Heinrich-Heine University Medical Center, Department of Vascular and Endovascular Surgery, Experimental Vascular Medicine, 40225 Düsseldorf, Germany.
Heinrich-Heine University Medical Center, Department of Cardiology, Pulmonology and Angiology, 40225 Düsseldorf, Germany.
Cells. 2022 Nov 4;11(21):3500. doi: 10.3390/cells11213500.
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.
The left anterior descending artery was ligated in C57/Bl6 mice and in two thrombocytopenic mouse models to induce AMI.
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 mice with chronic thrombocytopenia, but cardiac remodeling was unaltered. Consequently, left ventricular function, infarct size and scar formation in mice were comparable to controls.
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.
血小板是急性心肌梗死（AMI）后血栓形成和炎症的主要参与者。血小板减少对 AMI 后血小板诱导的细胞过程的影响尚未明确。
结扎 C57/Bl6 小鼠和两种血小板减少症小鼠模型的左前降支，以诱导 AMI。
STEMI 患者和 C57/Bl6 小鼠的血小板在 AMI 后显示出增强的血小板活化。这使得血小板能够迁移到梗死区，但不能迁移到左心室的远隔区。通过抗体诱导的血小板耗竭导致急性血小板减少症，可使 AMI 后 24 小时和 21 天的梗死面积减小和心功能改善。这是由于 AMI 后 24 小时血小板介导的炎症减少和 21 天后疤痕形成减少所致。由于血小板与心肌成纤维细胞的相互作用，左心室的胶原组成和间质胶原含量发生改变。慢性血小板减少症小鼠的急性炎症也明显减少，但心脏重塑没有改变。因此， 小鼠的左心室功能、梗死面积和疤痕形成与对照组相当。
本研究发现了血小板在心脏重塑中的新作用，并揭示了急性而非慢性血小板减少症可保护 AMI 后左心室功能。
