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- W2886201631 abstract "Introduction: Cardiac rupture is a major lethal complication of acute myocardial infarction (MI). Despite significant advances in reperfusion strategies, mortality from cardiac rupture remains high. Studies suggest that cardiac rupture is accelerated by thrombolytic therapy. However, the mechanisms by which thrombolytic therapy leads to the development of cardiac rupture remains largely unknown. Hypothesis: In this study, we tested the effect of thrombin protease activated receptor (PAR) 4 deficiency on cardiac rupture and function after MI. Methods and Results: PAR4 mRNA and protein expression were increased in human ischemic and dilated cardiomyopathy and in response to MI in mice. PAR4 gene deletion in mice protected the heart against acute MI by reducing inflammatory signals and cardiomyocyte apoptosis. However, PAR4-deficient mice showed significantly increased mortality and cardiac rupture rates (3-fold increase vs wild-type mice, P<0.05) along with impaired functional recovery after chronic MI. Pat..." @default.
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- W2886201631 date "2016-11-11" @default.
- W2886201631 modified "2023-09-26" @default.
- W2886201631 title "Abstract 14611: Protease-Activated Receptor 4 Deficiency Impairs Resolution of Inflammation and Predisposes the Heart to Cardiac Rupture After Myocardial Infarction" @default.
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