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myocardial infarction/− nicotin
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Tobacco cigarette smoking exacerbates aortic calcification in an early stage of myocardial infarction in a female mouse model.
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Despite increased social awareness, marketing restraints, tobacco taxation, and available smoking cessation rehab programs, active and passive smoking remain a worldwide challenging epidemic and a key risk factor for cardiovascular diseases development. Although cardiovascular (CV) protection is
Association of daily tar and nicotine intake with incident myocardial infarction: results from the population-based MONICA/KORA Augsburg Cohort Study 1984-2002.
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BACKGROUND
Cigarette smoking has been shown to be one of the most important risk factors for cardiovascular diseases. However, little is known about cumulative effects of daily tar and nicotine intake on the risk of incident myocardial infarction (MI) so far. To bridge this gap, we conducted an
Association between exposure to environmental tobacco smoke and biomarkers of oxidative stress among patients hospitalised with acute myocardial infarction.
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OBJECTIVE
To determine whether exposure to environmental tobacco smoke was associated with oxidative stress among patients hospitalised for acute myocardial infarction.
METHODS
An existing cohort study of 1,261 patients hospitalised for acute myocardial infarction.
METHODS
Nine acute hospitals in
Smokeless tobacco as a possible risk factor for myocardial infarction: a population-based study in middle-aged men.
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OBJECTIVE
To explore whether the use of snuff affects the risk of myocardial infarction (MI).
BACKGROUND
Snuff and other forms of smokeless tobacco are widely used in some populations. Possible health hazards associated with the use of smokeless tobacco remain controversial.
METHODS
In a
The effect of tobacco control measures during a period of rising cardiovascular disease risk in India: a mathematical model of myocardial infarction and stroke.
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BACKGROUND
We simulated tobacco control and pharmacological strategies for preventing cardiovascular deaths in India, the country that is expected to experience more cardiovascular deaths than any other over the next decade.
RESULTS
A microsimulation model was developed to quantify the differential
Nicotine and carbon monoxide content of cigarette smoke and the risk of myocardial infarction in young men.
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To evaluate whether the nicotine and carbon monoxide content of cigarette smoke is related to the risk of nonfatal first myocardial infarction in young men, we compared 502 cases with 835 hospital controls, all between the ages of 30 and 54 years. As expected, the estimated risk of myocardial
Chronic nicotine in hearts with healed ventricular myocardial infarction promotes atrial flutter that resembles typical human atrial flutter.
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The potential of chronic nicotine exposure for atrial fibrillation (AF) and atrial flutter (AFL) in hearts with and without chronic myocardial infarction (MI) remains poorly explored. MI was created in dogs by permanent occlusion of the left anterior descending coronary artery, and dogs were
Acute Myocardial Infarction in a Young Adult Male Associated with the use of Smokeless Tobacco (Sweka).
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Dipping smokeless tobacco (ST) is used worldwide. We report a case of acute myocardial infarction in a young patient, who consumed smokeless tobacco (Sweka) for over one year. ST may be as harmful as smoking and carries adverse cardiac complications. A prompt call for restriction and prohibition is
Retraction to: Electronic Cigarette Use and Myocardial Infarction Among Adults in the US Population Assessment of Tobacco and Health.
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After becoming aware that the study in the above-referenced article did not fully account for certain information in the Population Assessment of Tobacco and Health [PATH] Wave 1 survey, the editors of Journal of the American Heart Association reviewed the peer review process. During peer
Discontinuation of smokeless tobacco and mortality risk after myocardial infarction.
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BACKGROUND
Given the indications of increased risk for fatal myocardial infarction (MI) in people who use snus, a moist smokeless tobacco product, we hypothesized that discontinuation of snus use after an MI would reduce mortality risk.
RESULTS
All patients who were admitted to coronary care units
Increased risk of acute myocardial infarction associated with beedi and cigarette smoking in Indians: final report on tobacco risks from a case-control study.
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BACKGROUND
Tobacco smoking is an important risk factor for ischemic heart disease. In India, tobacco is smoked both as cigarettes and beedies. No studies have evaluated their importance as risk factors for ischemic heart disease among the Indian population. The present study explores the importance
[Effect of tobacco smoking on the incidence of recurrent myocardial infarction. A retrospective study of 208 cases].
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Two hundred and eight patients, less than 60 years of age at the time of their first myocardial infarction (MI), which occurred between 1 July 1976 and 30 September 1982, and with a mean recurrence-free follow-up period of 3450 +/- 142 days, were included in a retrospective survey. This concerned
CO inhalation at dose corresponding to tobacco smoke worsens cardiac remodeling after experimental myocardial infarction in rats.
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We hypothesized that inhalation of carbon monoxide (CO) (500 ppm), similar to that in tobacco smoke, disturbs the cardiovascular adaptation after myocardial infarction by increasing remodeling. Four groups of rats were assessed. Two groups had myocardial infarction induced by the ligation of the
Nicotine dependence and smoking cessation after hospital discharge among inpatients with coronary heart attacks.
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This study focuses on the predictability of two alternative questionnaires for nicotine dependence, i.e., the Fagerstrom Tolerance Questionnaire (FTQ) and the Tobacco Dependence Screener (TDS), each of which represents a different aspect of dependence, among patients with coronary heart disease
The role of oxidative stress and lipid peroxidation in ventricular remodeling induced by tobacco smoke exposure after myocardial infarction.
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OBJECTIVE
To evaluate the roles of oxidative stress and lipid peroxidation in the ventricular remodeling that is induced by tobacco smoke exposure after myocardial infarction.
METHODS
After induced myocardial infarction, rats were allocated into two groups: C (control, n=25) and ETS (exposed to
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