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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Over 1,200 middle-aged men with no apparent vascular disease participated in a 5-year multifactorial primary prevention trial, in which 612 received dietetic, hygienic and--when indicated--pharmacologic treatment for the following risk factors: hyperlipidemia, hypertension, smoking, obesity and abnormal glucose tolerance. Pharmacologic therapy included hypolipidemic agents (mainly probucol and clofibrate) and antihypertensive drugs (mainly diuretics and beta blockers). At the end of the 5 years, results in these men were compared with findings in 610 high risk and 593 low risk control subjects, none of whom had received treatment. Although intervention decreased the mean risk factor status of the treated men by 33%, their 5-year coronary incidence exceeded that of the high risk control subjects (3.1% vs 1.5%). Stroke incidence, however, was markedly reduced in the treated subjects (0% vs 1.3%). Multivariate analysis showed that the coronary events occurred in patients taking beta blockers or clofibrate, while few occurred in those receiving probucol or the diuretics. The decrease in mean serum cholesterol was 15% in men receiving only probucol, and ranged from 0% to 13% in those receiving different drug combinations, including clofibrate plus probucol (11%). Probucol also markedly decreased high density lipoprotein cholesterol levels, especially when combined with clofibrate. It is possible that adverse drug effects offset the probable benefit of an improved risk profile in the treated men, thereby explaining the greater than expected occurrence of cardiac events in this group. The probucol data, however, suggest that it may not be harmful to lower the high density lipoprotein cholesterol level when there is a significant decrease in total cholesterol as well.
Am J Cardiol 1986 Jun 27
PMID:Long-term use of probucol in the multifactorial primary prevention of vascular disease. 287 40

Almost all beta-adrenergic blockers, regardless of their pharmacologic characteristics, appear to have blood pressure-lowering activity in hypertensive patients. Comparisons between nonselective beta-blocking agents, such as propranolol and nadolol, with beta 1-selective drugs, such as metoprolol, atenolol and acebutolol, have demonstrated close similarities in their antihypertensive effects in patients. Similarly, beta blockers with and without intrinsic sympathomimetic activity (ISA) have comparable antihypertensive effects. However, beta-selective agents may offer some advantages over conventional beta blockers in hypertensive patients with concurrent conditions such as chronic obstructive airways disease, peripheral vascular disease, diabetes and hyperlipidemia. Beta 1-selective drugs are also preferred in diabetic patients receiving hypoglycemic agents because they do not interfere with glycogenolysis. Agents lacking ISA, such as propranolol, acutely increase peripheral resistance. beta blockers with ISA usually lower resistance. ISA may also minimize the bradycardia frequently found in elderly patients. Agents with ISA may protect against the decrease in high density lipoprotein cholesterol and the modest increase in triglycerides noted with some beta blockers that do not have ISA. Thus, in a large number of clinical situations in which hypertension is found, the properties of beta 1 selectivity and ISA allow beta blockers to be used with greater safety. Therefore, agents possessing both of these properties may be particularly valuable.
Am J Cardiol 1987 May 15
PMID:Clinical significance of beta 1-selectivity and intrinsic sympathomimetic activity in a beta-adrenergic blocking drug. 288 76

The treatment of high blood pressure with beta-blocking and other antihypertensive agents has been associated with a decrease in the incidence of stroke, progression of hypertension, heart failure, left ventricular hypertrophy, retinopathy and renal failure. Although hypertension increases the risk for developing coronary disease, the risk is heightened markedly if coexistent hyperlipidemia, smoking or glucose tolerance is present. Thiazide diuretics, primarily used as antihypertensive agents, compromise glucose tolerance and are associated with increases in plasma cholesterol, triglycerides and low density lipoprotein levels. Nonselective and beta 1-selective beta blockers have also been associated with increases in plasma triglycerides and very low density lipoproteins, as well as with decreases in high density lipoprotein levels. The effects of various antihypertensive agents on lipid levels, lipid metabolism, carbohydrate metabolism, left ventricular size and atherogenesis are discussed.
Am J Cardiol 1987 May 15
PMID:Effects of beta blockers and other antihypertensive drugs on cardiovascular risk. 288 79

Whether or not obesity per se is an independent risk factor remains controversial. However, a variety of studies have shown that obesity precipitates certain well-known risk factors, such as glucose intolerance, hyperlipidemia, hyperestrogenemia, hypertension, and left ventricular hypertrophy. Distribution of adipose tissue also seems to influence cardiovascular risk; patients with predominantly male-pattern obesity exhibit more profound risk for cardiovascular disease.
Cardiol Clin 1986 Feb
PMID:Risks for obesity. 293 52

Major risk factors have been identified that enhance the chances of cardiovascular morbidity and mortality. These include such modifiable factors as hypertension, hyperlipidemia, obesity, diabetes mellitus, smoking and hyperuricemia. Other factors that also increase risk are not modifiable and include advancing age, male gender and black race. The development of left ventricular (LV) hypertrophy imposes another significant risk for increased morbidity and mortality. Development of LV hypertrophy may be produced by hemodynamic as well as nonhemodynamic mechanisms. Included in the latter group are some of the same factors that in and of themselves participate in the production of increased LV mass (i.e., aging, gender and race, obesity, coronary disease, diabetes and the underlying mechanisms that subserve the hypertensive disease). This article discusses the concept, drawn from clinical and experimental studies, that demonstrate that the additional increased risk of LV hypertrophy may be ascribed to loss of reserve cardiac function, accelerated atherosclerosis, development of abnormal cardiac rhythm secondary to ischemia, fibrosis or drug-induced hypokalemia, inherent predisposition to ventricular dysrhythmias and sudden death, risks directly or coincidentally related to associated diseases or perhaps even the paradoxical risk of beneficial antihypertensive therapy.
Am J Cardiol 1987 Jan 23
PMID:Potential mechanisms explaining the risk of left ventricular hypertrophy. 294 82

