Fisiopatologia del cigarrillo

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The pathophysiology of cigarette smoking and cardiovascular disease: An update John A. Ambrose, and Rajat S. Barua J. Am. Coll. Cardiol. 2004;43;1731-1737 doi:10.1016/j.jacc.2003.12.047

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The online version of this article, along with updated information and services, is located on the World Wide Web at:http://content.onlinejacc.org/cgi/content/full/43/10/1731

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Journal of the American College of Cardiology © 2004 by the American College of Cardiology Foundation Published by Elsevier Inc.

Vol. 43, No. 10, 2004 ISSN 0735-1097/04/$30.00 doi:10.1016/j.jacc.2003.12.047

STATE-OF-THE-ART PAPER

The Pathophysiology of Cigarette Smoking and Cardiovascular Disease
AnUpdate
John A. Ambrose, MD, FACC,* Rajat S. Barua, MD, PHD† New York, New York
Cigarette smoking (CS) continues to be a major health hazard, and it contributes significantly to cardiovascular morbidity and mortality. Cigarette smoking impacts all phases of atherosclerosis from endothelial dysfunction to acute clinical events, the latter being largely thrombotic. Both active and passive(environmental) cigarette smoke exposure predispose to cardiovascular events. Whether there is a distinct direct dose-dependent correlation between cigarette smoke exposure and risk is debatable, as some recent experimental clinical studies have shown a non-linear relation to cigarette smoke exposure. The exact toxic components of cigarette smoke and the mechanisms involved in CS-related cardiovasculardysfunction are largely unknown, but CS increases inflammation, thrombosis, and oxidation of low-density lipoprotein cholesterol. Recent experimental and clinical data support the hypothesis that cigarette smoke exposure increases oxidative stress as a potential mechanism for initiating cardiovascular dysfunction. (J Am Coll Cardiol 2004;43:1731–7) © 2004 by the American College of Cardiology FoundationEpidemiologic studies strongly support the assertion that cigarette smoking (CS) in both men and women increases the incidence of myocardial infarction (MI) and fatal coronary artery disease (CAD) (1–11). Even low-tar cigarettes and smokeless tobacco have been shown to increase the risk of cardiovascular events in comparison to nonsmokers (12,13). Furthermore, passive smoking (environmentaltobacco exposure) with a smoke exposure about one-hundredth that of active CS is associated with approximately a 30% increase in risk of CAD, compared with an 80% increase in active smokers (14,15). Thus, the evidence linking cigarette smoke exposure with cardiovascular disease is clearly present, yet the exact components of cigarette smoke and the mechanisms responsible for this association have notbeen clearly elucidated. This article updates the present clinical and experimental observations on the potential pathobiology and mechanisms involved in smokingrelated cardiovascular disease (Fig. 1).

PHYSICAL AND BIOCHEMICAL PROPERTIES OF CIGARETTE SMOKE
Conventionally, cigarette smoke is divided into two phases: a tar phase and a gas phase. The tar or particulate phase is defined as thematerial that is trapped when the smoke stream is passed through the Cambridge glass-fiber filter that retains 99.9% of all particulate material with a size
From the *Comprehensive Cardiovascular Center, Saint Vincent Catholic Medical Centers of New York, New York Medical College, New York, New York; and †Department of Medicine, the Bronx Veteran Affairs Medical Center, Mount Sinai School of Medicine,New York, New York. Manuscript received September 24, 2003; revised manuscript received December 18, 2003, accepted December 23, 2003.

0.1 m (16). The gas phase is the material that passes through the filter. The particulate (tar) phase of cigarette smoke contains 1017 free radicals/g, and the gas phase contains 1015 free radicals/puff (16). The radicals associated with the tar phase are...
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