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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The impact of risk factors for sudden and non-sudden coronary death was investigated in 3,589 Finnish men aged 40-59 years at entry from a prospective population survey. During a mean follow-up time of 11 years, 234 coronary deaths occurred, 150 of which were sudden, i.e. ensuing within 1 hour of the onset of symptoms. The severity of the manifestations of CHD at baseline investigation appeared to be a powerful predictor of sudden coronary death. Smoking and high serum cholesterol were significant predictors of sudden coronary death. High serum cholesterol was an equally significant predictor of sudden and non-sudden coronary death. High blood pressure did not appear to significantly increase sudden coronary death but increased the incidence of non-sudden death significantly. Obesity and diabetes did not appear to be independent risk factors for sudden coronary death. Smoking and high serum cholesterol were significant risk factors for sudden coronary death in men with manifestations of coronary heart disease. The results suggest that reduction of primary risk factors, especially smoking and high serum cholesterol, is important even after coronary heart disease has become manifest.
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PMID:Risk factors for sudden and non-sudden coronary death. 334

In over 30 years of surveillance of 2873 women, 574 developed initial clinical manifestations of CHD. A number of antecedent metabolic risk factors proved atherogenic, including blood lipids, glucose tolerance, uric acid, and menopause. Serum total cholesterol predicts as strongly in women as in men. The predictive power of cholesterol is strengthened when the total cholesterol is partitioned into its atherogenic LDL and protective HDL fractions. Contrary to the case in men, triglyceride may be a contributor to risk in older women. A total-to-HDL cholesterol ratio exceeding 7.5 equalizes the risk in men and women. Impaired glucose tolerance also eliminates the female CHD risk advantage over men, conferring a three-fold increased risk. Serum uric acid, although lower in women than in men, is equally predictive in the sexes. Central obesity confers an increased CHD risk in women and predisposes to diabetes, hyperuricemia, hypertension, and an unfavorable LDL/HDL cholesterol ratio. A combination of obesity, low HDL cholesterol, and impaired glucose tolerance predisposes especially. Age-adjusted risk of CHD is increased two- to threefold compared to pre menopausal women, even when induced surgically without removing the ovaries. It is not clear whether post menopausal estrogen replacement eliminates this excess risk. Fibrinogen is higher in women than in men, and is increased with hypertension, diabetes, hypercholesterolemia, high hematocrit, and cigarette smoking. At any level of multivariate risk, fibrinogen added to the CHD risk in women.
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PMID:Metabolic risk factors for coronary heart disease in women: perspective from the Framingham Study. 360

Sudden death victims share most of the major risk factors for coronary disease in general; and the key to prevention is to reduce the risk of coronary attacks, especially by avoidance of cigarettes, correction of obesity, and reduction of blood pressure. The incidence increases with age, with sudden death incidence in women only a third that in men. By incorporating CHD risk factors into a multivariate logistic formulation, a composite estimate of risk is obtained over a wide range. A severely compromised coronary circulation manifested only by ECG abnormalities carries a high risk of sudden death. VPBs associated with sudden death often occur concurrently with ECG signs of LVH, intraventricular block, and nonspecific ST-T abnormalities. Convalescent MI patients with a low risk of sudden death are usually asymptomatic; have a normal creatinine, normal post-MI ECG, no tachycardia, a normal exercise ECG, few VPBs on monitoring, and normotension; and show no signs of cardiac failure.
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PMID:Epidemiology of sudden death: insights from the Framingham Study. 383 69

Analysis of the data derived in the course of examination of men aged 20 to 69 years demonstrates a distinct rise of the prevalence of CHD and AH with age. The level of the total cholesterol also increases with advancing age, reaching a maximum at 40 to 49 years as does the level of Tg (maximal at 50 to 59 years). The body weight also shows a linear increase. Emphasis should be placed on a high alpha-cholesterol content in persons aged 30 to 39 years. Analysis of the nutrition pattern of the male population aged 20 to 69 years revealed an atherogenic nature of nutrition marked by a high quota of fat, saturated fatty acids, low ratio of polyunsaturated to saturated fatty acids, and high cholesterol consumption with food. The highest consumption of energy sources and animal products was noted in persons aged 30 to 39 years. The same age demonstrated the lowest consumption of products of vegetable origin. Persons aged 50 to 59 years showed a reduction in consumption of protein of animal origin and essential polyunsaturated fatty acids as well as an increase in consumption of readily available sugars, which may lead to the development of obesity and hypertriglyceridemia and therefore to a higher risk of CHD development.
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PMID:[Age-related dynamics of the prevalence of ischemic heart disease and arterial hypertension and the mean level of basic risk factors in men 20 to 69 related to the nature of their nutrition]. 398 35

Lipids and lipoproteins were measured in 139 men and 145 women who were noninsulin-dependent diabetics (NIDDs) aged 45 to 64 years. Of these, 27 men and 16 women had had a previous definite myocardial infarction (MI). The NIDDs with MI (MI+) showed lower values of HDL and HDL2 cholesterol concentrations than NIDDs without previous MI (MI-) or NIDDS without any symptoms or electrocardiographic signs of coronary heart disease (CHD-). The inverse relationship between HDL, HDL2, and CHD was evident in both sexes, but it was particularly strong among male NIDDs. The difference in HDL and HDL2 cholesterol concentrations between the MI+ and MI- groups or between the MI+ and CHD- groups persisted after adjustment by analysis of covariance for the effect of physical activity, alcohol intake, obesity, duration of diabetes, and glycemic control. It is concluded that in a cross-sectional study, even among NIDDs with generally low HDL and HDL2 cholesterol concentrations, the presence of CHD is associated with a further depression of HDL and HDL2 cholesterol levels. Prospective studies are needed, however, to confirm that the association is predictive and not a consequence of CHD.
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PMID:Association of low HDL and HDL2 cholesterol with coronary heart disease in noninsulin-dependent diabetics. 407 98

It has become evident from a series of epidemiologic studies that an association exists between regular use of large amounts of alcoholic beverages and hypertension. In most studies, regular intake of smaller amounts of alcohol is not associated with hypertension but a possible threshold cannot be precisely defined at present. The relationship between alcohol and blood pressure is not attributable to demographic characteristics, obesity, reported salt use, smoking, or coffee use nor can it be explained by underreporting of alcohol consumption. If the relationship is causal then the pathogenesis is not yet firmly established. Multiple mechanisms, including direct effects of alcohol or of withdrawal from alcohol, are possible explanations. Alcohol shows a positive association with some sequelae of hypertension, but not to others. The most important exception is CHD, which is negatively associated with alcohol intake. Health professionals should not ignore the role of alcohol intake as a possible factor raising blood pressure in a certain proportion of hypertensive persons.
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PMID:The role of alcohol in the epidemiology of hypertension--is alcohol associated hypertension a common preventable disease? 639 87

The exceptional growth in risk factor assessment and the efficacy of primary prevention in childhood of atherosclerotic and hypertensive diseases is the subject of entire books that have recently collated the results of multiple investigators (58, 59). It is a topic well beyond the constraints of this review. It appears that the major "adult" CHD risk factors, including elevated total plasma and low-density lipoprotein cholesterol, elevated triglyceride, reduced high-density lipoprotein cholesterol, high blood pressure, obesity, and initiation of cigarette smoking can usually be recognized in children. There are, as yet, no longitudinal studies that control for one or more of these CHD risk factor variables to determine whether future development of CHD could be prevented or ameliorated. In the absence of unequivocal longitudinal studies of efficacy of intervention, prudent, safe, and well-supervised interventions should be carried out only after exhaustive proof of diagnosis (58). The recently summarized data suggest that they hyperlipoproteinemias, high blood pressure, obesity, and initiation of cigarette smoking can (with varying degrees of success) be dealt with during childhood and adolescence.
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PMID:Coronary risk factors in the young. 701 91

This study examines the relationship between obesity and low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, and very-low-density lipoprotein (VLDL) cholesterol in 4260 young adult men and women. The strongest association between obesity and LDL cholesterol was found in 20-29 yr-old males, the weakest in 40-49-yr-old males. Conversely, in women the relationship between LDL cholesterol and obesity was modest except in the oldest (40-49 yr) age group. An inverse relationship between obesity and HDL cholesterol was of similar shape and strength in all sex and age-specific groups. When the ratio of total cholesterol (TCHOL) to HDL cholesterol was compared in lean and grossly obese 20-29-yr-old males, substantial differences were found. Since other data show this index of the lipoprotein profile to be the single best indicator of CHD risk, it would appear that the atherogenic potential of obesity is greater than would be suggested by the relatively weak association between obesity and TCHOL or any single lipoprotein cholesterol. These data also suggest that the impact of obesity as a risk factor for CHD may have been underestimated. The paucity of lean males 40-49-yr-old prevents firm conclusions about the CHD risk in such a group. Indirect evidence indicates that lean 40-49-yr-old men would have a markedly more favorable lipoprotein profile and consequently a much lower risk of CHD.
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PMID:Obesity and lipoprotein cholesterol in the Framingham offspring study. 743 69

The prevention of cardiovascular diseases has been considered the first cause in diminishing coronary heart disease mortality. The main objective is the control of risk factors in primary as well as in secondary prevention. The correlation between diet rich in saturated fat and plasma cholesterol was the first milestone in this field followed by the improvement in cholesterol levels and subsequently in CHD mortality. Smoking cessation, physical exercise and control of blood pressure have shown to be efficacious. May be that Syndrome X that corresponds to insulin resistance, central obesity and low levels of HDL among other characteristics, reaches in the future a greater importance in CVD epidemiology. Other risk factors like those of psychosocial origin, thrombogenesis or hormones need more research in order to know their actual importance.
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PMID:[The epidemiology and risk factors of ischemic cardiopathy]. 749 37

A recent study (1) reported variation among men in clotting factor VIIc levels is associated with a genetic polymorphism detected by the restriction enzyme Msp I. The present study determined the Msp I genotype (Arg353, Gln353 alleles) for 189 women (mean age 53) who were subjects in the Healthy Women Study, a population study of CHD risk factor change at menopause. Women with the Arg/Arg genotype (n = 147) had an 16% higher (geometric) mean FVIIc level than those with the Arg/Gln (n = 41) genotype (1.21 vs 1.04 U/ml, p < 0.01), while the one subject with the Gln/Gln genotype had an FVIIc level of 1.00 U/ml. These results are consistent with those previously found in healthy men (1). In addition, women carrying the Gln allele did not exhibit the elevation in FVIIc with menopause and use of hormone therapy found among those with the Arg allele, suggesting that genotype may modify the observed rise in factor VIIc at menopause. Possibly because of the small sample size this interaction did not reach conventional levels of statistical significance. Results of multiple linear regression analyses controlling for age, hormone use, obesity, (ln) triglyceride levels, and family history of CHD found FVIIc levels to be significantly (p < 0.001) related to genotype. Thus, genotype appears to be a major determinant of FVIIc levels among women.
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PMID:Genetic determination of coagulation factor VIIc levels among healthy middle-aged women. 749 69


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