We report 41 patients with myocardial infarction who were less than forty years old and that had been studied by coronary angiography. 97.5% were male mostly in their thirties. Coronary risk factors in this group were similar to the old one; excepting for mental stress present in 75% of our patients. There was not predominant infarction site. We observed different disturbances of the cardiac rhythm but no patient had congestive heart failure or cardiogenic shock. Mortality due to the infarct itself was none .61% of the cases had univascular lesions or normal coronary angiography and only 12% had trivascular lesions. The patients with normal coronary angiography had no significant difference in the mayor coronary risk factors and in our group we found patients with arterial hypertension, hyperlipidemia, cigarette smoking and obesity. We suggest that mental stress is an important coronary risk factor; the evolution of these patients is favorable and the mortality is low as compared with previous reports.
Arch Inst Cardiol Mex
PMID:[Clinico-angiographic correlations in myocardial infarction in young people]. 295 73

Atherogenesis is a complex tissue reaction involving both vascular and circulating cells and components. The former include endothelial and smooth muscle cells, the latter circulating monocytes, platelets and lipoproteins. The role of growth factors secreted by platelets and all the cells involved in setting into motion a fibrocellular vascular reaction has been recently elucidated. Repeated injury or the presence of hyperlipidemia leads to occlusive disease. Many of these cellular events are also likely to be stimulated by the vascular injury that occurs as part of the angioplasty procedure. Restenosis, a major complication of the latter, may reflect the vascular response to iatrogenic injury. Progress in understanding the mechanisms involved in restenosis should also clarify important aspects of atherogenesis.
Am J Cardiol 1987 Jul 31
PMID:Insights into coronary angioplasty-induced restenosis from examination of atherogenesis. 295 47

The wealth of convincing evidence favouring the major role of lipids in atherosclerosis and the benefit of lipid lowering therapy for its prevention now sets the stage for more practical questions: "Whom to treat? When to treat? How to treat?". Although each patient must be considered individually, there are general rules and specific guidelines that should be underlined. An isolated finding of abnormal lipid levels should by no means be a systematic starting point for initiating treatment. In a step by step approach, guidelines for individual risk assessment, systematic search for specific clinical clues and pertinence of complementary investigative measures are given. In addition to ensuring a correct diagnosis, these recommendations will orient the physician's decision with respect to the necessity of initiating treatment and, if warranted, the choice of an optimal treatment algorithm. Therapeutic modalities are discussed both in general and specific terms, focusing mostly on pharmacologic agents. Clinical indications, mechanisms of action, adverse effects and expected efficacy are seen for each drug or family of drugs, including those with a promising future. In summary, 10 easy rules of thumb are provided to ensure adequate diagnosis and management of hyperlipidemia.
Can J Cardiol 1988 Jul
PMID:Identification of the patient at risk in the physician's office and drug management of dyslipoproteinemia. 305 39

Clinical therapy for hyperlipidemia and obesity mandates dietary changes. The rationale for modification of specific dietary components becomes more impressive with each decade, as research and epidemiologic studies continue. Treatment modalities should be based on lipid patterns and lipid aberrations. Intervention methods should become practical and behaviorally motivating for patients. The environment must be receptive, with sophisticated interaction between the physician and registered dietitian. Third party reimbursement trends should be considered, but should not deter nutrition care services essential for medical management of the individual with heart disease.
J Am Coll Cardiol 1988 Oct
PMID:Nutritional therapy for hyperlipidemia and obesity: office treatment integrating the roles of the physician and the registered dietitian. 307 26

Prior studies of the contribution of coronary disease risk factors to familial aggregation of premature coronary disease may have underestimated risk factors by relying on self-reported risk factor prevalence levels or, when risk factors have been measured, by using cut points in excess of the 90th percentile. To determine the actual prevalence of hyperlipidemia, hypertension and diabetes, and the awareness of these coronary risk factors in unaffected family members, 150 apparently coronary disease-free siblings of 86 people who had documented coronary disease before 60 years of age were studied. All subjects participated in a 1 day screening preceded by a self-administered risk factor questionnaire and a personal interview. Participation of both the index patients and siblings exceeded 86%. With the use of nationally established recommendations for blood pressure and lipids, which are based on coronary disease risk curves, screening revealed that 48% of brothers and 41% of sisters were hypertensive, 45% of brothers and 22% of sisters had a lipid abnormality, 38% of siblings were current cigarette smokers and 4.7% were diabetic. Two or more risk factors were present in 42% of brothers and 26% of sisters. More than 75% of siblings had one or more risk factors that would require intervention. When compared with a race-, gender- and age-matched reference population from the Lipid Research Clinics Prevalence Study, distributions for blood pressure and for total and low density lipoprotein cholesterol were higher for the siblings in every gender and age group.(ABSTRACT TRUNCATED AT 250 WORDS)
J Am Coll Cardiol 1988 Nov
PMID:Risk factors in siblings of people with premature coronary heart disease. 317 Sep 71


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