Heart Attack In Men Research Articles

Aspirin for Primary and Secondary Prevention of Cardiovascular Disease.

The first reported use of salicylate-rich plants as an analgesic and anti-inflammatory agent comes from the Ebers Papyrus, an Egyptian medical text from ca. 1,543 bc.1 It wasn't until the mid-1800s that silicon was isolated as the active component from willow tree bark extract, and then purified to acetylsalicylic acid. Bayer patented the compound in 1900, after the German chemist Felix Hoffmann's successful use of it to treat his father's severe arthritis. Finally, in 1950, the physician Lawrence Craven recognized that aspirin reduced the risk of heart attacks in men.2

The link between childhood sexual abuse and myocardial infarction in a population-based study

ObjectivesThis study examined the relationship between childhood sexual abuse (CSA) and myocardial infarction in men and women, while controlling for social determinants (i.e., socioeconomic status, social support, mental health) and traditional cardiovascular risk factors (i.e., age, race, obesity, smoking, physical inactivity, diabetes mellitus). MethodsPopulation-based data were obtained from the 2010 Behavioral Risk Factor Surveillance System. Myocardial infarction was ascertained by self-report of a health-professional diagnosis. CSA was defined as forced sex with someone at least 5 years older before the age of 18. The final sample included 5,095 men and 7,768 women. ResultsAfter adjustment for 15 factors, abused males had nearly 3 times the odds of heart attack compared to non-abused males (OR=2.96; 95% CI=1.12, 7.85). Among women, CSA was not associated with heart attack in the age–race adjusted (OR=1.20; 95% CI=0.39, 3.68) or fully-adjusted (OR=0.88; 95% CI=0.28, 2.75) analyses. ConclusionsCSA was associated with heart attack in men, even when controlling for traditional risk factors; however, no association was found among women. Future research is needed to replicate the study's unique findings.

2008 Stroke Council Award and Lecture—Brain and Heart: The Good, the Bad, and the Different

The brain and the heart are unique and essential organs, with autoregulated blood supplies and sophisticated electrical systems, functioning with harmonious complementarity in health; however, disease of one organ can threaten the other. Cardiac valvular disease, atrial fibrillation, and acute myocardial infarction carry a risk of stroke, and both ischemic and hemorrhagic strokes can lead to cardiac abnormalities and sudden death. Heart disease and stroke share most of the same risk factors, but not to the same degree, nor necessarily with the same consequences. For example, hypertension represents the single most powerful risk factor for stroke and can result in a major intracerebral hemorrhage, a condition without equivalent in any other organ. Despite the superficial resemblance between angina and transient ischemic attack, the mechanisms differ. Angina can be brought on by exercise, but no amount of mental exercise will lead to “brain angina.” Most cardiac patients can maintain a reasonable quality of life on half of their cardiac output. No meaningful quality of life is likely with half of brain output. Stroke recovery is complex. The brain is the only organ with which one can communicate directly and whose feelings have to be considered in recovery. Although stroke and heart disease prevention have much in common, puzzling differences remain. In primary prevention, aspirin prevents heart attacks in men but not in women, and strokes in women but not in men. Given the great commonalities and interrelationships between vascular brain and heart disease, it has been sensible and successful to have one organization encompassing cerebrovascular and cardiovascular health and diseases. To continue to progress at an accelerated pace, we need to become more familiar with the mutual relationship between cerebrovascular and cardiovascular disease, work together where we can, and separately where we must, but with the common aim of vanquishing both.

Traffic noise increases the risk of heart attack in men

Traffic noise increases the risk of heart attack in men

Summaries for patients. Helicobacter pylori infection and the risk for heart attacks in men.

Summaries for patients. Helicobacter pylori infection and the risk for heart attacks in men.

Risk of neoplastic and other diseases among people with heterozygosity for hereditary hemochromatosis.

