Transcriptome analysis constitutes one of the major methods of elucidation of the genetic basis underlying the pathogenesis of various diseases. The post-transcriptional regulation of gene expression is mainly provided by microRNAs. Their remarkable stability in biological fluids and their high sensitivity to disease alteration indicates their potential role as biomarkers. Given the high mortality and morbidity of cardiovascular diseases, novel predictive biomarkers are sorely needed. Our study focuses for the first time on assessing potential biomarkers of acute coronary syndrome (ACS) based on the microRNA profiles of platelets. The study showed the overexpression of eight platelet microRNAs in ACS (miR-142-3p; miR-107; miR-338-3p, miR-223-3p, miR-21-5p, miR-130b-3p, miR-301a-3p, miR-221-3p) associated with platelet reactivity and functionality. Our results show that the combined model based on miR-142-3p and aspartate transaminase reached 82% sensitivity and 88% specificity in the differentiation of the studied groups. Furthermore, the analyzed miRNAs were shown to cluster into two orthogonal groups, regulated by two different biological factors. Bioinformatic analysis demonstrated that one group of microRNAs may be associated with the physiological processes of platelets, whereas the other group may be linked to platelet–vascular environment interactions. This analysis paves the way towards a better understanding of the role of platelet microRNAs in ACS pathophysiology and better modeling of the risk of ACS.

Background: The study aimed to examine the relationship between vitamin D levels and the extent of coronary stenotic lesions in patients with ST-segment elevation myocardial infarction (STEMI). Experimental evidence points to the involvement of multiple factors in coronary plaque formation, including vitamin D. Little is known, however, about the association of vitamin D level with the intensity of atherosclerosis. Methods: Serum concentrations of 25-hydroxyvitamin D [25(OH)D] were measured in 130 consecutive patients with the first acute STEMI treated with primary percutaneous coronary intervention. STEMI was the first symptom of coronary artery disease (CAD). The study population was divided into patients with single and multi-vessel CAD. The angiographic severityof CAD was also determined based on the Gensini score. Results: The median 25(OH)D concentration was 11.12 ng/mL (25th and 75th percentile: 6.05; 17.12). Insufficient (20–30 ng/mL), deficient (10–20 ng/mL) and severely deficient(< 10 ng/mL) 25(OH)D levels were present in 18%, 35% and 45% of the individuals, respectively. Only 2 (2%) of patients had proper 25(OH)D levels (> 30 ng/mL). The 25(OH)D concentrations between patients with single- and multi-vessel CAD did not differ significantly (10.2 vs. 11.4 ng/mL, p = 0.62). There was no significant correlation between 25(OH)D levels and Gensini score (r = –0.0221, p = 0.81). Conclusions: The study demonstrated that vitamin D level is not associated with the severity of coronary lesions in patients with the first STEMI. A high prevalence of vitamin D deficiency in these patients was confirmed. Background: The study aimed to examine the relationship between vitamin D levels and the extent of coronary stenotic lesions in patients with ST-segment elevation myocardial infarction (STEMI). Experimental evidence points to the involvement of multiple factors in coronary plaque formation, including vitamin D. Little is known, however, about the association of vitamin D level with the intensity of atherosclerosis. Methods: Serum concentrations of 25-hydroxyvitamin D [25(OH)D] were measured in 130 consecutive patients with the first acute STEMI treated with primary percutaneous coronary intervention. STEMI was the first symptom of coronary artery disease (CAD). The study population was divided into patients with single and multi-vessel CAD. The angiographic severityof CAD was also determined based on the Gensini score. Results: The median 25(OH)D concentration was 11.12 ng/mL (25th and 75th percentile: 6.05; 17.12). Insufficient (20–30 ng/mL), deficient (10–20 ng/mL) and severely deficient(< 10 ng/mL) 25(OH)D levels were present in 18%, 35% and 45% of the individuals, respectively. Only 2 (2%) of patients had proper 25(OH)D levels (> 30 ng/mL). The 25(OH)D concentrations between patients with single- and multi-vessel CAD did not differ significantly (10.2 vs. 11.4 ng/mL, p = 0.62). There was no significant correlation between 25(OH)D levels and Gensini score (r = –0.0221, p = 0.81). Conclusions: The study demonstrated that vitamin D level is not associated with the severity of coronary lesions in patients with the first STEMI. A high prevalence of vitamin D deficiency in these patients was confirmed.

Context: Cardiogenic shock (CS) still remains one of the main causes of death in acute myocardial infarction (AMI).Objective: The aim of this study was to evaluate the prognostic value of midregional (MR)-proadrenomedullin in AMI complicated by CS.Methods: Forty-seven consecutive patients were included in our prospective observational study. All patients underwent coronarography and successful percutaneous coronary intervention (PCI). Plasma levels of MR-proADM were measured by a immunofluorescence method. The primary endpoint of the study, defined as cardiovascular death, occurred in 17 patients (36%).Results and conclusion: Elevated plasma level of MR-proADM, determined 24h after diagnosis of CS could be a predictor of in-hospital mortality in patients with AMI complicated by CS.

Before introduction of reperfusion therapy, fever was frequently observed in patients with acute myocardial infarction (AMI). Little is known about this symptom during the widespread use of primary percutaneous coronary intervention (pPCI). The aim of this study was to assess, whether body temperature is a predictor of impaired left ventricular systolic function in patients with AMI. Our cohort included 171 patients (48 women) aged 57 (51-67) years, admitted due to the first AMI with ST elevation treated with successful pPCI. Standard body temperature measurements were performed twice a day. Left ventricular function was assessed by echocardiography using the wall motion score index (WMSI) and ejection fraction (EF). The following inflammatory response markers were determined on admission: C-reactive protein, fibrinogen and white blood cell count. Within 48 h of observation the median (1(st); 3(rd) quartiles) peak body temperature was 37.0°C (36.7-37.2°C). A temperature above 37.5°C was observed only in 17 (10%) patients. There was no significant correlation between peak body temperature and any of the determined inflammatory response markers. WMSI was assessed at 1.3 (1.1-1.6), whereas EF at 56% (49-62%). There was no significant correlation between the left ventricular function and peak body temperature or determined markers of inflammation. In the era of pPCI and aggressive antiplatelet treatment, fever is not a common symptom associated with uncomplicated AMI and thus not correlated with left ventricular function and markers of inflammation.

Proteomic analyses based on mass spectrometry provide a powerful tool for the simultaneous identification of proteins and their signatures. Disorders detection at the molecular level delivers an immense impact for a better understanding of the pathogenesis and etiology of various diseases. Acute coronary syndrome (ACS) refers to a group of heart diseases generally associated with rupture of an atherosclerotic plaque and partial or complete thrombotic obstruction of the blood flow in the infarct-related coronary artery. The essential role in the pathogenesis of ACS is related to the abnormal, pathological activation of blood platelets. The multifactorial and complex character of ACS indicates the need to explain the molecular mechanisms responsible for thrombosis. In our study, we performed screening and comparative analysis of platelet proteome from ACS patients and healthy donors. Two-dimensional fluorescence difference gel electrophoresis and nanoscale liquid chromatography coupled to tandem mass spectrometry showed altered expressions of six proteins (i.e., vinculin, transgelin-2, fibrinogen β and γ chains, apolipoprotein a1, and tubulin β), with the overlapping increased expression at the mRNA level for transgelin-2. Dysregulation in protein expression identified in our study may be associated with an increased risk of thrombotic events, correlated with a higher aggregability of blood platelets and induced shape change, thus explaining the phenomenon of the hyperreactivity of blood platelets in ACS.