Key result
Elevated somatic depressive symptoms combined with 10 pack-years of smoking exposure significantly increased the odds of coronary artery calcification at 25 years (OR 2.06; 95% CI 1.08-3.93).
Why the study?
Does the interaction between cumulative smoking exposure and specific depressive symptom clusters associate with an increased risk of coronary artery calcification?
Cohort (n=3,189)
Does the interaction between cumulative smoking exposure and specific depressive symptom clusters associate with an increased risk of coronary artery calcification?
Somatic depressive symptoms synergistically interact with cumulative smoking exposure to significantly increase the risk of coronary artery calcification over 25 years.
Supports evaluating somatic depressive symptoms with smoking history for CAC risk; hypothesis-generating pending confirmatory studies.
OBJECTIVE: Depressive symptom clusters are differentially associated with prognosis among patients with cardiovascular disease (CVD). Few studies have prospectively evaluated the association between depressive symptom clusters and risk of CVD. Previously, we observed that smoking and global depressive symptoms were synergistically associated with coronary artery calcification (CAC). The purpose of this study was to determine whether the smoking by depressive symptoms interaction, measured cumulatively over 25 years, differed by depressive symptom cluster (negative affect, anhedonia, and somatic symptoms) in association with CAC. METHODS: Participants (N = 3,189: 54.5% female; 51.5% Black; average age = 50.1 years) were followed from 1985-1986 through 2010-2011 in the Coronary Artery Risk Development in Young Adults (CARDIA) study. Smoking exposure was measured by cumulative cigarette pack-years (cigarette packs smoked per day × number of years smoking; year 0 through year 25). Depressive symptoms were measured using a 14-item, 3-factor (negative affect, anhedonia, somatic symptoms) model of the Center for Epidemiologic Studies Depression (CES-D) Scale (years 5, 10, 15, 20, and 25). CAC was assessed at year 25. Logistic regression models were used to evaluate the association between the smoking by depressive symptom clusters interactions with CAC ( = 0 vs. > 0), adjusted for CVD-related sociodemographic, behavioral, and clinical covariates. RESULTS: 907 participants (28% of the sample) had CAC > 0 at year 25. The depressive symptom clusters did not differ significantly between the two groups. Only the cumulative somatic symptom cluster by cumulative smoking exposure interaction was significantly associated with CAC > 0 at year 25 (p = .028). Specifically, adults with elevated somatic symptoms (score 9 out of 18) who had 10, 20, or 30 pack-years of smoking exposure had respective odds ratios (95% confidence intervals) of 2.06 [1.08, 3.93], 3.71 [1.81, 7.57], and 6.68 [2.87, 15.53], ps < .05. Negative affect and anhedonia did not significantly interact with smoking exposure associated with CAC >0, ps > .05. CONCLUSIONS: Somatic symptoms appear to be a particularly relevant cluster of depressive symptomatology in the relationship between smoking and CVD risk.
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Carroll et al. (2017) conducted a cohort in Coronary artery calcification (n=3,189). Cumulative smoking exposure and somatic depressive symptoms vs. Lower smoking exposure and lower somatic symptoms was evaluated on Coronary artery calcification (CAC > 0) at year 25 (OR 2.06, 95% CI 1.08-3.93, p=0.028). Elevated somatic depressive symptoms combined with 10 pack-years of smoking exposure significantly increased the odds of coronary artery calcification at 25 years (OR 2.06; 95% CI 1.08-3.93).
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