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

The family at risk has at least one member who has (1) hyperlipidemia; (2) low HDL2-cholesterol; (3) essential hypertension; (4) a family history of premature CHD; or (5) actively smokes. The predictive value of CHD risk factors in adults is well documented and quantified. Familial aggregation, genetic studies, and tracking of blood pressure provide evidence that children born to families with a high prevalence of hypertension or who as adolescents track in the upper part of the blood pressure distribution are themselves at risk for hypertension. Similarly, familial aggregation, tracking, and autopsy studies provide evidence for the relationship of serum lipids to the subsequent development of coronary atherosclerosis. Smoking by parents adversely affects the hearts and lungs of children. In addition, the child with a parent who smokes is more likely to become an active smoker. Preventive strategies are now available to the pediatrician to reduce the risk of premature CHD.
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PMID:The management of the family at high risk for coronary heart disease. 265 86

Experimental and clinical evidence points to the existence of a cardiomyopathy associated with diabetes mellitus that is not due to coronary atherosclerosis. The condition is characterized by distinct clinical presentations and physiologic and biochemical abnormalities. Potential mechanisms for the development of diabetic cardiomyopathy are complex but are probably associated, in part, with hyperglycemia and hyperlipidemia. Primary hypertension is also associated with the development of myocardial abnormalities. Many of these changes are similar to those seen in diabetic cardiomyopathy. It is now clear that the co-existence of hypertension and diabetes mellitus produces a more severe cardiomyopathy than that produced by hypertension or diabetes alone. Potential mechanisms for interaction are numerous. Treatment of hypertension in diabetic patients must be targeted to more specific needs. Antihypertensive drugs should not worsen cardiac risk factors or glucose control and should have favorable effects on left ventricular function. The calcium antagonists and angiotensin-converting enzyme inhibitors have pharmacologic profiles that make them attractive as monotherapy for diabetic patients.
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PMID:Myocardial disease in hypertensive-diabetic patients. 268 10

Recent evidence suggests that metabolic changes that occur with antihypertensive agents may influence cardiovascular risk. Diuretic therapy is particularly appropriate for the salt-sensitive hypertensive patient. However, diuretic-induced electrolyte abnormalities may lead to ventricular arrhythmias, even in patients with uncomplicated essential hypertension. Antihypertensive drugs may change circulating lipoprotein levels, which may influence the development of atherosclerosis. Therefore, serum cholesterol and triglyceride levels should be monitored when antihypertensive drugs are administered that can cause hyperlipidemia. Weight reduction and diet therapy should be used because these may have a greater effect on reducing hyperlipidemia, though choice of antihypertensive agents is important. In addition, glucose tolerance may worsen with thiazide therapy, perhaps because newer evidence suggests that insulin resistance is common in essential hypertension. This glucose intolerance may be corrected with potassium repletion or substitution of bumetanide for thiazide. The calcium antagonists may be substituted for diuretic therapy, or other classes of antihypertensive drugs may be used with a reduced dose of diuretic drug if these metabolic changes persist. Thus, attention to metabolic changes may be as important as blood pressure reduction in treatment of the salt-sensitive hypertensive patient.
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PMID:Metabolic changes with antihypertensive therapy of the salt-sensitive patient. 328 52

Thiazide diuretics have been the 'mainstay' of antihypertensive therapy for three decades. They reduce arterial pressure, initially through a fall in plasma volume and cardiac output. However, in time, output returns towards pretreatment levels, thereby accounting for a long-term fall in pressure through decreased vascular resistance. At present, the precise mechanism for this reduced resistance remains unknown. Although the fall in arterial pressure is not due to direct vasodilation, it is not unlikely that it may operate, in part, indirectly through reduced vascular responsiveness, induced prostacyclins and other mechanisms. Attendant unwanted biochemical effects include hypokalaemia, hyperuricaemia, hyperglycaemia, reduced renal excretory function and hyperlipidaemia. Orthostatic hypotension and, of more recent emphasis, sexual impotence are among the more common side effects. A question has been raised as to whether hyperlipidaemia might explain the failure of some multicentre studies to prevent myocardial infarction or progression of coronary heart disease but this is more a 'non issue' although it must be considered. The present data continue to support the conclusion that diuretics are safe, effective and economical for the treatment of hypertension, and they remain a major cornerstone of initial as well as multipharmacological therapy, particularly in volume-dependent forms of essential hypertension, steroid-dependent hypertensions, renal parenchymal disease and in special patient groups (black, obese and elderly.
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PMID:Diuretics in hypertension. 331 27

During three-month therapy with small doses of guanfacine (Estulic Sandoz) that were sufficient to control blood pressure in patients with stage II essential hypertension and led to a decrease in excretion of noradrenaline and vanillylmandelic acid, the authors found a decrease in the level of blood cholesterol in patients with hyperlipidaemia. There was no adverse effect on the levels of triglycerides, beta, pre-beta and alpha lipoproteins. The authors conclude that Estulic therapy is indicated in patients who, in addition to essential hypertension, have hyperlipidaemia.
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PMID:The effect of small doses of guanfacine (Estulic Sandoz) on the lipid levels and catecholamine excretion in patients with essential hypertension. 331 51

