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Cited by 2,394Smoking Behavior and CessationNitric Oxide and Endothelin EffectsAntioxidant Activity and Oxidative Stress

The pathophysiology of cigarette smoking and cardiovascular disease

Open access
Ambrose, John A, Barua, Rajat S·2004·Journal of the American College of Cardiology
DOI 10.1016/j.jacc.2003.12.047
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Abstract

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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Crossref · 10.1016/j.jacc.2003.12.047

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  • Other evidence shows that effects diminish with increasing exposure for active smoking, a pattern incorporated into the exposure-response curves.

    “Other evidence161 shows that the effects diminish with increasing exposure for active smoking, a pattern incorporated into our exposure– response curves.”

    From A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990–2010: a systematic analysis for the Global Burden of Disease Study 2010 (2012) · cites this paper as [161]

  • Mechanisms point towards the effect of smoking on endothelial function, oxidative processes, platelet function, fibrinolysis, inflammation, and modification of lipids and vasomotor function.

    “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]

  • Most current evidence suggests that nicotine exposure from smoking has only minor effects on the atherosclerotic process.

    “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]

  • Lifestyle risk factors (dietary habits, physical inactivity, smoking, adiposity) strongly influence established cardiovascular risk factors and also affect novel pathways of risk such as inflammation/oxidative stress, endothelial function, thrombosis/coagulation, and arrhythmia.

    “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 patients with established cardiovascular disease, physical activity reduces angina symptoms, benefits heart failure, decreases claudication, and lowers mortality after myocardial infarction.

    “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]

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1 of the 111 references couldn’t be matched to a known paper.

Research works printed but not linked: 1

  1. Tappia PS, Troughton KL, Langley-Evans SC, Grimble RF. Ciga- rette smoking influences cytokine production and antioxidant de- fenses. Clin Sci (Lond) 1995;88:485-9.

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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
ORCID
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)
DOI
10.1016/j.jacc.2003.12.047
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
Licence
Locations
  • Journal of the American College of Cardiology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Health Sciences › Medicine › Biochemistry › 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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