Abstract 13115: Risk Markers for Minimal Coronary Artery Calcification in Persons With Significant Aortic Valve Calcium: The Multi-Ethnic Study of Atherosclerosis

Abstract

Introduction: Calcific aortic valve disease is the most common valve disorder affecting >5 million US adults. The underlying pathobiology for the early stages of aortic valve calcification (AVC) and coronary artery calcium (CAC) includes many shared ASCVD risk factors, but a considerable proportion of individuals with significant AVC have little to no CAC. Hypothesis: Among persons with significant AVC (>100 AU), those with a low CAC burden (CAC <100 AU) would be younger and have a lower prevalence of both traditional and novel ASCVD risk factors compared to persons with CAC ≥100. Methods: After excluding 2 persons with bicuspid aortic valve, 325 participants from the Multi-Ethnic Study of Atherosclerosis without clinical ASCVD and with AVC >100 at Visit 1 (2000-02) were included (34% women, 23% African American). We used Poisson regression to calculate adjusted prevalence ratios for CAC <100 versus CAC >100, using traditional and novel ASCVD risk markers. Results: Participants had a mean age of 72.1 years and 133 (41%) had CAC <100 of whom 46/133 had CAC=0. Those with CAC <100 were younger (70 vs. 74 years), had a lower prevalence of both hypertension (74% vs. 87%) and statin use (16% vs. 29%), but otherwise similar risk factor profiles compared to those with CAC ≥100. There were no significant differences in median Lp(a) (19.1 vs. 19.7 mg/dL) or hsCRP values (2.3 vs. 1.9 mg/L). A higher likelihood of CAC <100 was observed per 10 years younger age (PR=1.41, 95% CI: 1.22-1.62), female sex (PR=1.68, 95% CI: 1.28-2.20), and a total cholesterol-HDL cholesterol ratio <3.5 (PR=1.37, 95% CI: 1.02-1.85). There was no significant association between other individual risk factors and CAC <100, but an ASCVD risk of <7.5% had a prevalence ratio of 2.30 (95% CI: 1.85-2.85). Among nontraditional risk factors, only the absence of thoracic calcification was associated with a higher prevalence of CAC <100 (PR=1.71, 95% CI: 1.28-2.28). Conclusions: More than 40% of persons with significant AVC had a low burden of CAC, which is incompletely explained through traditional and novel ASCVD risk markers. These results suggest that unmeasured risk markers, genetics, and/or the non-ASCVD pathways of later stage AVC may be more important in understanding the observed discordance between AVC and CAC.