Observational study of circulating endothelial cell profiles in patients with non-ST-elevation myocardial infarction stratified by plaque erosion or rupture identified by optical coherence tomography: The Plaque Erosion Pilot Study ii (PEPSii)

Introduction Myocardial infarction (MI) remains a leading global cause of death and disability. There is growing evidence that about 40% of MI cases have plaque erosion due to mass endothelial cell apoptosis and exposure of pro-thrombotic underlying extracellular matrix, in contrast to shearing of endothelial cells during more conventional plaque rupture events. This hypothesis suggests that circulating endothelial cells (CEC) would be higher in MI cases of plaque erosion compared to plaque rupture. Accordingly, I set up a study to measure levels of CEC in patients with non-ST elevation MI (NSTEMI) who underwent plaque morphology evaluation to stratify cases into plaque erosion or rupture. Methods This was an observational study which enrolled patients undergoing elective percutaneous coronary intervention (PCI), a feasibility group to establish and refine research methods, and NSTEMI undergoing PCI (cases). Peripheral venous blood samples were obtained to assess CEC and platelet-leukocyte aggregates (PLAs) using flow cytometry. Culprit plaques were imaged using optical coherence tomography (OCT) and independently classified as plaque rupture or erosion. CEC levels in NSTEMI patients were compared between plaque erosion and plaque rupture cases. Results Overall, 22 NSTEMI patients and 11 feasibility patients were recruited. Of the NSTEMI patients, 7 did not have plaque morphology, either due to missing data, or inability to agree on a classification. CEC levels, as a percent CD45-ve PBMCs, were significantly higher in the plaque erosion group (17.4%; n=7) compared to the plaque rupture group (9%; n=8: p=0.0012). PLA analysis showed no significant differences between erosion and rupture (p=0.8665). Conclusion Higher levels of CEC in the plaque erosion group compared to rupture supports the hypothesis of mass endothelial cell denudation as a causative mechanism. Further research is needed to investigate trigger factors for erosion and to understand if specific therapeutic strategies are needed for these patients