Associations of cigarette smoking with coronary artery and extra-coronary calcification in older adults: The Atherosclerosis Risk in Communities study.

BACKGROUND AND AIMS: Smoking is a major risk factor for atherosclerosis, yet its impact on coronary artery calcium (CAC) and extra-coronary calcification (ECC), which commonly manifests at older age, has not been fully characterized. We aimed to evaluate the relationships between smoking (status, pack-years, and years since cessation) and CAC and ECC among older adults.

METHODS

In 1901 Atherosclerosis Risk in Communities (ARIC) Study (United States) participants (mean age 81 ± 4 years, 62% female, 20% Black) without a clinical history of coronary heart disease at visit 7 (2018-19), we quantified the associations of key smoking parameters (status, pack-years, and years since cessation) with CAC and ECC (thoracic aorta and aortic/mitral valve calcification) using multivariable logistic regression models adjusted for other risk factors. Smoking parameters were lagged by 5 years. High CAC and ECC were defined as sex-race specific >75th percentile of Agatston score.

RESULTS

Current and former smoking were significantly associated with high CAC (adjusted odds ratio [aOR] 2.57 [95%CI 1.58-4.19] and 1.66 [1.30-2.12], respectively) and ECC except for the aortic valve. Pack-years demonstrated a robust dose-response relationship with CAC and ECC, but less so for the aortic and mitral valves. The association was particularly strong for calcification at aortic valve ring, ascending aorta, and descending aorta (e.g., aOR 4.10 [2.57- 6.55], 4.07 [2.56, 6.46], and 3.97 [2.45, 6.43], respectively, for current vs. never smokers). The odds of high vascular calcification declined with progressively longer years of smoking cessation.

CONCLUSIONS

Cigarette smoking was strongly associated with vascular calcification, especially calcification in the aorta, but less so for valvular calcification. These findings reinforce the harm of smoking on broad ranges of vascular beds and simultaneously support unique pathophysiology across different vascular beds and cardiac valves.