Abstract 4363463: The Association of AHA Cardiovascular-Kidney-Metabolic Syndrome and PREVENT ASCVD Risk with Abdominal Aortic Calcification in US Adults

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Background: Abdominal aortic calcification (AAC) is a marker of subclinical atherosclerotic cardiovascular disease (ASCVD). Cardiovascular-kidney-metabolic (CKM) syndrome reflects dysfunction across cardiovascular, renal, and metabolic systems. The relationship between AAC and CKM is poorly understood. This study examined associations of CKM stages and predicted 10-year ASCVD risk with AAC in US adults aged ≥40 years. Methods: This cross-sectional study used National Health and Nutrition Examination Survey (NHANES) 2013–2014 data. AAC was measured by dual-energy X-ray absorptiometry and scored via the Kauppila method (range: 0–24). AAC was categorized as absent (score = 0), present (score > 0 to ≤ 6), and severe (score > 6). CKM stages (0–3+) were characterized as follows: Stage 0 included healthy individuals with normal BMI and waist circumference without other risk factors; Stage 1 included elevated BMI/waist circumference or prediabetes; Stage 2 included hypertension, diabetes, hypertriglyceridemia, metabolic syndrome, or moderate-to-high-risk CKD; Stage 3+ included very-high-risk CKD or ASCVD risk ≥20%. Multivariable linear and multinomial logistic regression were used to examine associations of ASCVD risk and CKM stage with AAC. Results: A total of 3140 participants (mean age 57.4 years, 48.1% male, 71% Non-Hispanic White) were included. Mean AAC scores progressively increased across CKM stages: 0.42 (stage 0), 0.81 (stage 1), 1.96 (stage 2), and 4.61 (stage 3+) (p<0.001). Each 10% ASCVD risk increase correlated with a 1.46-point higher AAC score (95% CI: 1.19–1.74). CKM stage 3+ was linked to a 1.16-point higher AAC score vs. stage 0 (95% CI: 0.43–1.89). Odds of any AAC increased 80% per 10% ASCVD increase (OR=1.80; 95% CI: 1.47–2.20), and odds of severe vs. absent AAC were over threefold higher (OR=3.45; 95% CI: 2.78–4.28). CKM stage 3+ had 3.38-fold greater odds of severe vs. absent AAC (95% CI: 1.29–8.86). Race/ethnicity modified AAC–ASCVD (p<0.01) and AAC–CKM (p<0.01) associations. Compared to stage 0, CKM stage 3+ was linked to AAC score increases of 3.37 (95% CI: 2.61–4.12) in Non-Hispanic White, 3.66 (95% CI: 1.75–5.57) in Asian, 2.01 (95% CI: 0.974-3.060) in Non-Hispanic Black, and 1.76 (95% CI: 0.40–3.13) in Hispanic populations. Conclusions: CKM stage and ASCVD risk are associated with AAC, with the magnitude of associations varying by race/ethnicity. AAC may serve as a useful imaging marker for early cardiometabolic risk detection.

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