Abstract P404: Coronary Artery Calcification Presence and Progression by Obesity Phenotypes: The Coronary Artery Risk Development in Young Adults (CARDIA) Study
Authors: Camhi Sarah M , Must Aviva , Gona Philimon N , Hankinson Arlene , Odegaard Andrew O , Reis Jared P , Carnethon Mercedes R 
Published: December 2020

Background:
Past research findings regarding whether metabolically healthy obesity (MHO) is a healthier state within obesity have been mixed and often controversial. Coronary artery calcification (CAC) can provide insight into subclinical atherosclerosis burden and progression. The purpose of this study was to compare CAC presence and progression between non-obese and obese phenotypes (MHO and metabolically unhealthy obesity, MUO).

Methods:
Young adults (18-30 years of age in 1985-86) enrolled in the CARDIA study were excluded if they had baseline obesity, had undergone bariatric surgery or were pregnant/breastfeeding. CAC was estimated with computed tomography using standardized procedures at all coronary arteries and summed across all arteries at year (Y) Y15 and Y25 (Agatston units, AU). Presence of CAC (n=2546) was defined as any score >0 AU at Y15. Progression of CAC (ΔCAC, n=2035) was a dichotomous variable indicating any incident CAC at Y25 for participants without CAC at Y15 or an increase in CAC ≥20 AU from Y15-Y25. Obesity onset (BMI ≥30 kg/m
2
) was identified at Y7, Y10, Y15. MHO was defined as obesity and 0-1 risk factor: SBP/DBP ≥130/85mmHg; glucose ≥100mg/dL; triglycerides ≥150mg/dL; and HDL-C men <40, women <50mg/dL or on relevant medication. MUO was defined as obesity and ≥2 risk factors. MHO duration was estimated as years from identification of MHO to either Y15 or transition to MUO. Phenotypes were categorized by MHO duration (MHO duration×obesity duration): stable MHO (100%); transient MHO (1-99%); MUO (0%). Logistic regression analysis was used to estimate the odds of CAC presence or ΔCAC between obesity phenotypes adjusting for age, sex, race, smoking, alcohol and physical activity.

Results:
Participants were 42% black and 52% female, 25.2±3.6 years at baseline with BMI 23.3±2.9 kg/m
2
at baseline, and BMI 27.4±5.1 kg/m
2
at Y15. CAC presence was 9% (n=173) among non-obese (n=1849); 6% (n=23) among stable MHO (n=373), 10% (n=12) among transient MHO (n=115), and 1% (n=39) among MUO (n=209). ΔCAC was 26% (385/1467), 18% (54/298), 31% (31/100) and 46% 79/170) for non-obese, stable MHO, transient MHO and MUO, respectively. Compared to stable MHO, MUO had higher odds of CAC presence (OR, 95% CI: 3.26, 1.73-6.15) and ΔCAC (3.30, 2.14-5.11); transient MHO had higher odds of ΔCAC (1.88, 1.10-3.20); with no significant differences between transient MHO vs. stable MHO for CAC presence. There were also no significant differences between non-obese and stable MHO for either CAC presence or ΔCAC. Among those who developed obesity, each additional 5 years of MHO duration was associated with lower odds of ΔCAC (0.60, 0.46-0.78).

Conclusion:
Our findings suggest that subclinical coronary calcified atherosclerosis burden is similar for non-obese and stable MHO, and higher in MUO vs. non-obese. Future studies should confirm results and examine possible biological mechanisms.