Anatolian Journal of Cardiology最新文献

Background: To explore the impacts of cardiac rehabilitation exercise plus sacubitril valsartan sodium on cardiac function, lung function, and quality of life in chronic heart failure (CHF) patients.

Methods: One hundred and forty-six CHF patients admitted to the hospital from January 2023 to December 2024 were chosen and divided into a control group (conventional treatment + sacubitril valsartan sodium) and a study group (conventional treatment + sacubitril valsartan sodium + cardiac rehabilitation exercise).

Results: The total effective rate of the study group was higher when comparing with the control group (P < .05). The study group had higher left ventricular ejection fraction level as well as lower left ventricular end-systolic diameter, left ventricular end-diastolic diameter, and N-terminal pro B-type natriuretic peptide levels when comparing with the control group after 3 months of intervention (P < .01). The study group had higher forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and FEV1/FVC levels when comparing with the control group following 3 months of intervention (P < .01). The study group had higher SpO2, PaO2, and PaO2/FiO2 levels after 3 months of intervention (P < .01). The study group had longer 6-minute walking test after 3 months of intervention (P < .01). The study group had lower MLHFQ score when comparing with the control group after 3 months of intervention (P < .01). The rate of rehospitalization and incidence of major adverse cardiovascular event (MACE) in the study group were lower than in the control group (P < .05).

Conclusion: Cardiac rehabilitation exercise combined with sacubitril valsartan sodium is effective in treating CHF patients, which improves cardiac function, lung function and blood gas levels, promotes exercise endurance and quality of life, and reduces the rehospitalization rate and MACE incidence in CHF patients.

Objective: Electrocardiogram (ECG) remains an essential tool in cardiology. Coronary artery calcium (CAC) score, measured via computed tomography, is a well-established predictor of cardiovascular risk. However, its cost and availability limit widespread use. This study introduces a novel ECG-based index, the PARLA (Prediction of Ischemia via Angle of QRS-T and corrected QT Length Assessment) Index, combining the QTc interval and frontal QRS-T (fQRS-T) angle, to assess its association with CAC severity.

Methods: This retrospective, cross-sectional study included patients who underwent ECG and coronary computed tomography angiography. Exclusion criteria encompassed conduction abnormalities, significant valvular disease, cardiomyopathy, prior coronary interventions, and medications affecting ECG parameters. The PARLA Index was defined as the sum of the QTc interval and absolute fQRS-T angle. Patients were classified based on CAC score: <100 (low CAC score) vs. ≥100 (high CAC score). Statistical analyses, including logistic regression and receiver operating characteristic (ROC) curve analysis, assessed the predictive value of the PARLA Index for CAC severity.

Results: Among 595 patients (mean age 53.4 ± 11.6 years, 39.5% female), the high-CAC group had older age, higher prevalence of hypertension and diabetes, and greater left ventricular wall thickness. The PARLA Index was significantly higher in the high-CAC group (440± 26 vs. 465 ± 37, P < .001). Multivariate regression identified the PARLA Index as an independent predictor of CAC ≥100 (OR: 1.021, P < .001). ROC analysis determined an optimal PARLA Index cut-off of 450 (AUC: 0.705, sensitivity: 63%, specificity: 66%).

Conclusions: The PARLA Index is a novel, simple ECG-derived parameter that correlates with CAC severity and may serve as a noninvasive tool for cardiovascular risk stratification. Future studies should validate its prognostic value.

Background: Intermediate-high-risk (IHR) pulmonary embolism (PE) is defined by right ventricular (RV) dysfunction and elevated cardiac troponin in the absence of hemodynamic instability. While full-dose thrombolysis may improve outcomes, it poses a high bleeding risk. This study assessed the safety and efficacy of a reduced-dose, slow-infusion thrombolytic regimen.

Methods: This single-center retrospective study included 124 patients with acute IHR PE who met at least one of the following criteria: systolic blood pressure ≤110 mm Hg, heart rate >100 bpm, SpO2 <90% on room air, respiratory rate >20/min, or lactate >2 mmol/L. Patients with contraindications to thrombolysis or symptom onset >14 days were excluded. Patients received 25 mg intravenous alteplase (t-PA) infused over 4-6 hours, along with standard anticoagulation according to the institutional protocol. Following the initial dose, a repeat infusion of 25 mg over 4-6 hours was administered if tachycardia, hypoxia, or signs of organ hypoperfusion persisted on re-evaluation.

Results: Syncope was the presenting symptom in 27.4%, and 49.2% had deep vein thrombosis. Median t-PA dose was 50 mg and median infusion duration was 6 hours. Significant improvements were observed in RV and RA size/function, thrombus burden, and clinical parameters (all P < .001). Qanadli score and RV/LV ratio decreased by 55% and 29%, respectively. Major and minor bleeding occurred in 4.8% and 3.2%. In-hospital mortality was 4.8%; 12-month survival was 89.5%. Chronic thromboembolic pulmonary hypertension developed in 3.2%.

Conclusion: Low-dose, slow-infusion t-PA therapy appears effective and well-tolerated, offering hemodynamic and clinical benefit with fewer bleeding complications in patients with IHR PE.

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.