Tobacco and Coronary Disease

English, John P.; Willius, Fredrick A.; Berkson, Joseph

doi:10.1001/jama.1940.02810420013004

Cited by 97 publications

(26 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The association between smoking and coronary disease was first described in 1940 by English et al [15] , and was subsequently demonstrated in other longitudinal work such as the Framingham study [16] . Four major mechanisms have been described explaining how smoking contributes to the appearance of cardiovascular events [17] .…”

Section: Discussionmentioning

confidence: 87%

Acute versus Chronic Myocardial Ischemia: A Differential Biological Profile Study

Sagastagoitia

Sáez²,

Vacas³

et al. 2007

Pathophysiol Haemos Thromb

View full text Add to dashboard Cite

Objective: To determine the possible differences in lipid, thrombogenic and inflammatory marker concentrations and the presence of chronic and acute coronary artery disease (stable and unstable angina, respectively), comparing them with a group of control patients with normal coronary arteries. Material and Methods: This prospective cohort study included 125 patients with unstable angina, 189 with stable angina and a control group of 83 patients with normal coronary arteries. Marker concentrations were measured in all 3 groups. Logistic regression analysis was performed to determine whether such factors could predict unstable or stable angina. Results: Lipid parameter concentrations were similar in the 2 coronary disease groups and significantly lower than in controls. Haemostatic and inflammatory marker concentrations were higher in patients with coronary disease, but were statistically significant only when comparing unstable angina patients with normal controls. Unstable angina patients had significantly higher levels of lipoprotein (a) [Lp(a)], fibrinogen, C-reactive protein (CRP) and leucocytes. Multiple logistic regression analysis showed that CRP (OR 2.635, 95% CI 1.417–4.898), smoking (OR 3.416, 95% CI 1.773–6.584), leucocytes (OR 2.034, 95% CI 1.079–3.836) and Lp(a) (OR 2.269, 95% CI 1.188–4.334) were independent risk factors of unstable versus stable angina. Conclusions: Patients with unstable angina present a more atherogenic profile than patients with stable angina. Together with smoking, elevated Lp(a), CRP and leucocyte concentrations proved to be associated with the presence of unstable angina.

show abstract

Section: Discussionmentioning

confidence: 87%

Acute versus Chronic Myocardial Ischemia: A Differential Biological Profile Study

Sagastagoitia

Sáez²,

Vacas³

et al. 2007

Pathophysiol Haemos Thromb

View full text Add to dashboard Cite

show abstract

“…The composition of the Krebs-Henseleit solution 13 3 . The partial pressure of oxygen in the solution was maintained between 550 and 600 mmHg.…”

Section: Methods -mentioning

confidence: 99%

Behavior of cardiac variables in animals exposed to cigarette smoke

Paiva¹,

Zornoff²,

Okoshi³

et al. 2003

Arq. Bras. Cardiol.

