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Passive tobacco exposure may impair symptomatic improvement in patients with chronic angina undergoing enhanced external counterpulsation

DOI: 10.1186/1471-2261-8-23

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Abstract:

This observational study included 1,026 non-smokers (108 exposed and 918 not-exposed to SHS) from the Second International EECP Patient Registry. We also assessed angina response in 363 current smokers. Patient demographics, symptomatic improvement and quality of life assessment were determined by self-report prior and after EECP treatment.Non-smoking SHS subjects had a lower prevalence of prior revascularization (85% vs 90%), and had an increased prevalence of stroke (13% vs 7%) and prior smoking (72% vs 61%; all p < 0.05) compared to non-smokers without SHS exposure. Despite comparable degrees of coronary disease, baseline angina class, medical regimens and side effects during EECP, fewer SHS non-smokers completed a full 35-hour treatment course (77% vs 85%, p = 0.020) compared to non-smokers without SHS. Compared to non-smokers without SHS, non-smoking SHS subjects had less angina relief after EECP (angina class decreased ≥ 1 class: 68% vs 79%; p = 0.0082), both higher than that achieved in current smokers (66%). By multivariable logistic regression, SHS exposure was an independent predictor of failure to symptomatic improvement after EECP among non-smokers (OR 1.81, 95% confidence intervals 1.16–2.83).Non-smokers with SHS exposure had an attenuated improvement in anginal symptoms compared to those without SHS following EECP.Epidemiological evidence has unequivocally confirmed that active smoking is a risk factor for cardiovascular disease and the leading cause of preventable death [1,2]. The impact of passive smoking on the cardiovascular system was recognized nearly two decades ago, when evidence of the harmful effects of second-hand smoke (SHS) began to emerge [3,4]. In the past decade, clinical data from the Atherosclerosis Risk in Communities (ARIC) studies demonstrated that both active and passive smoking were associated with accelerated atherosclerosis progression [5]. Steenland et al reported that the risk of death due to cardiovascular disease (CVD) incr

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