Associations of cigarette smoking and burden of thoracic aortic calcification in asymptomatic individuals: A dose-response relationship.
Jui-Peng TsaiYa-Ting JanChun-Ho YunKuo-Tzu SungChuan-Chuan LiuJen-Yuan KuoChung-Lieh HungTung-Hsin WuJiun-Lu LinCharles Jia-Yin HouHung-I YehHiram G BezerraAaron SoPublished in: PloS one (2020)
Smoking is known as a powerful predictor of pathological coronary atherosclerosis. Thoracic aortic calcification (TAC), an alternative marker for pathological atherosclerosis, has also been shown to be associated unfavorable cardiovascular outcomes. We aimed to investigate the dose-response relationship between cigarette use and calcification burden in subjects free from clinical symptoms. Among 3109 patients enrolled in this analysis, we categorized study participants according to smoking exposure pattern as: non-smokers, ex-smokers and current smokers. Smoking dose (cigarette/day), duration (years) and pack-years were semi-quantified as smoking dose exposure variables. Thoracic aortic calcification burden (including TAC score, plaque volume and plaque density) were determined and related to smoking dose and pattern information. TAC burdens (including TAC score, plaque volume and density) were highest in current smoker compared to non-smoker group, with ex-smoker showing TAC burdens in-between (all ANOVA p<0.05). Linear regression models consistently demonstrated that TAC burdens as continuous variables were independently higher in a dose-dependent manner with smoking exposure, particularly in high-dose (> 10 cigarettes/day) and the long-duration (> 3 years) smokers, even after adjusting for baseline demographic differences (all p<0.05). By logistic regression, subjects who never smoke consistently demonstrated reduced risk of TAC existence (adjusted OR: 0.65 [95% CI: 0.48-0.86], P = 0.003) in contrary to those current smokers (adjusted OR: 1.47 [95% CI: 1.10-1.89], P = 0.009). A dose-response relationship between active cigarette use and TAC burden was observed, with those who never exposed to smoking or quitted demonstrating partial protective effects. Our data provided imaging-based evidence about the potential deleterious biological hazards of long-term and high-dose cigarette consumption.
Keyphrases
- smoking cessation
- replacement therapy
- high dose
- coronary artery disease
- aortic valve
- chronic kidney disease
- spinal cord
- low dose
- cardiovascular disease
- left ventricular
- type diabetes
- coronary artery
- stem cell transplantation
- heart failure
- high resolution
- depressive symptoms
- pulmonary arterial hypertension
- machine learning
- human health
- ejection fraction