactivity [ [2] Gurbel P.A. Bliden K.P. Guyer K. et al. Adenosine diphosphate-induced platelet-fibrin clot strength: a new thrombelastographic indicator of long-term poststenting ischemic events. Am Heart J. 2010; 160: 346-354 Abstract Full Text Full Text PDF PubMed Scopus (139) Google Scholar ]. Interestingly, it has been demonstrated that MAthrombin exhibited significant correlation with other prothrombotic markers and with C-reactive protein and were increased in patients with angina as compared to asymptomatic patients [ [3] Tantry U.S. Bliden K.P. Suarez T.A. et al. Hypercoagulability, platelet function, inflammation and coronary artery disease acuity: results of the Thrombotic RIsk Progression (TRIP) study. Platelets. 2010; 21: 360-367 Crossref PubMed Scopus (61) Google Scholar ]. Taken together, these findings suggest the potential of MAthrombin for diagnostic evaluation of pathophysiological state of hypercoagulability in AMI patients. However, the association between MAthrombin and AMI has not yet been clarified. In the present study, we investigated the level of MAthrombin in patients with AMI and other forms of coronary atherosclerosis disease (CAD) and found that there is a dynamic elevation of MAthrombin after the onset of myocardial infarction.