View full text Add to dashboard Cite

Among health hazards caused by smoking, cardiovascular changes stand out. Smoking influences the prevalence of infarction through several mechanisms, such as endothelial dysfunction, greater oxidation of LDL-cholesterol, a reduction in HDL-cholesterol, an increase in the levels of adhesion molecules and fibrinogen, an increase in platelet aggregation, and an increase in the prevalence of vascular spasm 1,2 . English et al 3 were the first to report a close relation between smoking and mortality due to ischemic heart disease, and they were followed by other authors who stressed that association 4,5 . The proposed mechanisms, by which the constituents of cigarette smoke (carbon monoxide, nicotine, tar, and the substances contained in vapor) may cause myocardial infarction, are as follows: thrombosis, formation of atherosclerotic plaque, platelet aggregation, vasoconstriction, hypoxia, and arrhythmia induction 6 . Although the association between the smoking habit and coronary heart disease is universally accepted, little is known about the morphofunctional effects of smoking directly on the heart. Thus, the objective of this study was to assess the behavior of the variables related to myocardial mechanical function and also to in situ heart function of the animals exposed to cigarette smoke. MethodsThe study comprised 51 male Wistar rats weighing between 200 and 250 g divided into 2 groups as follows: control group (C) -formed by 28 animals, receiving the diet routinely used in our laboratory adjusted according to the daily ingestion observed in group S during smoke exposure; and smoking group (S) -formed by 23 animals receiving the unrestricted diet routinely used in our laboratory for 3 months and exposed to tobacco smoke in the last 30 days.The method used was that proposed by Simani et al 7 and implemented by Wang et al 8 to expose the animals to cigarette smoke in a modified incubator. The rats, 5 each time, were placed in the clear chamber connected to the smoking device. Smoke puffs were drawn from a cigarette Objective -To assess the behavior of cardiac variables in animals exposed to cigarette smoke. (C= 3.39 ± 0.4 mm and S= 3.71 ± 0.51 mm, P=0.02). A significant reduction was observed in systolic shortening fraction (C= 56.7 ± 4.2% and S= 53.5 ± 5.3%, P=0.02) and in ejection fraction (C= 0.92 ± 0.02 and S= 0.89 ± 0.04, P=0.01). Methods - Conclusion -The rats exposed to cigarette smoke had a reduction in left ventricular systolic function, although their myocardial function was preserved.

show abstract

“…D) CIGARETTE SMOKING. The notion that cigarette smoking is linked to heart disease dates back to a series of studies that unequivocally linked smoking and the incidence of myocardial infarction (208,231,355). More recently, the Surgeon General's report estimates that smoking in-creases atherosclerotic disease by ϳ50% and doubles the incidence of coronary artery disease (962a).…”

Section: Epidemiology and Risk Factorsmentioning

confidence: 99%

Role of Oxidative Modifications in Atherosclerosis

Stocker¹,

Keaney²

2004

Physiological Reviews

2,248

1,756

View full text Add to dashboard Cite

This review focuses on the role of oxidative processes in atherosclerosis and its resultant cardiovascular events. There is now a consensus that atherosclerosis represents a state of heightened oxidative stress characterized by lipid and protein oxidation in the vascular wall. The oxidative modification hypothesis of atherosclerosis predicts that low-density lipoprotein (LDL) oxidation is an early event in atherosclerosis and that oxidized LDL contributes to atherogenesis. In support of this hypothesis, oxidized LDL can support foam cell formation in vitro, the lipid in human lesions is substantially oxidized, there is evidence for the presence of oxidized LDL in vivo, oxidized LDL has a number of potentially proatherogenic activities, and several structurally unrelated antioxidants inhibit atherosclerosis in animals. An emerging consensus also underscores the importance in vascular disease of oxidative events in addition to LDL oxidation. These include the production of reactive oxygen and nitrogen species by vascular cells, as well as oxidative modifications contributing to important clinical manifestations of coronary artery disease such as endothelial dysfunction and plaque disruption. Despite these abundant data however, fundamental problems remain with implicating oxidative modification as a (requisite) pathophysiologically important cause for atherosclerosis. These include the poor performance of antioxidant strategies in limiting either atherosclerosis or cardiovascular events from atherosclerosis, and observations in animals that suggest dissociation between atherosclerosis and lipoprotein oxidation. Indeed, it remains to be established that oxidative events are a cause rather than an injurious response to atherogenesis. In this context, inflammation needs to be considered as a primary process of atherosclerosis, and oxidative stress as a secondary event. To address this issue, we have proposed an “oxidative response to inflammation” model as a means of reconciling the response-to-injury and oxidative modification hypotheses of atherosclerosis.

show abstract

Tobacco and Coronary Disease

Cited by 97 publications

References 7 publications

Acute versus Chronic Myocardial Ischemia: A Differential Biological Profile Study

Acute versus Chronic Myocardial Ischemia: A Differential Biological Profile Study

Behavior of cardiac variables in animals exposed to cigarette smoke

Role of Oxidative Modifications in Atherosclerosis

Contact Info

Product

Resources

About