Population-based sibships with essential hypertension diagnosed before the age of 60 years are being screened in Utah to find two or more hypertensive siblings with the same biochemical abnormality as a clue to an inherited cause for their specific type of hypertension. Among 131 hypertensive subjects in 58 sibships, concordant abnormalities in fasting serum lipid concentrations were observed in two or more siblings in 48% of the sibships. After adjusting for effects of antihypertensive medications, abnormal values reported in only 10% of the Lipid Research Clinics data were observed in 30% of patients for serum triglycerides, 19% for serum low-density lipoprotein cholesterol, and 39% for high-density lipoprotein cholesterol. More than one lipid level was abnormal in almost all concordant sibships, suggesting an association between hypertension and a syndrome of mixed lipid abnormalities, probably familial combined hyperlipidemia (renamed "familial combined dyslipidemia" because of common low high-density lipoprotein cholesterol levels). We conclude that familial dyslipidemic hypertension may be a specific syndrome with lipid abnormalities more severe than blood pressure elevations.
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PMID:Familial dyslipidemic hypertension. Evidence from 58 Utah families for a syndrome present in approximately 12% of patients with essential hypertension. 337 5

Red cell Na-Li countertransport was measured in 78 normal subjects, 64 patients with essential hypertension, and 67 patients with hyperlipidemias. Both hypertensive and hyperlipidemic patients had elevated Na-Li countertransport compared to normal controls (p less than 0.001). Subjects with hyperlipidemia and hypertension had higher countertransport (p less than 0.02) than patients with only hyperlipidemia. Normotensive hyperlipidemic subjects had higher countertransport than normotensive and normolipidemic controls (p less than 0.02). This suggest that hypertension and high plasma lipids can influence independently the Na-Li countertransport. In another group of 52 normotensive subjects, Na-Li countertransport was positively correlated with serum total and free (unesterified) cholesterol, phospholipids and triglycerides. No correlations were found with HDL-cholesterol or HDL-phospholipids. A very high positive correlation was found between Na-Li countertransport and plasma acetylcholinesterase (p less than 0.005). These findings suggest that plasma lipids, probably through membrane lipids, can affect the maximal rate of the Na-Li exchange in red cells. The relationship between plasma or membrane lipids and cation transport should be further studied in erythrocytes and other cells.
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PMID:Elevation of red cell sodium-lithium countertransport in hyperlipidemias. 396 81

The authors examined 40 patients with chronic ischemic pancreatitis without concomitant pathology of the alimentary organs in order to define the features of the disease clinical picture and progress. It was found that patients with disseminated atherosclerosis, especially when it is coupled with essential hypertension, and with extravasal stenosis of the celiac trunk are predisposed to the development of chronic ischemic pancreatitis. Factors promoting pancreatic ischemia include abnormalities of the blood rheological properties seen in vascular pathology and alimentary hyperlipidemia.
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PMID:[Various characteristics of chronic ischemic pancreatitis]. 652 92

Essential hypertension, a disease that affects about 60 million Americans, is not a homogeneous clinical entity. The disease is caused by altered regulation of mechanisms that control arterial pressure. Because the manifestations of the abnormally regulated pressure have many factors, the approaches to treatment likewise may be expected to be multifactorial. Hemodynamic, neural and catecholamine, renopressor, renal excretory and volume, hormonal, electrolyte, and depressor mechanisms are discussed. Associated conditions that must be considered include exogenous obesity, hyperuricemia, coronary artery disease, carbohydrate intolerance, and hyperlipidemia. Clearer understanding of the role of each of these factors in essential hypertension should provide a rationale for wise selection of antihypertensive therapy and allow reversal of the very high rates of cardiovascular morbidity and mortality associated with the disease.
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PMID:Mechanisms contributing to high blood pressure. 684 8

Hypertensive patients with hyperlipidemia are at high risk to develop coronary heart disease (CHD). Chemotherapeutic correction of hyperlipidemia seems most reliable modality to prevent CHD. Hypolipidemic effect and tolerance of leskol (fluvastatin) in dietotherapy-resistant hypercholesterolemia were studied in 74 patients with essential hypertension treated with hypotensive drugs. The patients were included in a multicenter trial. A 12-week course reduced total cholesterol level under 6.2 mmol/l in 59% of the patients, under 5.2 mmol/l in 29% of them. LDLP cholesterol lowered to 3.5% in 34% of the patients. Mean apo B diminished by 23%. There was a 27% decrease in the proportion of atherogenic fraction apo B to antiatherogenic fraction of transport proteins apo A-I. Leskol is well tolerated and effective against hypercholesterolemia, it is safe in relation to side effects and blood biochemistry.
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PMID:[The hypolipidemic effect of and tolerance for Lescol in treating hypercholesterolemia in hypertension patients (an analysis of the data from a multicenter study)]. 770 57


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