Nutritional and inflammatory status in the obesity paradox of coronary artery disease

The "obesity paradox," where higher body mass index (BMI) is linked to lower mortality, has been observed in coronary artery disease (CAD) patients. One hypothesis is that weight loss in cancer patients may confound this association. This study examined the obesity paradox in CAD patients without cancer and investigated the roles of nutritional and inflammatory status.

We analysed 1,252 CAD patients without a history of cancer who underwent percutaneous coronary intervention. Patients were categorized into BMI <25 kg/m² (n = 843) and BMI ≥25 kg/m² (n = 409). The primary outcome was 5-year all-cause mortality. Nutritional status was evaluated using the prognostic nutritional index (PNI) and geriatric nutritional risk index (GNRI), while inflammation was assessed by neutrophil-lymphocyte ratio (NLR), platelet-lymphocyte ratio (PLR), and monocyte-lymphocyte ratio (MLR).

During the follow-up period, 73 deaths occurred (56 in BMI <25 kg/m² vs. 17 in BMI ≥25 kg/m²). Patients with low BMI had significantly lower PNI and GNRI (both P < 0.001), but no significant differences in NLR or PLR. Kaplan-Meier analysis showed poorer survival in people without obesity (P < 0.001). In multivariable analysis, higher BMI remained an independent protective factor (HR 0.87, 95 % CI 0.81-0.94, P < 0.001). However, PNI and GNRI had superior prognostic discrimination compared to BMI. The predictive model's C-statistic improved significantly when PNI and NLR were added to conventional risk factors, with notable gains in net reclassification and discrimination indices (both P < 0.001).

The obesity paradox in non-cancer CAD patients remains evident and appears more closely related to nutritional status than BMI alone. Lower BMI was associated with malnutrition, not increased inflammation. Simple markers such as PNI and NLR offer additional prognostic value and may aid in better risk stratification of CAD patients.