Correlation between burst of thrombin and microvacular obstruction (no reflow) during ST Elevation Myocardial Infarction treated by primary percutaneous coronary Intervention

Abstract

Background: The thrombotic burden at the acute phase of STEMI is a consequence of platelet and coagulation activation. Objective: To evaluate the generation of thrombin during acute phase of STEMI. In order to study the consequence, thrombin generation was correlated with other markers of coagulation activation, markers of cellular activation, microvascular injury and infarct size. Methods: Thirty six STEMI patients admitted for primary Percutaneous Coronary Intervention (PCI) were enrolled. Blood samples were collected before angioplasty, at the end of angioplasty and 2, 6, 12 and 24 hours after angioplasty. Plasma thrombin antithrombin complexes and d-dimers were evaluated by ELISA methods, fibrinogen by clothing test. Platelets and endothelial microparticles were determined by flow cytometry analysis. Microvascular obstruction was assessed by the myocardial blush grade. Myocardium at risk was determined on angiography and infarct size was assessed by area under the curve of plasma troponin and CK-MB. Results: A burst of thrombin occurred during PCI in 69% of patients and was associated with increased fibrinogen, d-dimer, circulating platelets and endothelials microparticles, when compared with patient without burst (p<0.05). Prolonged ischemic time and significant myocardium at risk were correlated with a higher level of thrombin generation (p<0.05). Thrombin generation was correlated with alteration of myocardial blush (p<0.05) and higher troponin I and CK levels (p<0.05). Conclusion: This study showed a burst of thrombin at the time of primary PCI during STEMI in two third of patients. When present, this burst was associated with more cellular, myocardial and micro-vascular damage.