European Heart Journal Advance Access published online on October 17, 2005
European Heart Journal, doi:10.1093/eurheartj/ehi601
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1 Department of Cardiology and Pulmonology, University Clinic, Georg August University of Goettingen, D-37099 Goettingen, Germany
* To whom correspondence should be addressed. The evidence that active smoking is a risk factor for cardiovascular disease (CVD) and the leading cause of preventable death is overwhelming. However, numerous epidemiological findings indicate that even passive exposure to cigarette smoke may exert detrimental effects on vascular homoeostasis. Recent experimental data provide a deeper insight into the pathophysiological mechanisms linking secondhand smoke (SHS) to CVD. Importantly, most of these effects appear to be characterized by a rapid onset. For example, the relatively low doses of toxins inhaled by passive smoking are sufficient to elicit acute endothelial dysfunction, and these effects may be related, at least in part, to the inactivation of nitric oxide. Moreover, passive smoking may directly impair the viability of endothelial cells and reduce the number and functional activity of circulating endothelial progenitor cells. In addition, platelets of non-smokers appear to be susceptible to pro-aggregatory changes with every passive smoke exposure. Overall, SHS induces oxidative stress and promotes vascular inflammation. Apart from vascoconstriction and thrombus formation, however, the myocardial oxygen balance is further impaired by SHS-induced adrenergic stimulation and autonomic dysfunction. These data strongly suggest that passive smoking is capable of precipitating acute manifestations of CVD (atherothrombosis) and may also have a negative impact on the outcome of patients who suffer acute coronary syndromes.
Received June 29, 2005
Revised September 23, 2005
Accepted September 29, 2005
Review
Secondhand smoke as an acute threat for the cardiovascular system: a change in paradigm
Stavros Konstantinides, E-mail: skonstan{at}med.uni-goettingen.de
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