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Several studies have shown that high uric acid (UA) and low serum albumin (SA) values increase the risk of cardiovascular disease and mortality in ST-elevation myocardial infarction (STEMI). We determined whether the uric acid/albumin ratio (UAR) is a predictor of mortality in STEMI patients. All patients who presented at our center with a diagnosis of STEMI and underwent percutaneous intervention from 2015 to 2020 were screened consecutively; 4599 patients were included. A Cox proportional hazards model was used to evaluate UAR, and adjusted predictors obtained from laboratory findings and clinical characteristics contributed to mortality. Also, a regression model was presented with a directed acyclic graph (DAG). The median age of the patients was 58 years (IQR [interquartile range]: 50–67); 3581 patients (77.9%) were male. The incidence of mortality in the entire patient group was 11.9%. Median follow-up duration of all groups was 42 months. Multivariate Cox proportional regression (model-1) analysis showed age (increase 50 to 67 years; HR [hazard ratio]: 1.34, 95% CI 1.18–1.52) and UAR (increase 1.15–1.73; HR: 1.33, 95% CI 1.16–1.52) were associated with mortality. UAR may be a prognostic factor for mortality in STEMI patients and an easily accessible parameter to identify high-risk patients.

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Background:Coronary artery ectasia (CAE) is defined as localized or diffuse dilatation of the coronary arteries. There are scarce data about the role of inflammation in CAE. In the present study, the plasma soluble adhesion molecules intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) levels in CAE were investigated. Methods: The study population (n = 67) consisted of four groups. Group 1: patients with normal coronary artery (NCA); group 2: patients with isolated ectasia without stenotic lesion; group 3: patients with obstructive coronary artery disease (OCAD) without CAE; group 4: patients with both OCAD and CAE. Results: Plasma concentrations of ICAM-1 and VCAM-1 were higher in patients with isolated ectasia than in cases with NCA (p < 0.001 and p < 0.001, respectively). Compared with OCAD patients, patients with CAE had significantly elevated concentrations of ICAM-1 and VCAM-1 (p < 0.001 and p < 0.05, respectively). The levels of ICAM-1 and VCAM-1 of the CAE and OCAD group were higher than in patients in the OCAD group (p < 0.05 and p < 0.05, respectively). We detected a positive correlation between the presence of CAE and the levels of ICAM-1 and VCAM-1. Multivariate logistic regression analyses revealed a significant independent relation between the presence of CAE and ICAM-1 and VCAM-1. Conclusion: We found elevated plasma levels of ICAM-1 and VCAM-1 in patients with CAE and OCAD + CAE compared with subjects with NCA and OCAD. These data strongly suggest that more severe vascular wall inflammation may play a role in the pathogenesis of CAE.

RVEIO index is a useful, simple, accurate, and independent predictor of severe TR that adds incrementally to traditional methods of quantifying TR severity. Accurate quantification and classification of TR severity is critical for clinical decision-making and management; therefore, the incorporation of RVEIO index into the integrative approach to grading TR severity should be considered.