Increased body iron stores have been associated with risk of heart attack in men and risk of cancer and colonic adenoma in both sexes. Because heterozygous carriers of hereditary hemochromatosis (HH) have on the average increased iron stores compared with noncarriers of the HH gene and comprise as much as 15% of the American population, disease risk in HH heterozygotes was investigated. A community-based cohort was defined, in which the exposure variable was heterozygosity for HH. Heterozygotes were identified by mailing individuals homozygous for HH questionnaires concerning the health histories of their parents (predominantly heterozygotes or exposed). Spouses of the HH homozygotes were asked to complete accompanying questionnaires concerning their parents (unexposed). The frequencies for exposed and unexposed, age-adjusted relative risks (RR), and 95% confidence intervals (CI), of cancer, heart disease, and stroke as causes of death as well as the cumulative incidence of heart attack, diabetes, stroke, hypertension, colonic adenoma, and cancers of the lung, colorectum, breast, cervix, pancreas, stomach, and blood were estimated. Data were available for 1950 HH heterozygotes and 1656 unexposed subjects. Elevated RR were observed in HH heterozygotes in males for diabetes (RR, 1.16; 95% CI, 1.01-1.33), colorectal cancer (RR, 1.28; CI, 1.07-1.53), and hematologic malignancy (RR, 1.30; CI, 1.30-1.63), for colonic adenoma in females (RR, 1.29; CI, 1.08-1.53) and males (RR, 1.24; CI, 1.05-1.46), and for stomach cancer in females (RR, 1.37; CI, 1.04-1.79). Heterozygosity for HH is associated with increased risk for colorectal neoplasia, diabetes, hematologic malignancy, and gastric cancer. No increased risk of heart disease, cancer death, or cancers of the lung, breast, or cervix were demonstrated.

Changes in drug treatment and case fatality of patients with acute myocardial infarction. Observations from the Newcastle MONICA Project, 1984/1985 to 1988/1990.

To describe changes in medications administered to patients with acute myocardial infarction between 1984/1985 and 1988/1990 and changes in case fatality. Descriptive study from the Newcastle MONICA Project, which monitors all heart attacks in men and women aged 25 to 69 years in the Lower Hunter Region of New South Wales. All patients admitted to hospital with a "definite" acute myocardial infarction who survived at least 28 days during periods in 1984/1985 (513 events) and 1988/1990 (790 events). Changes in drugs being taken immediately before the onset of the myocardial infarction, prescribed during hospitalisation and on discharge from hospital, and changes in case fatality rates. From the first time period to the second there were significant increases in the use of aspirin, calcium channel blockers, angiotensin-converting enzyme (ACE) inhibitors and hypolipidaemic agents, and significant reductions in the use of diuretics. In 1988/1990, 34% of patients with a definite myocardial infarction received thrombolytic therapy compared with fewer than 1% in 1984/1985. Among those patients who survived at least one hour from onset of symptoms, the case fatality rate declined from 13.5% to 7.9% (change -5.6%; 95% confidence limits, -8.9%, -2.2%). Large changes in drug treatment of patients with acute myocardial infarction have occurred in the second half of the 1980s. These may be responsible for the reduction in case fatality. Nevertheless, use of drugs of proven effectiveness in acute care and for secondary prevention is surprisingly low in this population.

Physical activity and stroke in British middle aged men.

To assess the relation between physical activity and stroke and to determine the overall benefit of physical activity for all major cardiovascular events. Prospective study of a cohort of men followed up for 9.5 years. General practices in 24 towns in England, Wales, and Scotland (British regional heart study). 7735 men aged 40-59 at screening, selected at random from one general practice in each of 24 towns. Fatal and non-fatal strokes and heart attacks. 128 major strokes (fatal and non-fatal) occurred. Physical activity was inversely associated with risk of stroke independent of coronary risk factors, heavy drinking, and pre-existing ischaemic heart disease or stroke (relative risk 1.0 for inactivity, 0.6 moderate activity, and 0.3 vigorous activity; test for trend p = 0.008). The association remained after excluding men reporting regular sporting (vigorous) activity. However, vigorous physical activity was associated with a marginally significant increased risk of heart attack compared with moderate or moderately vigorous activity in men with no pre-existing ischaemic heart disease or stroke (relative risk 1.6%; 95% confidence interval 0.96 to 2.8). In men with symptomatic ischaemic heart disease or stroke those doing moderately vigorous or vigorous activity had a risk of heart attack slightly higher than that in inactive men (relative risk = 1.6; 0.8 to 3.3). Moderate physical activity significantly reduces the risk of stroke and heart attacks in men both with and without pre-existing ischaemic heart disease. More vigorous activity did not confer any further protection. Moderate activity, such as frequent walking and recreational activity or weekly sporting activity, should be encouraged without restriction.

