Halaman 1 dari 985 hasil
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
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
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
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
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
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
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
BACKGROUND: The influence of a pharmacologic agent on wavefront dynamics during ventricular fibrillation (VF) in a setting of remodeled and healed myocardial infarction (MI) remains poor explored. We hypothesized that nicotine, by virtue of its complex direct and indirect cardiovascular effects,
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
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
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
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
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
This study examined the effects of L-arginine on myocardial infarct size, hemodynamics, and vascular reactivity in environmental tobacco smoke (ETS)-exposed and non-ETS-exposed rats. We previously demonstrated that exposure to ETS increased myocardial infarct size in a rat model of ischemia and
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