BACKGROUND:This study assessed the association between a novel inflammatory marker, uric acid (UA)-to-albumin ratio (UAR), and preprocedural intracoronary artery thrombus (ICAT) in ST elevation myocardial infarction (STEMI). MATERIAL AND METHODS:A total of 171 STEMI patients treated by primary percutaneous coronary intervention between February and December 2023 were evaluated prospectively in this cross-sectional study. The patients were stratified into 2 groups as low (grades 1 to 3) and high-(ICAT) groups (grades 4 and 5). To determine the independent predictors of lower and higher ICAT, multivariate regression analysis was performed. RESULTS:C-reactive protein (CRP), UA, and UAR were significantly higher in the high ICAT group (1.11 (0.3-2.8) vs 0.80 (0.10-2.8), P=0.037; 5.4 (3.5-7.2) vs 4.9 (3.4-5.6), P<0.001; 1.78 (0.82-3) vs 1.48 (0.77-2.57), P<0.001, respectively). However, albumin levels were similar between groups (3.1 (2.1-4.4) vs 3.3 (2.1-4.4), P=0.243). Higher UAR (OR: 3.95% CI: 1.23-12.7, P=0.021), lower left ventricular ejection fraction (LVEF) (OR=0.802; 95% CI 0.7537-0.872; P<0.001), longer pain-wire crossing time (OR=1; 95% CI: 1-1.02; P<0.001), and diabetes mellitus (OR=0.181; 95% CI 0.46-0.7; P<0.001) were independent predictors of ICAT. CONCLUSIONS:UAR, a marker of inflammation, is an independent predictor of ICAT in patients with STEMI.

Myocardial infarction (MI) is defined as a clinical event in which myocardial damage is evidenced in the setting of myocardial ischemia. However, patients without occlusive coronary artery stenosis can also have myocardial infarction, which is titled Myocardial Infarction with Non-Obstructive Coronary Arteries (MINOCA). In our study, we aimed to evaluate oxidative stress and inflammation responses between MINOCA and MI with coronary artery disease (CAD) patients. In this prospective, cross-sectional study, patients with elevated cardiac markers who were admitted to the cardiology clinic between March 2024 and May 2024 with the preliminary diagnosis of acute coronary syndrome were included. Patients were consecutively collected as those with an occlusive lesion on coronary angiography and those without. Routine blood samples and oxidative stress parameters were obtained and compared between groups. A total of 88 patients, including 44 MINOCA and 44 MI-CAD patients, were included in the study. The MINOCA group was significantly younger than the MI-CAD group (56.2 ± 12.5, vs. 64.7 ± 9.3, p: 0.001). While inflammatory parameters were similar between groups, dityrosine (5708 FU/mL (5311–6417) vs. 4488 FU/mL (3641–5238), p < 0.001), lipid hydroperoxide (3.6 nmol/mL (3.4–3.9) vs. 3.4 nmol/mL (3.1–3.9), p: 0.023), kynurenine (3814 ± 621 FU/mL vs. 3319 ± 680 FU/mL, p: 0.001), and malondialdehyde (17.4 nmol/mL (13.7–19.1) vs. 13.1 nmol/mL (12–14.9), p < 0.001) levels were higher in the MI-CAD group than in the MINOCA group. Although inflammation parameters did not differ between MI-CAD and MINOCA patients, oxidative stress parameters were higher in the MI-CAD group. Regardless of the presence and severity of inflammation, oxidative markers can help to assess the level of myocardial cell damage, risk stratification, and diagnosis of myocardial infarction.

Objectives: The inflammation-based Glasgow prognostic score (GPS), which comprises elevated serum C-reactive protein (CRP) and decreased albumin concentration, is the most valid inflammatory risk score in cancer. New prognostic markers are needed to predict high-risk infective endocarditis (IE) patients. In the present study, we investigated the in-hospital mortality estimation of GPS in infective endocarditis patients. Methods: The retrospectively designed study included 53 IE patients diagnosed according to Duke criteria. Demographic and clinical data of the patients were recorded and GPS levels were measured. Patients were divided into two groups according to in-hospital mortality outcomes. Glasgow prognostic score was rated as 0, 1, or 2 points based on serum albumin and C-reactive protein levels. Results: The nonsurvivor group was older and the number of patients with kidney failure or diabetes was higher in this group. Glasgow prognostic score was higher in the nonsurvivor group, while albumin levels were lower. Thirty-four patients died during intensive care unit follow-up, and the mean follow-up period was 24.1 ± 18.6 days. ROC analysis showed that the Glasgow prognostic score had a sensitivity of 82.4% and a specificity of 36.8% at a cut-off value of ≥1.5 in predicting in-hospital mortality. Chronic renal failure (OR: 6.720; 95% CI: 1.907-23.684; p = 0.003) and age (OR: 1.040; 95% CI: 1.001-1.081; p = 0.044) were the independent variables of the mortality prediction in univariate logistic regression analysis. In multivariate logistic regression analysis, only chronic renal failure (OR: 0.153; 95% CI: 0.036-0.653; p = 0.011) was found to be a significant predictor of mortality. Kaplan–Meier survival analysis revealed that long-term survival was reduced in patients with a high GPS (Log-rank: p = 0.003). Conclusions: Glasgow prognostic score level is associated with increased in-hospital mortality in IE patients. Chronic renal failure and GPS are the independent predictors of mortality.

Background and Objectives: The genetic architecture underlying myocardial infarction with nonobstructive coronary arteries (MINOCA) remains incompletely understood. While genetic research in coronary artery disease has largely focused on individual variants and susceptibility loci, genome-wide structural genomic alterations have received limited attention. We aimed to characterize and compare copy number variation (CNV) profiles in patients with MINOCA and atherosclerotic acute coronary syndrome (ACS) using high-resolution molecular karyotyping. Materials and Methods: This observational study included 83 patients with myocardial infarction, comprising 39 with MINOCA and 44 with atherosclerotic ACS. Genome-wide molecular karyotyping was performed using the CytoScan HT-CMA 1000K chromosomal microarray platform(Thermo Fisher Scientific, Waltham, MA, USA). Genomic gains and losses were systematically characterized according to their chromosomal location, recurrence, and associated gene annotations, enabling a comprehensive comparison of structural genomic patterns between the two clinical phenotypes. Results: Genome-wide analysis identified 221 CNV events, including 109 in MINOCA and 112 in atherosclerotic ACS. Copy number gains accounted for 65 and 78 events, respectively, whereas losses accounted for 44 and 34 events. Recurrent alterations involved 17q21.31, 19p12, and 2q37.3, revealing shared structural genomic patterns across both phenotypes. Notably, distinct CNV regions were identified exclusively in MINOCA, including 6q24.1, 4q13.3, and 17q11.2, with the latter encompassing genes involved in inflammatory and cellular signaling pathways. Other recurrent alterations, including 8q24.13 and 16q21, were observed exclusively in atherosclerotic ACS. Conclusions: High-resolution genome-wide molecular karyotyping revealed a complex landscape of shared and distinct structural genomic alterations in MINOCA and atherosclerotic ACS. These findings highlight candidate genomic regions that may provide new insights into the biological heterogeneity of myocardial infarction and its underlying mechanisms.