Association between visceral adiposity index and heart failure: A cross‐sectional study

**Background:** Obesity is a well-established risk factor for heart failure (HF), but the relationship between visceral adiposity and HF is less clear. The Visceral Adiposity Index (VAI) is a simple, noninvasive metric that estimates visceral fat using body mass index (BMI), waist circumference (WC), triglycerides (TG), and high-density lipoprotein cholesterol (HDL-c). While VAI has been linked to diabetes, hypertension, and atherosclerosis, its association with HF had not been studied. This study aimed to evaluate the association between VAI and HF in a large, nationally representative US sample.

**Methods:** This cross-sectional study used data from the National Health and Nutrition Examination Survey (NHANES) cycles 2009–2018. After excluding participants <18 years and those with missing HF data, 28,764 adults were included. VAI was calculated using sex-specific formulas based on BMI, WC, TG, and HDL-c. HF was defined by self-reported physician diagnosis. Covariates included demographics, comorbidities (hypertension, diabetes, coronary heart disease, kidney disease, liver disease), lifestyle factors (smoking, alcohol), laboratory values (eGFR, serum uric acid, albumin, hemoglobin, hematocrit, neutrophil-lymphocyte ratio), and medication use. Logistic regression models were used to estimate odds ratios (OR) and 95% confidence intervals (CI) for HF per unit increase in VAI and across VAI quartiles (Q1–Q4), with progressive adjustment for covariates. Restricted cubic spline analysis assessed dose-response relationships. Subgroup analyses were performed by sex, age, race, smoking, hypertension, diabetes, coronary heart disease, liver disease, serum uric acid, eGFR, and albumin.

**Key Results:** The study included 28,764 participants (weighted mean age 50 years; 48.4% male). Participants with HF had significantly higher VAI than those without HF (p<0.001). In unadjusted analysis, each one-unit increase in VAI was associated with a 4% higher odds of HF (OR 1.04, 95% CI 1.02–1.05). After full adjustment (Model 3: age, sex, race, hypertension, diabetes, smoking, alcohol, coronary heart disease, kidney disease, liver disease, eGFR, systolic and diastolic blood pressure, serum uric acid, albumin, hemoglobin, hematocrit, and neutrophil-lymphocyte ratio), the association remained significant (OR 1.03, 95% CI 1.00–1.05, p=0.031). When VAI was categorized into quartiles, the highest risk was observed in Q3 (OR 1.55, 95% CI 1.24–1.94) compared to Q1 in the fully adjusted model. Q4 showed a non-significant increased risk (OR 1.19, 95% CI 0.93–1.51). The p for trend across quartiles was 0.014. Restricted cubic spline analysis revealed a linear relationship between VAI and HF odds (p for nonlinearity=0.151). Subgroup analyses showed consistent positive associations across most subgroups, with no significant interactions.

**Clinical Implications:** This study demonstrates that VAI, a simple and inexpensive index, is independently associated with HF prevalence in a large US adult population. The linear dose-response relationship suggests that even modest increases in visceral adiposity may elevate HF risk. VAI could serve as a practical screening tool for identifying individuals at higher risk for HF, potentially enabling earlier preventive interventions. However, due to the cross-sectional design, causality cannot be established. The reliance on self-reported HF diagnosis and lack of HF subtype classification are limitations. Future prospective studies are needed to confirm these findings and explore VAI's utility in predicting incident HF and differentiating HF phenotypes.