Anatolian Journal of Cardiology最新文献

Objective: This study was conducted to investigate the clinical value of microRNA (miR)-212-3p in acute coronary syndrome (ACS) patients.

Methods: This study involved 128 ACS patients and 110 patients with coronary arterial atherosclerosis. Real-time fluorescence quantitative polymerase chain reaction was employed to measure serum miR-212-3p levels and assessed its correlation with disease severity. The diagnostic efficacy of miR-212-3p was evaluated through receiver operating characteristic (ROC) curve and logistic regression modeling. Furthermore, Kaplan-Meier and Cox regression analyses were utilized to determine the predictive value of miR-212-3p for the occurrence of major adverse cardiovascular events (MACE).

Results: The serum miR-212-3p was elevated in ACS patients, with levels in acute myocardial infarction (AMI) patients being greater than unstable angina pectoris (UAP) patients. Serum miR-212-3p demonstrated considerable diagnostic utility in the identification of ACS patients and in differentiating between AMI and UAP cases. Furthermore, miR-212-3p levels correlated with myocardial injury markers [cardiac troponin I (cTnI), high-sensitivity C-reactive protein (hs-CRP), and creatine kinase-MB (CK-MB)], as well as with coronary artery scores (Gensini and SYNTAX). Elevated levels of miR-212-3p were asso-ciated with MACE incidence. Serum miR-212-3p, cTnI, Gensini, and SYNTAX score served as independent risk factors for MACE occurrence, with higher expression of miR-212-3p being linked to a poorer clinical prognosis.

Conclusion: Serum miR-212-3p might serve as a non-invasive biomarker for ACS diagnosis and MACE prediction and as a supplementary molecular tool in clinical practice.

Background: Patients with rheumatoid arthritis (RA) have an increased risk of developing cardiovascular disease (CVD). However, the mechanisms underlying the comorbidity between RA and CVD remain poorly understood. This study aimed to identify the shared genes between RA and CVD and to explore their functional relationships.

Methods: Rheumatoid arthritis- and CVD-associated genes were obtained from the DisGeNET and Malacards databases, respectively. Shared genes between the 2 diseases were identified, and gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed using WebGestalt and Cytoscape (v3.9.0). To further investigate potential molecular interactions, protein-protein interaction networks were constructed based on data from the STRING database. Finally, the in silico Tabula Muris single-cell transcriptomic dataset was used to assess the tissue-specific expression of candidate genes and evaluate their potential roles in specific tissues and cell types.

Results: A total of 108 genes were shared between RA and CVD, out of the 898 and 552 genes identified for each condition. Functional enrichment analysis showed that these shared genes were predominantly associated with inflammation and immune response-related pathways. Among them, 42 candidate genes were identified, of which 7 (i.e., IFNG, CCL5, CXCL10, FN1, EGFR, CXCL1, and CD44) were highlighted based on their strong connectivity and biological relevance. For validation, the validation, Tabula Muris single-cell transcriptomic dataset revealed that these genes were highly expressed in mouse cardiac tissues.

Conclusion: Seven shared genes associated with both RA and CVD were identified, which may contribute to the comorbidity between the 2 diseases.

Environmental noise, particularly from road, rail, and aircraft traffic, is now firmly recognized as a widespread risk factor for cardiovascular disease. About 1 in 3 Europeans is exposed to chronic noise exposure above the guideline thresholds recommended by the World Health Organization (WHO), thus contributing substantially to cardiovascular morbidity and mortality. Robust evidence from recent meta-analyses links transportation noise to ischemic heart disease, heart failure, stroke, hypertension, and type 2 diabetes mellitus. Findings from experimental studies in both humans and animal models reveal biologically plausible mechanisms involving sympathetic nervous system activation, oxidative stress, inflammation, endothelial dysfunction, and disruption of circadian rhythms. The adverse health effects are particularly pronounced for nighttime noise, which disrupts restorative sleep and alters neurohormonal balance. Emerging research using the exposome framework highlights the cumulative toll of environmental stressors, including noise, on vulnerable populations. This review combines the latest evidence from epidemiology, mechanistic research, and intervention studies and outlines a road-map for incorporating noise into cardiovascular prevention strategies. Figures illustrate key concepts such as the noise reaction model, oxidative stress pathways, and practical mitigation measures. The conclusion calls for noise to be treated as a fully recognized cardiovascular risk factor-in parallel with traditional risks-and to address it through coordinated efforts in urban planning, public health policy, and clinical practice.