Physical activity and ischaemic heart disease in middle-aged British men.

To assess the relation between reported physical activity and the risk of heart attacks in middle aged British men. Prospective study of middle-aged men followed for a period of eight years (The British Regional Heart Study). One general practice in each of 24 British towns. 7735 men aged 40-59 years at initial examination. Heart attacks (non-fatal and fatal). During the follow up period of eight years 488 men suffered at least one major heart attack. A physical activity score used was developed and validated against heart rate and lung function (FEV1) in men without evidence of ischaemic heart disease. Risk of heart attack decreased significantly with increasing physical activity; the groups reporting moderate and moderately vigorous activity experienced less than half the rate seen in inactive men. The benefits of physical activity were seen most consistently in men without preexisting ischaemic heart disease and up to levels of moderately vigorous activity. Vigorously active men had higher rates of heart attack than men with moderate or moderately vigorous activity. The relation between physical activity and the risk of heart attack seemed to be independent of other cardiovascular risk factors. Men with symptomatic ischaemic heart disease showed a reduction in the rate of heart attack at light or moderate levels of physical activity, beyond which the risk of heart attack increased. Men with asymptomatic ischaemic heart disease showed an increasing risk of heart attack with increasing levels of physical activity, but with a progressive decrease in case fatality. Overall, men who engaged in vigorous (sporting) activity of any frequency had significantly lower rates of heart attack than men who reported no sporting activity. However, when all men reporting regular sporting activity at least once a month were excluded from analysis, there remained a strong inverse relation between physical activity and the risk of heart attack in men without pre-existing ischaemic heart disease. This study suggests that the overall level of physical activity is an important independent protective factor in ischaemic heart disease and that vigorous (sporting) exercise, although beneficial in its own right, is not essential in order to obtain such an effect.

Blood pressure, cigarette smoking and heart attack in the WHO co-operative trial of clofibrate.

In the WHO sponsored trial of clofibrate and its follow-up, about 15,000 men were observed for a mean period of 13.2 years. As expected, incidence of heart attacks (HA) was directly related to serum cholesterol, blood pressure (BP) and cigarette smoking. The previously reported lower incidence of HA in men receiving clofibrate compared with controls was most noticeable in hypertensive heavy smokers (P less than 0.01). BP was slightly lower in smokers than non-smokers (P less than 0.01). The difference in BP was greater in the trial visit before HA. Smokers also had higher plasma fibrinogen levels (P less than 0.05). The combination of reduced diastolic BP, and therefore myocardial perfusion pressure, with an increased thrombogenic tendency, might explain the high incidence of HA in smokers. Clofibrate apparently reduced fibrinogen levels, which might account for its specially good effect in preventing HA in smokers. However, the ill effects of smoking are still evident at a lower level in the men taking clofibrate and the drug is no substitute for giving up the habit. Clofibrate is not recommended for widespread use, except in subjects with marked lipid and/or blood fibrinogen abnormalities after dietary measures have been tried.

Electrocardiograms in the Busselton population.

Summary: In 1972, electrocardiograms were recorded on members of the Busselton community and classified according to nine major categories of the Minnesota code. Men showed a higher prevalence of abnormalities than women except for ST depression in 60–69 year old women.Comparisons with the 1959‐60 Tecumseh population revealed a significantly lower prevalence of T waves and tall R waves in Busselton people, and a tendency to fewer abnormal Q waves, abnormal ST segments and ectopic beats in Busselton men. The moderate prevalence of Q waves in Busselton compared with elsewhere is consistent with lower death rates from CVD observed in Busselton men over 60 years compared with urban men in Australia.Concerning the predictive value of including electrocardiography in mass health examinations, Busselton's 1966 ECGs were classified into one of three categories—those with either no evidence of ischaemic heart disease (IHD), with suspect IHD, or with probable IHD. All subjects have since been followed for six years. In those with evidence of suspect IHD, the annual death rates for heart attacks in men and women between 1967‐72 was 7–9 times that of those whose ECG showed no evidence of IHD. Men with probable IHD suffered about 20 times the annual risk and women about 47 times the risk of those whose ECG showed no evidence of IHD.