Author + information
- Received September 24, 2003
- Revision received December 18, 2003
- Accepted December 23, 2003
- Published online May 19, 2004.
- ↵*Reprint requests and correspondence:
Dr. John A. Ambrose, The Comprehensive Cardiovascular Center, Saint Vincent Catholic Medical Centers of New York, 170 West 12th Street, New York, New York 10011, USA.
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 cardiovascular dysfunction 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.
- Received September 24, 2003.
- Revision received December 18, 2003.
- Accepted December 23, 2003.
- American College of Cardiology Foundation
- Physical and biochemical properties of cigarette smoke
- Cs and atherosclerosis: clinical and experimental observations
- Cs and thrombosis—clinical and experimental observations
- Factors and mechanisms responsible for smoking-mediated vascular dysfunction
- Nonlinear dose effect of smoking on cardiovascular function