Journal of Cardiovascular Development and Disease

Cardiovascular disease (CVD) remains the leading cause of death among women worldwide and accounts for a substantial proportion of global morbidity, mortality, and disability, as well as healthcare expenditure [...]

The worse nutritional status of patients without obesity after an acute coronary syndrome (ACS) could explain their worse prognosis and the so-called obesity paradox. We performed a retrospective study of all consecutive patients admitted to a hospital for ACS between 2009 and 2020. Nutritional status was analyzed using the CONUT scale, and values > 4 were categorized as moderate-severe malnutrition. We included 2789 patients with a mean BMI of 28.0 (4.6) kg/m² and 26.4% with obesity. The mean CONUT index was 2.4 (2.2), and 24.3% had moderate-severe malnutrition. Obese patients had a lower prevalence of moderate-severe malnutrition: 20.0% vs. 25.9% (p = 0.003). The median follow-up was 3 years. A significant interaction between BMI and the CONUT for mortality was verified, and both variables behaved in the opposite way in relation to risk. BMI was associated with lower all-cause (HR: 0.93, 95% CI 0.89–0.98) and cardiovascular (HR: 0.93, 95% CI 0.87–0.98) mortality risk only in patients with CONUT > 4; however, in patients without malnutrition, BMI obesity was not associated with increased mortality or major cardiovascular events. In conclusion, CONUT-defined nutritional-inflammatory status may partly contribute to the observed obesity paradox in ACS patients.

Background: The non-high-density lipoprotein cholesterol (non-HDL-C) / high-density lipoprotein cholesterol (HDL-C) ratio has emerged as a marker of residual vascular risk; however, its role in patent foramen ovale (PFO)-associated cryptogenic stroke (CS) remains unclear. We investigated the association between the non-HDL-C/HDL-C ratio and CS in patients with PFO and evaluated its incremental predictive value beyond the Risk of Paradoxical Embolism (ROPE) score. Methods: This retrospective study included 316 patients with confirmed PFO, including 56 patients with CS. Multivariable logistic regression, restricted cubic spline analysis, ROC analysis, net reclassification improvement (NRI), integrated discrimination improvement (IDI), decision curve analysis, and bootstrap internal validation were performed. Results: Patients with CS had significantly higher non-HDL-C/HDL-C ratio levels than those without CS (p < 0.001). In multivariable analysis, the non-HDL-C/HDL-C ratio remained independently associated with CS (OR: 1.881, 95% CI: 1.310–2.700, p < 0.001). Restricted cubic spline analysis demonstrated a significant nonlinear association between the non-HDL-C/HDL-C ratio and CS risk (overall p = 0.001; nonlinear p = 0.015). Addition of the non-HDL-C/HDL-C ratio to the ROPE score improved discrimination, increasing the AUC from 0.781 to 0.819 (DeLong p = 0.010), and significantly improved risk reclassification (continuous NRI: 0.555, p = 0.002; IDI: 0.057, p = 0.002). Internal validation demonstrated stable model performance with minimal optimism. Conclusions: The non-HDL-C/HDL-C ratio was independently associated with CS and demonstrated potential incremental predictive value beyond the ROPE score in patients with PFO. These findings suggest that metabolic lipid burden may contribute to thromboembolic susceptibility and may improve individualized risk stratification in PFO-related stroke.