Introduction: Reticulated platelets (RPs), represent the youngest subpopulation of the platelet pool. RPs are characterized by increased RNA content, more dense granules, higher levels of surface activation markers, and probably increased reactivity. In the acute inflammatory phase of post-Ischemia/Reperfusion (I/R) lesions, reticulated platelets may contribute to adverse outcome through through evasion of conventional antiplatelet therapy and interaction with endothelial cells and CM, as well as by leukocyte recruitment and activation. 

Methods: REPL-AMI (reticulated platelets in myocardial infarction) is an observational clinical study in patients with ST-elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI). To elucidate the potential pathophysiologic relevance of RPs in STEMI patients, the temporal kinetics of circulating RPs as well as correlating RPs with post-I/R infarct size and cardiac function are examined. Immature platelet fraction (%IPF) and immature platelet counts (IPC) are measured in blood samples from STEMI patients and patients with stable coronary artery disease (CCS) before and after successful angioplasty. Leukocyte-platelet aggregates (LPA) are measured as a marker of platelet reactivity and heterocellular interaction. From contrast enhanced CINE and late gadolinium enhancement (LGE) imaging, myocardial salvage index is calculated for every patient with available MRI data. The primary endpoint is to detect a correlation between %IPF and salvage index, exploratory analyses evaluate for correlations between %IPF or LPA and the extent of LGE. 

Results: So far, 83 patients with STEMI (57 with a cardiac MRI performed) and 17 patients with CCS were enrolled. Median myocardial salvage index was 38.0 % [16.65 to 56.50], median left ventricular ejection fraction was 49.00 % [41.50 to 56.50], median IPF at presentation in CCS and STEMI patients was 3.0 [2.2 to 3.9] and 3.8 [2.7 to 5.8], respectively. Currently, no significant correlation between RP levels at presentation and myocardial salvage index and no significant kinetic of RP levels following STEMI was observed. 

We found significantly higher granulocyte-platelet aggregate levels in CCS vs STEMI patients on day 1 after PCI. Additionally, we see a trend towards this effect for other leukocyte populations. More detailed analyses and updated data will be reported.

Conclusion: The anticipated output of the project is to understand how RPs contribute to myocardial damage following I/R, in comparison to non-RP. So far, we could find significantly lower granulocyte-platelet aggregates in peripheral blood samples of STEMI patients. This effect could be caused by a shift of these aggregates into the infarcted myocardium.