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Original Research: PULMONARY HYPERTENSION |

Tobacco Smoke: A Risk Factor for Pulmonary Arterial Hypertension?: A Case-Control Study

Regula Schiess, MSc; Oliver Senn, MD; Manuel Fischler, MD; Lars C. Huber, MD; Serap Vatandaslar, MD; Rudolf Speich, MD, FCCP; Silvia Ulrich, MD
Author and Funding Information

From the Clinic of Internal Medicine (Ms Schiess, and Drs Fischler, Huber, Vatandaslar, Speich, and Ulrich), and the Clinic of Pulmonology (Dr Ulrich), University Hospital Zurich; and the Institute for General Practice (Dr Senn), University of Zurich, Zurich, Switzerland.

Correspondence to: Silvia Ulrich, MD, Clinic and Policlinic of Internal Medicine, University Hospital of Zurich, Raemistrasse 100, 8091 Zurich, Switzerland; e-mail: ulris@bluewin.ch


Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2010 American College of Chest Physicians


Chest. 2010;138(5):1086-1092. doi:10.1378/chest.09-2962
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Background:  Smoking is a well-known risk factor for cardiovascular, lung, and many other diseases. Smoking can induce pulmonary arterial hypertension (PAH) in animal models; PAH is common in smokers with COPD and thereby not correlated with the degree of airway obstruction. The impact of tobacco smoke exposure on the development of PAH in humans is not known.

Methods:  In a case-control study we assessed smoking and secondhand smoke exposure in all patients with PAH and chronic thromboembolic pulmonary hypertension (CTEPH) seen at our pulmonary hypertension clinic from 2002 until July 2008. Data from patients with PAH were compared with CTEPH and healthy control subjects from the Swiss Health Survey 2007.

Results:  Ninety-one patients with PAH were compared with 64 patients with CTEPH and 18,747 control subjects (women 58, 36, 10,331, respectively). Tobacco smoking was significantly more common in PAH compared with CTEPH and control subjects. This difference could be attributed to men. Patients with PAH also smoked longer and more heavily compared with patients with CTEPH. In addition, secondhand smoke exposure was significantly longer in nonsmokers with PAH compared with control subjects.

Conclusion:  Our data indicate that tobacco smoke exposure may be a risk factor for men with PAH. Considering smoking as a risk factor for PAH will have implications in counseling patients and especially their hitherto unaffected relatives. Further research on the pathogenetic role of smoking in PAH is warranted.


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