Abstract
Objective Although blood thrombogenicity seems to be one of the determinant factors for the development of acute myocardial infarction (MI), it has not been dealt with in-depth. This study aimed to investigate blood thrombogenicity and its change in acute MI patients. Methods and Results We designed a prospective, observational study that included 51 acute MI patients and 83 stable coronary artery disease (CAD) patients who underwent cardiac catheterization, comparing thrombogenicity of the whole blood between: (1) acute MI patients and stable CAD patients; and (2) acute and chronic phase in MI patients. Blood thrombogenicity was evaluated by the Total Thrombus-Formation Analysis System (T-TAS) using the area under the flow pressure curve (AUC 30 ) for the AR-chip. Acute MI patients had significantly higher AUC 30 than stable CAD patients (median [interquartile range], 1,771 [1,585–1,884] vs. 1,677 [1,527–1,756], p = 0.010). Multivariate regression analysis identified acute MI with initial TIMI flow grade 0/1 as an independent determinant of high AUC 30 ( β = 0.211, p = 0.013). In acute MI patients, AUC 30 decreased significantly from acute to chronic phase (1,859 [1,550–2,008] to 1,521 [1,328–1,745], p = 0.001). Conclusion Blood thrombogenicity was significantly higher in acute MI patients than in stable CAD patients. Acute MI with initial TIMI flow grade 0/1 was significantly associated with high blood thrombogenicity by multivariate analysis. In acute MI patients, blood thrombogenicity was temporarily higher in acute phase than in chronic phase.
Highlights
Acute myocardial infarction (MI) is caused by plaque disruption and subsequent thrombotic coronary occlusion
Blood thrombogenicity was significantly higher in acute MI patients than in stable coronary artery disease (CAD) patients
Acute MI with initial TIMI flow grade 0/1 was significantly associated with high blood thrombogenicity by multivariate analysis
Summary
Acute myocardial infarction (MI) is caused by plaque disruption and subsequent thrombotic coronary occlusion. Plaque disruptions and mural thrombus formation are often detected in the coronary arteries without causing any coronary event, that is, silent plaque disruptions [1,2]. The determinant factors for mural thrombus at disrupted plaque to become occlusive have been unknown. Blood thrombogenicity is one of the well-known determinant factors of thrombus formation. It is not always stable, of which change is likely to influence the development of acute MI. A hypothesis that a temporary rise in blood thrombogenicity triggers thrombotic coronary occlusion after plaque disruption has been presented [8], it appears not to be adequately established. Previous studies investigated thrombogenic components of blood in MI patients, such as platelet function or coagulation factors activities, and suggested that blood thrombogenicity was temporarily increased in the acute phase of MI patients [9,10,11,12,13,14]; these thrombogenic components only partially reflect thrombogenicity of whole blood, which in acute MI patients has not been adequately elucidated
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