Background: Currently, recommended pre-operative risk assessment models including the revised cardiac risk index (RCRI) are not very effective in predicting postoperative myocardial damage after non-elective surgery, especially for elderly patients. Aims: This study aimed to create a new risk prediction model to assess myocardial injury after non-cardiac surgery (MINS) in elderly patients and compare it with the RCRI, a well-known pre-operative risk prediction model. Materials and Methods: This retrospective study included 370 elderly patients who were over 65 years of age and had non-elective surgery in a tertiary hospital. Each patient underwent detailed physical evaluations before the surgery. The study cohort was divided into two groups: patients who had MINS and those who did not. Results: In total, 13% (48 out of 370 patients) of the patients developed MINS. Multivariable analysis revealed that creatinine, lymphocyte, aortic regurgitation (moderate-severe), stroke, hemoglobin, ejection fraction, and D-dimer were independent determinants of MINS. By using these parameters, a model called “CLASHED” was developed to predict postoperative MINS. The ROC analysis comparison demonstrated that the new risk prediction model was significantly superior to the RCRI in predicting MINS in elderly patients undergoing non-elective surgery (AUC: 0.788 vs. AUC: 0.611, p < 0.05). Conclusions: Our study shows that the new risk preoperative model successfully predicts MINS in elderly patients undergoing non-elective surgery. In addition, this new model is found to be superior to the RCRI in predicting MINS.

Background and Objectives: Studies have shown that inflammation markers can be used as prognostic tools in predicting acute ischemic stroke. In this study, we conducted a comparison of several inflammation scores in predicting left atrial thrombosis (LAT) in patients with ischemic stroke without AF. Materials and Methods: In this single-center, retrospective study, we included 303 consecutive patients with ischemic stroke. Each patient underwent a transesophageal echocardiography (TEE) examination within 10 days of admission to detect the presence of LAT. To identify independent predictors of LAT, we conducted a multivariate logistic regression analysis. Results: In total, 303 patients who had ischemic stroke were included in the analysis. LAT was detached in 34 patients at the time of the TEE examination. The patients were categorized into two groups based on their LAT status. The Prognostic Nutritional Index (PNI), HALP score, and C-reactive Protein–Albumin Ratio (CAR) were identified as statistically significant predictors of LAT. Based on the results of the multivariate regression analysis, the CAR emerged as the only independent predictor of LAT. Conclusions: Among several inflammation scores, the PNI, HALP, and CAR were statistically significant predictors of LAT in ischemic stroke patients without AF. CAR was identified as the optimal score for the prediction of LAT in patients with stroke and without AF.

This study evaluates the association between the Intermountain Risk Score (IMRS) and coronary artery ectasia (CAE) to determine its predictive value. A retrospective study was conducted at a tertiary hospital from January 2019 to January 2024. A total of 446 patients (226 with CAE, 220 controls) were included. Clinical, laboratory, and angiographic data were analyzed. IMRS was calculated based on routine demographic and laboratory parameters. Statistical analyses included logistic regression and receiver operating characteristic (ROC) curve analysis. Patients with CAE had significantly higher IMRS scores (p = 0.011) and were more likely to fall into high-risk IMRS categories (p = 0.002). Smoking (HR: 3.744, p = 0.045), mean corpuscular volume (HR: 1.105, p = 0.019), and IMRS color category (HR: 5.255, p = 0.016) were independent predictors. ROC analysis showed an AUC of 0.617 for IMRS score and 0.627 for IMRS color category. IMRS is a significant predictor of CAE and may serve as a practical risk stratification tool. Higher-risk patients could benefit from closer monitoring and targeted interventions. Further validation in prospective studies is needed.

Excessive alcohol consumption causes significant cardio‐hepatic damage. This study investigated the effects of standard (10 mg/kg) and high (40 mg/kg) doses of atorvastatin on fibrosis, hypertrophy, apoptosis, inflammation, oxidative stress, mitochondrial‐mediated apoptotic pathways, and thiol/disulfide balance in alcohol‐induced heart and liver injury. Forty Sprague‐Dawley rats were divided into five groups ( n = 8; 4 male/4 female): Control (CONT), ALCOHOL (2.5 g/kg 20% ethanol i.p./28 days), ATOR (10 mg/kg o.g./28 days), ALCOHOL + ATOR (10 mg/kg o.g./28 days) and ALCOHOL+ hATOR (40 mg/kg o.g./28 days). Histopathologically, alcohol caused cardiac myocyte dilation, vacuolization, inflammation, and hepatic cord disruption. While standard ATOR partially improved tissue architecture ( p < 0.001), the ALCOHOL+ hATOR group showed the lowest severity. Alcohol exposure significantly increased apoptosis (Caspase‐3, M30, M65), oxidative stress (TOS, OSI, MDA), ischemia (IMA), and inflammatory cytokines (IL‐1β, TNF‐α, HsCRP, Endothelin‐1) across serum, heart, and liver samples, while decreasing TAS, total thiol, and native thiol levels ( p < 0.001 for all vs. CONT). Conversely, high‐dose atorvastatin (ALCOHOL + hATOR) significantly reversed alcohol‐induced toxicity by decreasing Caspase‐3, M30, M65, TOS, OSI, MDA, TNF‐α, HsCRP, Endothelin‐1, and disulfide levels, while significantly restoring TAS, total thiol, and native thiol levels ( p < 0.001 vs. ALCOHOL). TAS was significantly higher in the ALCOHOL+hATOR group than the ALCOHOL + ATOR group ( p < 0.001). Despite marked improvements by hATOR, OSI, TOS, IL‐1β, and HsCRP levels remained higher than CONT ( p < 0.001). High‐dose atorvastatin (40 mg/kg) exerts robust pleiotropic, anti‐apoptotic, and antioxidant cytoprotection. By preserving thiol‐disulfide homeostasis and limiting inflammation, high‐dose atorvastatin effectively mitigates alcohol‐induced subchronic cardiac and hepatic injury.