Acute thrombocytopenia by antibody-induced platelet depletion, but not chronic thrombocytopenia, reduced infarct size and improved cardiac function 24 hours and 21 days post-AMI in mice.
Does acute or chronic thrombocytopenia protect against left ventricular dysfunction after acute myocardial infarction in mice?
Acute, but not chronic, thrombocytopenia protects left ventricular function and reduces infarct size post-myocardial infarction in mice by reducing platelet-mediated inflammation and scar formation.
Background: Platelets are major players of thrombosis and inflammation after acute myocardial infarction (AMI). The impact of thrombocytopenia on platelet-induced cellular processes post AMI is not well defined. Methods: The left anterior descending artery was ligated in C57/Bl6 mice and in two thrombocytopenic mouse models to induce AMI. Results: Platelets from STEMI patients and from C57/Bl6 mice displayed enhanced platelet activation after AMI. This allows platelets to migrate into the infarct but not into the remote zone of the left ventricle. Acute thrombocytopenia by antibody-induced platelet depletion resulted in reduced infarct size and improved cardiac function 24 h and 21 days post AMI. This was due to reduced platelet-mediated inflammation after 24 h and reduced scar formation after 21 days post AMI. The collagen composition and interstitial collagen content in the left ventricle were altered due to platelet interaction with cardiac fibroblasts. Acute inflammation was also significantly reduced in Mpl−/− mice with chronic thrombocytopenia, but cardiac remodeling was unaltered. Consequently, left ventricular function, infarct size and scar formation in Mpl−/− mice were comparable to controls. Conclusion: This study discovers a novel role for platelets in cardiac remodeling and reveals that acute but not chronic thrombocytopenia protects left ventricular function post AMI.
Reusswig et al. (Fri,) conducted a other in Acute myocardial infarction. Acute and chronic thrombocytopenia vs. Controls was evaluated on Infarct size and cardiac function. Acute thrombocytopenia by antibody-induced platelet depletion, but not chronic thrombocytopenia, reduced infarct size and improved cardiac function 24 hours and 21 days post-AMI in mice.
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