Literature DB >> 11583703

Particulate and vapor phase constituents of cigarette mainstream smoke and risk of myocardial infarction.

C J Smith1, T H Fischer.   

Abstract

On pharmacological and compositional grounds, cigarette mainstream smoke (MS) aerosol can be broadly categorized as consisting of the following constituents: carbon monoxide, other vapor phase components, particulate matter ('tar') and nicotine. The relative risk of coronary artery disease for smoking 20 cigarettes per day has been estimated by meta-analysis of five large prospective epidemiology studies to be 1.78. These four major smoke components are simultaneously delivered to the active smoker as a complex aerosol composed of several billion semi-liquid particles per cm(3) within the mixture of combustion gases. Fractional attribution of the 78% increase in reported risk to a given constituent is problematic because of the complex mixture. However, a significant literature exists which suggests that some general statements regarding smoke constituent-associated risks for development or exacerbation of myocardial infarction are supportable. First, the atherogenic potential of MS is associated with the particulate and vapor phases and not with CO. Nicotine might exert an indirect effect on atherosclerotic plaque development by increasing shear forces in main conduction arteries. Similarly, the thrombogenic potential is associated primarily with the particulate and vapor phases and also possibly with nicotine via platelet aggregation. Vasoconstriction probably results from the actions of nicotine and hypoxia from carbon monoxide. Finally, the arrhythmia-inducing potential may result from catecholamine release following nicotine exposure, with a questionable contribution from carbon monoxide.

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Year:  2001        PMID: 11583703     DOI: 10.1016/s0021-9150(01)00570-6

Source DB:  PubMed          Journal:  Atherosclerosis        ISSN: 0021-9150            Impact factor:   5.162


  41 in total

1.  Left ventricular growth response to exercise and cigarette smoking: data from LARGE Heart.

Authors:  J R Payne; K I Eleftheriou; L E James; E Hawe; J Mann; A Stronge; P Kotwinski; M World; S E Humphries; D J Pennell; H E Montgomery
Journal:  Heart       Date:  2006-06-27       Impact factor: 5.994

2.  Cured meat consumption, lung function, and chronic obstructive pulmonary disease among United States adults.

Authors:  Rui Jiang; David C Paik; John L Hankinson; R Graham Barr
Journal:  Am J Respir Crit Care Med       Date:  2007-01-25       Impact factor: 21.405

Review 3.  Role of Advanced Glycation End Products and Its Receptors in the Pathogenesis of Cigarette Smoke-Induced Cardiovascular Disease.

Authors:  Kailash Prasad; Indu Dhar; Gudrun Caspar-Bell
Journal:  Int J Angiol       Date:  2015-06

4.  Exposure to acrolein by inhalation causes platelet activation.

Authors:  Srinivas D Sithu; Sanjay Srivastava; Maqsood A Siddiqui; Elena Vladykovskaya; Daniel W Riggs; Daniel J Conklin; Petra Haberzettl; Timothy E O'Toole; Aruni Bhatnagar; Stanley E D'Souza
Journal:  Toxicol Appl Pharmacol       Date:  2010-08-03       Impact factor: 4.219

Review 5.  The biology behind the atherothrombotic effects of cigarette smoke.

Authors:  Adam Csordas; David Bernhard
Journal:  Nat Rev Cardiol       Date:  2013-02-05       Impact factor: 32.419

6.  Smoking among women following heart transplantation: should we be concerned?

Authors:  Lorraine Evangelista; Alvina Ter-Galstanyan; Debra K Moser; Kathleen Dracup
Journal:  Prog Cardiovasc Nurs       Date:  2009-12

7.  Current smoking and the risk of non-fatal myocardial infarction in the WHO MONICA Project populations.

Authors:  M S Mähönen; P McElduff; A J Dobson; K A Kuulasmaa; A E Evans
Journal:  Tob Control       Date:  2004-09       Impact factor: 7.552

8.  Adaptive regression modeling of biomarkers of potential harm in a population of U.S. adult cigarette smokers and nonsmokers.

Authors:  John H Warner; Qiwei Liang; Mohamadi Sarkar; Paul E Mendes; Hans J Roethig
Journal:  BMC Med Res Methodol       Date:  2010-03-16       Impact factor: 4.615

9.  Glutathione-S-transferase P protects against endothelial dysfunction induced by exposure to tobacco smoke.

Authors:  Daniel J Conklin; Petra Haberzettl; Russell A Prough; Aruni Bhatnagar
Journal:  Am J Physiol Heart Circ Physiol       Date:  2009-03-06       Impact factor: 4.733

10.  Smoking reduction, smoking cessation, and incidence of fatal and non-fatal myocardial infarction in Denmark 1976-1998: a pooled cohort study.

Authors:  N S Godtfredsen; M Osler; J Vestbo; I Andersen; E Prescott
Journal:  J Epidemiol Community Health       Date:  2003-06       Impact factor: 3.710

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