Nutritional and Inflammatory Status are Associated with Obesity Paradox in Coronary Artery Disease Patients Without Cancer

Background/Introduction The "obesity paradox," a phenomenon where obesity is associated with lower mortality rates in patients with coronary artery disease (CAD), remains controversial. One explanation is the confounding influence of cancer, which is associated with weight loss and worse prognosis. However, the relationship between obesity, nutritional status, inflammation, and prognosis in CAD patients without cancer remains unclear. Purpose This study aimed to investigate the obesity paradox in CAD patients while excluding those with a history of cancer. Additionally, we sought to determine the role of nutritional and inflammatory parameters in this paradoxical association. Methods A single-center, observational cohort study was conducted on 1,252 CAD patients without a history of cancer. Participants were stratified into high- and low-BMI groups. Nutritional status was assessed using the prognostic nutritional index (PNI) and geriatric nutritional risk index (GNRI). Inflammatory markers included platelet-lymphocyte ratio (PLR), neutrophil-lymphocyte ratio (NLR), and monocyte-lymphocyte ratio (MLR). The primary endpoints were all-cause mortality and cardiovascular death within five years. Kaplan–Meier survival analysis and Cox proportional hazards models were used to evaluate prognostic factors. The C-statistic, net reclassification improvement (NRI), and integrated discrimination improvement (IDI) were calculated to assess predictive performance. Results Non-obese individuals had significantly lower PNI (P < 0.001) and GNRI (P < 0.001), indicating poorer nutritional status. No significant differences were observed in inflammatory markers between groups. During follow-up, 75 deaths occurred. Kaplan–Meier analysis showed a significantly worse prognosis for non-obese patients (log-rank P < 0.001) (Figure 1), although cardiovascular death did not differ significantly (log-rank P = 0.201). Multivariable analysis adjusted for nine conventional risk factors identified BMI as an independent protective factor for all-cause mortality (HR, 0.87; 95% CI, 0.81-0.94). Adding BMI, PNI, and NLR to the model improved risk prediction (C-statistic increase from 0.755 to 0.838, P < 0.001) (Figure 2). Conclusion The obesity paradox persisted in CAD patients after excluding cancer. Poorer nutritional status in non-obese individuals may contribute to worse outcomes. Simple nutritional and inflammatory markers, particularly PNI and NLR, enhance risk stratification and should be incorporated into clinical assessment models.