Biological profiling in the spectrum of acute coronary syndrome: characterizing patients from MINOCA to NSTEMI with different features of the culprit plaque

Abstract Background In the last two decades, the development of procedures and tools such as coronary angiography and optical coherence tomography (OCT) have made it possible to highlight several aspects of acute coronary syndromes (ACS), identifying multiple subgroups such as patients with myocardial infarction with non-obstructive coronary arteries (MINOCA) and patients with Non-ST-Elevation Myocardial Infarction (NSTEMI) and ruptured fibrous cap (RFC) or intact fibrous cap (IFC) culprit lesions. The aim of the study is to better characterize the ACS spectrum by evaluating the biological profile of non-characterized NTSEMI, RFC-NSTEMI, IFC-NSTEMI, and MINOCA patients. Methods We enrolled 56 consecutive patients presenting with ACS, specifically 16 patients with non-characterized NSTEMI, 12 patients with RFC-NSTEMI, 8 patients with IFC-NSTEMI, and 20 patients with MINOCA. Biological samples were collected and stored. We performed gene expression analysis through qRT-PCR technique for 21 genes. Results Our data displayed several differences in gene expression levels involved in inflammation, cellular adhesion, extracellular matrix turnover, and oxidative stress between the groups under examination. We observed no significant difference between non-characterized NSTEMI and MINOCA for all the studied genes. Alongside, MINOCA displayed significantly lower levels of the following genes than RFC and IFC patients: CD44, GPX1, ICAM1, PLA2G7, SOD1, and VEGFA. Furthermore, when compared with IFC patients, MINOCA showed lower levels of EDN1, LGALS8, MMP1, and TNF, and non-characterized NSTEMI showed a lower gene expression of CD31, ICAM1, and PI16. Finally, CD44, EDN1, GPX1, LGALS8, NOS3, SOD1, TFRC, and VEGFA were more expressed in RFC and IFC compared to non-characterized NSTEMI patients. Conclusions Our preliminary data, besides exploring new pathways in MINOCA patients, reflects the need for characterization and patients’ stratifications in the clinical management of ACS, since no differences were observed between non-characterized NSTEMI and MINOCA. This result may indicate that a one size fits all approach is not the most suitable since a plaque could be an innocent bystander and should be treated accordingly. A precision medicine approach that recognizes the presence of obstructive plaque and defines the type of culprit plaque (i.e., RFC or IFC) could identify better treatment, for a tailored therapy, allowing better prognosis and quality of life.Figure