The DOI matches its Crossref record; 109 of the 111 references it cites were found in a registry or an index.
The pathophysiology of cigarette smoking and cardiovascular disease
Open accessAbstract
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.
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“Other evidence161 shows that the effects diminish with increasing exposure for active smoking, a pattern incorporated into our exposure– response curves.”
In the citing paper
“Mechanisms have been elucidated through observational cohort studies, experimental observations, and laboratory studies in humans and animals, 225,227 -229 and point towards the effect of smoking on endothelial function, 230,231 oxidative processes, 232 platelet function, 233 fibrinolysis, inflammation, 234 -238 and modification of lipids and vasomotor function.”
From European Guidelines on cardiovascular disease prevention in clinical practice (version 2012) (2012) · cites this paper as [227]
In the citing paper
“Most current evidence suggests that nicotine exposure from smoking has only minor effects on the atherosclerotic process, 227,245”
From European Guidelines on cardiovascular disease prevention in clinical practice (version 2012) (2012) · cites this paper as [227]
In the citing paper
“Notably, lifestyle risk factors, including dietary habits, physical inactivity, smoking, and adiposity, strongly influence the established cardiovascular risk factors and also affect novel pathways of risk such as inflammation/oxidative stress, endothelial function, thrombosis/coagulation, and arrhythmia.”
From Beyond Established and Novel Risk Factors: Lifestyle Risk Factors for Cardiovascular Disease (2008) · cites this paper as [38]
In the citing paper
“In patients with established cardiovascular disease, physical activity reduces angina symptoms, benefits heart failure, decreases claudication, and lowers mortality after myocardial infarction.38”
From Beyond Established and Novel Risk Factors: Lifestyle Risk Factors for Cardiovascular Disease (2008) · cites this paper as [38]
In the citing paper
“Consistent with these pleiotropic benefits, physical activity and fitness are associated with 30% to 50% lower risk of cardiovascular events.38,40,67”
From Beyond Established and Novel Risk Factors: Lifestyle Risk Factors for Cardiovascular Disease (2008) · cites this paper as [38]
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Citations
Cites
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2 of the 111 references couldn’t be matched to a known paper.
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Raza, H., John, A., & Nemmar, A. (2013) · Cellular Physiology and Biochemistry · doi:10.1159/000350087 · Cited by 47,311
Lim, S. S., Vos, T., Flaxman, A. D., Danaei, G., Shibuya, K., Adair-Rohani, H., AlMazroa, M. A., Amann, M., Anderson, H. R., Andrews, K. G., et al. (2012) · The Lancet · doi:10.1016/s0140-6736(12)61766-8 · Cited by 11,805
European Guidelines on cardiovascular disease prevention in clinical practice (version 2012)
Authors/Task Force Members:, Perk, J., De Backer, G., Gohlke, H., Graham, I., Reiner, Ž., Verschuren, M., Albus, C., Benlian, P., Boysen, G., et al. (2012) · European Heart Journal · doi:10.1093/eurheartj/ehs092 · Cited by 8,490
European guidelines on cardiovascular disease prevention in clinical practice: executive summary
Graham, I., Atar, D., Borch‐Johnsen, K., Boysen, G., Burell, G. K., Cífková, R., Dallongeville, J., Backer, G. D., Ebrahim, S. B. J., Gjelsvik, B., et al. (2007) · European Heart Journal · doi:10.1093/eurheartj/ehm316 · Cited by 3,865
Graham (2007) · doi:10.1097/01.hjr.0000277983.23934.c9 · Cited by 1,647
Metadata
- Authors
- Ambrose, J. A., & Barua, R. S.
- Affiliations
- Saint Vincent's Catholic Medical Center (US)
- Icahn School of Medicine at Mount Sinai (US)
- Corresponding author
- Ambrose, John A
- Venue
- Journal of the American College of Cardiology
- Publisher
- Elsevier BV
- Published
- 2004-05
- Volume
- 43
- Issue
- 10
- Pages
- 1731-1737
- ISSN
- 0735-1097 (ISSN-L)
- OpenAlex
- W1559813904
- Cited by
- 2,394
- References
- 111
- Citations by year
- 2026: 127 · 2025: 153 · 2024: 141 · 2023: 123 · 2022: 130 · 2021: 151 · 2020: 153 · 2019: 120 · 2018: 115 · 2017: 114 · 2016: 110 · 2015: 107 · 2014: 129 · 2013: 119 · 2012: 112
- FWCI
- 6.01
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of the American College of Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Smoking Behavior and Cessation
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
- Keywords
- cigarette smoking, cardiovascular disease, atherosclerosis, endothelial dysfunction, thrombosis, passive smoking, oxidative stress, LDL oxidation, inflammation, dose-response relationship
- MeSH terms
- Arteriosclerosis, Blood Vessels, Cardiovascular Diseases, Coronary Thrombosis, Female, Humans, Male, Smoke, Smoking, Nicotiana, Tobacco Smoke Pollution, Oxidative Stress
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