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Smoking and depression are risk factors for acute coronary syndrome (ACS) that often co-exist. We investigated the evolution of depression according to smoking cessation one-year after ACS. Data from 1822 ACS patients of the Swiss multicenter SPUM-ACS cohort study were analyzed over a one-year follow-up. Participants were classified in three groups based on smoking status one-year post-ACS - continuous smokers, smokers who quit within the year, and non-smokers. Depression status at baseline and one-year was assessed with the Center for Epidemiologic Studies Depression scale (CES-D) and antidepressant drug use. A CES-D score ≥ 16 defined depression. A multivariate-adjusted logistic regression model was used to calculate odds ratios (OR) between groups. The study sample mean age was 62.4 years and females represented 20.8%. At baseline, 22.6% were depressed, 40.9% were smokers, and 47.5% of these quit smoking over the year post-ACS. In comparison to depressed continuous smokers, depressed smokers who quit had an adjusted OR 2.59 (95% confidence interval (CI) 1.27-5.25) of going below a CES-D score of 16 or not using antidepressants. New depression at one-year was found in 24.4% of non-depressed smokers who quit, and in 27.1% of non-depressed continuous smokers, with an adjusted OR 0.85 (95% CI 0.55-1.29) of moving to a CES-D score of ≥16 or using antidepressants. In conclusion, smokers with depression at time of ACS who quit smoking improved their depression more frequently compared to continuous smokers. The incidence of new depression among smokers who quit after ACS was similar compared to continuous smokers.

Background: Alterations in heart rate variability (HRV) are a potential link between exposure to traffic-related air pollution and cardiovascular mortality. Objectives: We investigated whether long-term exposure to traffic-related PM10 (TPM10) is associated with HRV in older subjects and/or in participants taking specific cardiovascular treatment or with self-reported heart disease. Methods: We included 1607 subjects from the general population aged 50 to 72 years. These participants from the SAPALDIA cohort underwent ambulatory 24-hr electrocardiogram monitoring. Associations of average annual exposure to TPM10 over 10 years with HRV parameters from time and frequency domains were estimated using multivariable mixed linear models. Effect estimates are expressed as percent changes in geometric means. Results: HRV was only associated with TPM10 in participants under ACE inhibitor therapy (N=94). A 1 μg/m3 increment, approximately equivalent to an interquartile range, in 10 year average TPM10 was associated with decrements of 14.5% (95% confidence interval (CI), −25.9 to −1.3) in high frequency (HF) power, of 4.5% (−8.2 to −0.5) in the standard deviation of all normal-to-normal RR intervals (SDNN), of 10.6% (−18.5 to −1.9) in total power (TP) and an increase of 9.2% (0.8 to 20.2) in the LF/HF power ratio. Conclusions: In the absence of an overall effect our results suggest that alterations in HRV, a measure of autonomic control of the cardiac rhythm, may not be a central mechanism by which long-term exposure to TPM10 increases cardiovascular mortality. Novel evidence on an effect in persons under ACE inhibitor treatment needs to be confirmed in future studies. Keywords: HRV, Traffic-related PM10, Cardiovascular medication, ACE inhibitors, SAPALDIA