Background: The risk of coronary artery disease (CAD) in different valve dysfunction has been unclear. Methods: We reviewed patients, who underwent valve heart surgery and coronary angiography from 2008 to 2021, at our center. Results: A total of 7,932 patients were included in the present study, and 1,332 (16.8%) had CAD. The mean age of the study cohort was 60.5±7.9 years, and 4,206 (53.0%) were male. CAD was 21.4% in aortic disease, 16.2% in mitral valve disease, 11.8% in isolated tricuspid valve disease, and 13.0% in combined aortic and mitral valve disease. Patients with aortic stenosis were older than those with regurgitation (63.6±7.4 years vs. 59.5±8.2 years, P < 0.001), and the CAD risks also were higher (28.0% vs. 19.2%, P < 0.001). The age difference was minimal (60.6±8.2 years vs. 59.5±6.7 years, P = 0.002) between patients with mitral valve regurgitation and stenosis, but the risks of CAD were twice high in regurgitation (20.2% vs. 10.5%, P < 0.001). When the type of valve impairment was not considered, non-rheumatic etiology, advanced age, male sex, hypertension, and diabetes were independent predictors of CAD. Conclusion: In patients undergoing valve surgery, the prevalence of CAD was influenced by conventional risk factors. Importantly, CAD also was associated with the type and etiology of valve diseases.

Background: Previous studies have shown the importance of energy deficiency and malfunctioning mitochondria in the pathophysiology of hypertrophic cardiomyopathy (HCM). There has been a little research into the relationship between plasma free fatty acids (FFA), one of the heart’s main energy sources, and HCM. We evaluated its clinical importance in HCM to see if there was a link between plasma FFA metabolism and HCM. Methods: In a single-center retrospective observational study, we investigated 420 HCM patients diagnosed at Beijing Anzhen Hospital between January 1, 2018, and December 31, 2022. Meanwhile, 1372 individuals without HCM (non-HCM) were recruited. 391 non-HCM patients were chosen as controls via a propensity score matching (PSM) study with a 1:1 ratio. Results: FFA in HCM patients showed statistically significant correlations with creatinine (r = 0.115, p = 0.023), estimated GFR (r=-0.130, p = 0.010), BNP (r = 0.152, p = 0.007), LVEF (r=-0.227, p < 0.001), LVFS (r=-0.160, p = 0.002), and LAD (r = 0.112, p = 0.028). Higher FFA levels were found in HCM patients who had atrial fibrillation and NYHY functional classes III or IV (p = 0.015 and p = 0.022, respectively). In HCM patients, multiple linear regression analysis revealed that BNP and LVEF had independent relationships with increasing FFA (Standardized = 0.139, p = 0.013 and =-0.196, p < 0.001, respectively). Conclusions: Among HCM patients, the plasma FFA concentration was lower, and those with AF and NYHY functional class III or IV had higher FFA levels, and LVEF and BNP were independently associated with increasing FFA. The findings of the study should help inspire future efforts to better understand how energy deficiency contributes to hypertrophic cardiomyopathy (HCM) development.

Calcific aortic valve disease (CAVD) and atherosclerotic cardiovascular disease (ASCVD) represent two major cardiovascular disorders that frequently coexist and share overlapping risk factors and pathophysiological processes, yet also exhibit distinct features that shape their progression and management. This review synthesizes current evidence on their common mechanisms—including endothelial dysfunction, lipid infiltration, oxidative stress, and inflammatory activation—and highlights disease-specific pathways in CAVD versus ASCVD. Therapeutically, both conditions benefit from risk factor modification, diabetes control, and emerging agents such as glucagon-like peptide-1 receptor agonists. Divergent treatment strategies are defined by surgical or transcatheter valve replacement for CAVD, often integrated with percutaneous or surgical revascularization for concomitant ASCVD. This review underscores the need for mechanistically informed and integrative approaches to improve outcomes in patients burdened by these interrelated conditions.

Cardiogenic shock secondary to concomitant severe aortic stenosis (AS) and coronary artery disease (CAD) is a critical clinical condition requiring comprehensive management. A 75-year-old man presented with cardiogenic shock resulting from severe AS and CAD. Emergency surgery was performed. It involved initiation of extracorporeal circulatory support, followed by percutaneous coronary intervention (PCI) and, subsequently, transcatheter aortic valve replacement (TAVR) using a TaurusElite valve (Peijia Medical). This strategy resulted in marked hemodynamic improvement. This case highlights the efficacy and safety of concurrent PCI and TAVR as a lifesaving strategy for cardiogenic shock patients with concomitant severe CAD and AS. Emergency PCI with concurrent TAVR represents a viable lifesaving strategy for cardiogenic shock patients with coexisting severe CAD and AS. Prophylactic extracorporeal circulation initiation is critical in TAVR procedures for patients with cardiogenic shock to prevent circulatory collapse and maintain systemic perfusion.

The triglyceride-glucose (TyG) index is highly correlated with cardiovascular diseases, but the relationship between TyG index changes and hypertrophic car

Background: Insulin resistance (IR) and obesity are key drivers of atrial fibrillation (AF). However, the comparative predictive value of the Triglyceride-Glucose (TyG) index versus composite indices combining IR and anthropometric measures—such as TyG-BMI, TyG-Waist Circumference (TyG-WC), and Waist-to-Height Ratio (WHtR)—remains undefined. We aimed to evaluate these associations and the modifying effect of genetic susceptibility. Methods: We analyzed 293,318 UK Biobank participants free of AF at baseline. Hazard ratios (HRs) were estimated using Cox proportional hazards models, and non-linearity was assessed using restricted cubic splines. Incremental predictive value was evaluated via Net Reclassification Improvement (NRI). Interactions with AF Polygenic Risk Scores (PRS) were examined. Results: During follow-up, 22,707 incident AF cases occurred. While the TyG index was associated with AF in unadjusted models, this association was nullified after full adjustment. In contrast, composite indices (TyG-BMI, TyG-WC) and WHtR showed robust, positive associations (WHtR HR per SD: 1.30, 95% CI 1.28–1.32). Spline analysis identified non-linear threshold effects (e.g., WHtR inflection at 0.556). Adding WHtR or TyG-BMI to baseline models significantly improved risk reclassification (NRI ∼10.3–11.8%, P<0.001), whereas TyG alone did not (P=0.73). Elevated metabolic risk increased AF incidence across all genetic categories, with significant interactions suggesting greater relative impact in low-genetic risk groups. Conclusions: Composite indices integrating central obesity and insulin resistance are superior to the TyG index alone in predicting incident AF. The identification of specific risk thresholds and genetic interactions highlights "metabolic health" as a crucial, modifiable target for AF prevention. Research Insights: