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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

WHO mortality statistics are subject to severe criticism all over the world due to the ICD code, the monocausal evaluation and th inhomogenity of data which are only partially verified by post mortem findings. Despite this fact WHO statistics are the only possibility to compare morality in different areas. In order to prove their reliability we have collected data of patients who have died in 9 Vienna hospitals. Our material consists of more than 15000 out of 25000 death cases in the year 1976. The autopsy rate was about 70%. To handle this amount of datas a computer system was used. In comparison with the official Austrian statistics our total atherosclerosis rate was higher due to the multicausal evaluation and the much higher percentage of CHD. Atherosclerosis of the brain was found in a lower percentage than officially mentioned when autopsy was performed. An example for single case studies is the myocardial infarction in a defined age group to support the importance of statistics based on a high rate of autopsies and the use of electronic data processing.
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PMID:Atherosclerosis and mortality statistics. 721 44

Prepubertal boys and pubertal girls and boys selected because of the occurrence of acute myocardial infarction in their father or mother were characterized by a low HDL cholesterol when compared to healthy controls. This observation extends our previous observations of low HDL cholesterol in adult relatives of CHD patients to the children of the same patients. The occurrence of an HDL abnormality in young children demonstrates that the low HDL cholesterol precedes the occurrence of cardiovascular disease. Low HDL cholesterol was associated with increased VLDL cholesterol in prepubertal children and pubertal boys without significant increase in VLDL triglycerides. Smoking and drinking habits, and physical activity which are environmental factors known to affect HDL did not differ between these children and the controls and cannot account for the observed differences. The results show that the low HDL cholesterol is detectable early in life in close relatives of CHD patients, persists throughout the lifespan and is possibly genetically determined.
Atherosclerosis 1980 May
PMID:Decreased HDL cholesterol in prepubertal and pubertal children of CHD patients. 738 69

Death or disability from CHD is a major public health problem that costs the Air Force about $50 million annually. Statistically, 20% of 30,000 pilots in the Air Force could have a significant degree of coronary atherosclerosis. In-flight incapacitation due to "heart attack" is a real possibility. Fortunately, aircraft accidents related to coronary events have been very uncommon. The basic mechanisms leading to the development of CHD, a multifactorial condition, are not fully understood. The significance of various risk factors associated with an increased incidence of CHD are discussed. It is hoped that preventive programs designed to identify, educate, and treat those at high risk will reduce the incidence of premature death and disability due to CHD. Two such programs (HEW's MRFIT and USAF's HEART) are briefly described. The costs, benefits, risks, sensitivity, and predictive value of tests available to detect CHD in asymptomatic individuals are outlined.
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PMID:Coronary heart disease: an expensive Air Force problem. 741 79

The link between impaired fibrinolytic function and CHD has been reinforced considerably in the past couple of years. This has been achieved by a combination of epidemiological, clinical, cell biological and molecular biological studies. The molecular mechanisms for the identified associations between more established risk factors for atherosclerotic disease and impaired fibrinolytic function now need to be disentangled to promote the design of specific drugs that may pave the way for intervention. The possibility that some of the observed relations are epiphenomena should also not be disregarded. The concept of genotype-specific differences in the susceptibility of the individual to common metabolic disturbances needs to be examined in greater detail. Basic research on the role of fibrinolysis in atherosclerosis and its thrombotic complications should be given high priority, because the modulation of fibrinolytic function is likely to become an important approach to prevention.
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PMID:Fibrinolysis and atherosclerosis. 754 67

Several clinical trials have provided compelling evidence in support of the benefits of lipid-lowering therapy for primary and secondary prevention of atherosclerosis. The results of primary prevention trials have demonstrated that coronary morbidity can be reduced and survival improved with effective lipid-lowering regimens. There has been concern, however, regarding harmful effects (e.g., increased rate of suicide and increased risk of gastrointestinal cancer) of cholesterol-lowering therapies in primary prevention trials. These concerns are not well supported by strong evidence, and there has been lack of a dose-response relationship. It is generally believed that for 1% reduction in serum cholesterol, there is a 2% reduction in the risk of coronary events. The results of numerous secondary prevention trials have clearly demonstrated the benefit of lipid-lowering therapies in reducing the risk of future cardiac events and cardiac mortality in patients with preexistent coronary artery disease. Several studies have shown that treatment regimens effective in reducing LDL cholesterol levels lead to regression of atherosclerotic plaques as well as retard the progression of the disease process. Interestingly, some of these studies have also shown that when measured angiographically, the luminal diameter at the site of stenotic lesions might improve only by an average of 2% to 3%; however, this small degree of improvement is associated with a remarkable reduction by 35% to 25% in the risk of future coronary events. These findings further corroborate the hypothesis about the importance of a lipid-rich cap of the vulnerable plaques and suggest that the reduction in lipid levels is associated with the efflux of lipids from the plaque, thus converting it from a vulnerable to a stable state. The most recent data from the 4S trial have unequivocally demonstrated the benefits of treatment with HMG coenzyme-A reductase inhibitors in reducing the risk of future coronary events and improving the overall survival in patients with established CHD. Although there is still ongoing controversy regarding the precise course of action for primary prevention of CHD, the results of a large number of studies provide overwhelming evidence in support of aggressive lipid-lowering therapy for secondary prevention of CHD. Based on the findings of these studies, it seems prudent that clinicians become actively involved in the evaluation and management of lipid abnormalities and other risk factors in patients with CHD.
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PMID:Clinical perspectives on primary and secondary prevention of coronary atherosclerosis. 767 95

Despite recent advances in both prevention and treatment, cardiovascular disease (CVD) remains the leading cause of mortality in the US. The Framingham Study was a landmark in defining CHD-related risk factors; unfortunately, very few minorities were included. A major preventable risk factor for CHD continues to be lipid abnormalities, but its association within minority populations is unclear. The few studies that have examined the association of hyperlipidemia with CHD in minorities have shown that total cholesterol was a predictor of CHD risk (e.g., black men aged 35-64). Several researchers have reported higher levels of HDL for black men and women compared to white men and women. Since HDL was shown to be inversely related to CHD, this discrepancy in HDL is hypothesized to account for the lower than expected mortality rate. Lipoprotein(a) has been identified as an independent risk factor for CHD; blacks have considerably higher levels than whites. Data also indicate the following: Hispanics have lower CVD mortality rates than the general population despite having known risk factors (e.g., obesity, diabetes, low socioeconomic status); Hispanic women have lower levels of HDL cholesterol; Native-American populations have lower prevalence of CHD associated with lower LDL-cholesterol and higher HDL-cholesterol. Understanding epidemiologic and pathophysiologic data regarding differences between various racial groups should help reduce CVD-related morbidity and mortality in minority populations.
Atherosclerosis 1994 Aug
PMID:Lipids, lipoproteins and coronary heart disease in minority populations. 780 31

This paper deals with the comparison of European and American guidelines for prevention of CHD, screening and management of hyperlipidemia. The revised EAS guidelines consist of 4 chapters: the scientific basis of CHD prevention; strategies for prevention of CHD; setting up a primary care system for CHD prevention, and the fourth focuses on clinical management with healthy diet, lifestyle and drug treatment of risk factors for CHD. The EAS guidelines emphasize that therapeutic decisions are based on the assessment of the global risk of CHD. In both EAS and American guidelines, optimal total plasma cholesterol and triglyceride target values recommended are < 200 mg/dl for both parameters. Both guidelines state that the initial approach to the treatment of hyperlipidemia should involve diet, increased physical activity, and weight reduction. If target levels are not achieved, the physician should determine whether drug therapy is appropriate. Conservative measures (diet and exercise) are recommended in particular for premenopausal women, elderly subjects and adolescents. There is complete agreement on the importance of secondary prevention of CHD.
Atherosclerosis 1994 Oct
PMID:Comparison of European and USA guidelines for prevention of coronary heart disease. 785 83

As a part of the EARS study we assessed the role of the common apo A-IV polymorphism in determining the hereditary predisposition to cardiovascular disease. The study population consisted of 1261 controls and 629 cases (students whose father had MI before 55 years) from five different European regions. The apo A-IV 1-1 phenotype accounted for 85% of the individuals. One per cent of subjects were homozygous for the apo A-IV2 allele. There was significant regional variation in the apo A-IV allele frequencies from North to South in Europe, with the lowest A-IV2 frequency in Finland. The distribution of the apo A-IV phenotypes was similar in cases and controls, as was the regional variation. The apo A-IV polymorphism did not affect HDL cholesterol. There was no correlation between apo A-IV alleles and the plasma concentration of apo A-IV. The plasma concentration of apo A-IV was lower in females than in males; furthermore, there was a significant difference in apo A-IV concentrations between oral contraceptive users and nonusers: users had the lowest values. As no strongly significant genetic difference could be demonstrated between plasma lipid concentration in cases and controls, and as the apo A-IV polymorphism did not significantly influence plasma lipid concentration, we conclude that the apo A-IV gene is not a major determinant of the risk for MI and/or CHD.
Atherosclerosis 1994 Jun
PMID:Genetic polymorphism of apolipoprotein A-IV in five different regions of Europe. Relations to plasma lipoproteins and to history of myocardial infarction: the EARS study. European Atherosclerosis Research Study. 798 Jun 97

High body iron stores have been proposed as a risk factor for advanced atherosclerosis. We investigated the prevalence of early atherosclerotic changes, and their relation to conventional CHD risk factors and body iron status. A cross-sectional study was carried out in 206 men aged 50 to 60 years (6% random population sample). Intima-media thickness (IMT) of the carotid artery was evaluated with high-resolution B-mode ultrasonography. Statistical analyses were performed separately for men with and without cardiovascular disease (CVD). Among all the study participants, 6.6% had IMT > 1.3 mm in the common carotid artery, whereas 53.8% had IMT > 1.5 mm in the carotid bifurcation. Respective values were 4.8% and 46.8% for those without CVD, and 8.5% and 62.2% for those with CVD. Mean IMT in the carotid bifurcation, the predilection site for atherosclerosis, was 1.85 mm (95% CI 1.72; 1.98) in the men with CVD, as compared to 1.65 mm (95% CI 1.56; 1.73) in the men free of CVD. Serum LDL cholesterol (beta = 0.26), saturated fat intake (beta = 0.20), blood haemoglobin (beta = -0.29), systolic blood pressure (beta = 0.21) and smoking (beta = 0.19), jointly explained 23% of the variance in the carotid bifurcation IMT in the men without CVD. Neither serum ferritin, transferrin nor dietary iron levels were associated with carotid bifurcation atherosclerosis. On the other hand, in the men with CVD, age (beta = 0.34) and physical activity (beta = -0.25) jointly explained 16.5% of the IMT variance in the carotid bifurcation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Association of risk factors and body iron status to carotid atherosclerosis in middle-aged eastern Finnish men. 798 92

We investigated the role of adrenal androgens, cortisol, testosterone and sex-hormone binding globulin (SHBG) as coronary risk factors using a nested case-control design. The study population consisted of 62 cases with cardiac end-points and 97 controls on placebo during the last 4 years in the Helsinki Heart Study. Serum concentrations of dehydroepiandrosterone, dehydroepiandrosterone sulfate (DHEAS), androstenedione, androstanediol glucuronide, cortisol, testosterone, and SHBG at the first annual visit of the 5-year study period were determined by radioimmunoassays. The only significant difference was found in DHEAS, with cases having higher levels than controls (P < 0.04). DHEAS levels were positively associated with smoking (P < 0.001), alcohol consumption (P < 0.04) and triglyceride levels (P < 0.002) and with systolic (P < 0.04) and diastolic (P < 0.006) blood pressures, and negatively associated with age (P < 0.01) and HDL-cholesterol (P < 0.03). The association between DHEAS and the CHD risk was studied using logistic regression analyses with the classical risk factors--age, smoking, blood pressure, and lipid levels--as covariates in the models. Studies of the joint effects of age and DHEAS disclosed that the risk associated with elevated DHEAS was confirmed to older men (odds ratio (OR) 7.3, 95%, CI 2.3-23.3). A similar analysis with smoking revealed that the DHEAS-related risk was mainly found in smokers (OR 3.4, 95% CI 1.5-8.2). One possible explanation for these results is that some form of mild steroid biosynthetic defect of the adrenals or functional adrenal hyperplasia associated with high DHEAS levels increases the CHD risk in this population.
Atherosclerosis 1994 Feb
PMID:Adrenal androgens and testosterone as coronary risk factors in the Helsinki Heart Study. 800 95


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