Background: Platelets play a crucial role in ischemic diseases, which can lead to myocardial infarction (MI), the most leading cause of death in Western countries. In the acute phase of myocardial infarction (AMI) in patients antiplatelet intervention inhibits inflammatory cell recruitment into the infarcted myocardium. In mice knock down or inhibition of specific platelets proteins like PAR-4, GPVI or P-selectin leads to reduced infarct size and reduced inflammation in the acute phase after I/R injury.

Aims: Aim of this project is to analyze the influence of platelets in processes of inflammation and remodeling after I/R in mice besides of their thrombotic potential.

Methods: In vitro and in vivo analysis of thrombocytopenic mice after I/R injury.

Results: In the acute phase after I/R injury platelets showed enhanced integrin activation and degranulation. Thrombocytopenia in mice leads to reduced infarct size and an improved left ventricular function 24 hours and 21 days after myocardial infarction. Improved heart function was accompanied by reduced inflammation, including decreased cell-migration into the infarcted myocardium and improved cell survival in the infarct border zone as detected by reduced expression of pro-apoptotic proteins in the acute phase and reduced active caspase3 5 days after I/R.

Conclusions: Our results show that platelets modulate inflammation and cell-survival after myocardial infarction indicating platelet interaction with inflammatory and endothelial cells and migration into the infarcted border zone to induce cell apoptosis of cardiomyocytes and / or inflammatory leukocyte.

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ISTH Congress Abstracts - https://abstracts.isth.org/abstract/role-of-platelets-in-processes-of-myocardial-healing-after-myocardial-ischemia-and-reperfusion-in-mice/