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

In this unifying hypothesis directed to the etiology and pathogenesis of atherosclerosis, the importance of focal arterial lesion-prone sites has been emphasized. Key initial participants in these sites include the focal intimal influx and accumulation of low-density lipoprotein (LDL) and a preferential recruitment of blood monocytes. Both are further enhanced in the presence of hyperlipidemia, when the quantity of intimal LDL and the oxidative potential of the intima exceed the capacity of macrophages to remove, via the non-down-regulating scavenger receptor, cytotoxic anionic (Ox-LDL) macromolecules. Foam cells, pathognomonic of the fatty streak, form during the receptor-mediated uptake of Ox-LDL by the macrophages. Interstitial free radicals and the excess of Ox-LDL particles injure and kill cells, including the foam cells, with the formation of the necrotic extracellular lipid core, a key transitional step in lesion progression. Monocyte-macrophage recruitment to the intima is likely to be regulated not only by a multiplicity of endothelial adhesive cytokines, integrins, and selectins, but also by the monocyte-specific chemoattractant, MCP-1, constitutively synthesized and secreted by intimal smooth muscle and endothelial cells. Its synthesis and secretion is augmented by mildly oxidized LDL. Free radicals, pivotal in the oxidation of LDL, and derived from activated macrophages, and also endothelial and smooth muscle cells. Smooth muscle cells migrate from the media through the intimal endothelial layer (IEL) and proliferate under the regulation of a number of mitogens, including platelet-derived growth factor (PDGF). Collagen synthesis by smooth muscle cells is substantial. Lymphocytes, as a source of interferons, invade the plaque and are present in the adventitia in substantial numbers, likely representing an autoimmune response in the later stages of plaque development. Platelets and mural thrombosis directly contribute to subsequent plaque growth, particularly after plaque rupture or fissure and disruption of the thromboresistant endothelial cells (EC). Plaque regression in all likelihood involves the conversion of the inert pool of extracellular lipid to a metabolically active intracellular pool and subsequent clearance by the high-density lipoprotein mediated reverse cholesterol transport system. The atherogenic cascades so described conceptually represent arterial inflammatory and healing processes occurring in a hyperlipidemic environment. Many components of pathogenesis are the targets for modulation by genetic, hemodynamic and selected risk factors. The prevention and treatment of the disease should logically target reduction in plasma LDL levels, the inhibition of the oxidative modification of lipoproteins, including LDL, by free radical scavengers, and augmentation of the reverse cholesterol transport system.
Clin Cardiol 1991 Feb
PMID:The pathogenesis of atherosclerosis: an overview. 204 53

The mechanisms responsible for reocclusion after percutaneous transluminal angioplasty are still poorly understood. The effects of angioplasty on arterial morphology, deoxyribonucleic acid (DNA) synthesis (3H-thymidine incorporation) and lipid metabolism (14C-oleate incorporation) were studied in renal arteries of 24 male mongrel dogs. Balloon-dilated (identified by Evans blue dye accumulation) and adjacent normal arterial segments were collected 90 min and 2, 5 and 14 days after the procedure. The immediate vascular response was endothelial cell denudation and platelet accumulation. Two weeks after angioplasty, healing of the luminal surface by "endothelial-like" cells, mild smooth muscle cell proliferation and an angiogenic response with capillary growth into the media were observed. DNA synthesis was increased in balloon-dilated segments at day 5 compared with adjacent nonballoon-dilated artery. This increase in DNA synthesis persisted in the 2 week postangioplasty segments. Additionally, angioplasty produced both quantitative and qualitative changes in arterial lipid synthesis. The most dramatic change was an increase in sterol esterification that was apparent as early as 90 min after angioplasty; the change persisted through day 5 but diminished toward baseline by day 14. Angioplasty-induced alterations of arterial metabolism parallel aspects of the atherogenic process and may be involved in the pathogenesis of postangioplasty reocclusion, particularly in the presence of additional risk factors, such as hyperlipemia.
J Am Coll Cardiol 1990 May
PMID:Proliferative and lipid metabolism response to balloon angioplasty in canine renal arteries. 213 45

Clinical, electrocardiographic and echocardiographic findings of 69 subjects aged 80 years or over were analyzed in order to assess the prevalence of left ventricular mass, hyperlipidemia, hypertension and cigarette smoking. Of the 69 subjects studied, 41 had no symptoms or sign of cardiovascular disease, 28 had one or more cardiac symptoms (NYHA stage 2-4). 25 had electrocardiographic evidence of left ventricular hypertrophy and there were no differences between the asymptomatic and symptomatic groups. Echocardiographically, the left ventricular mass index ranged between 103 to 247 g/m2 in men and 170 to 251 g/m2 in women. In 36 subjects with high left ventricular mass index, the ventricular septal thicknesses ranged from 12 mm to 15 mm in 19 subjects, and posterior wall thicknesses ranged from 12 mm to 16 mm in 17 subjects. Of the 58 patients with an adequate echocardiogram, 47 had clinically diagnosed hypertension (81%). In our study population, a prevalence of left ventricular hypertrophy (62%), isolated systolic hypertension (26%), definite hypertension (33.3%), high LDL-cholesterol (63%), low HDL-cholesterol (26%), abnormal Q wave (16%), cigarette smoking (47.8%) and diabetes mellitus (1.4%) were found.
Int J Cardiol 1990 Dec
PMID:Left ventricular mass index and prevalence of heart disease in the population aged 80 years and over. 214 63

Four-week-old Wistar and Wistar-Kyoto (WKY) and 12-year-old Wistar rats treated with streptozotocin (55 or 65 mg/kg) were studied to assess the relationship between diabetes-induced alterations in lipid and thyroid hormone concentrations and myocardial tissue function. In the Wistar rats, both doses of streptozotocin resulted in hyperlipidemia and hypothyroidism. However, the higher dose was associated with: greater increases in plasma lipid levels in both age groups; larger increases in plasma lipid levels in older rats; and decreases in myocardial sensitivity to isoproterenol and beta-adrenoceptor density. The diabetic state in WKY rats, while also accompanied by hypothyroidism, was not differentially affected by the two doses of streptozotocin, nor associated with severe hyperlipidemia, nor associated with alterations in the myocardial beta-adrenoceptor system. These findings, as expected, reveal that the dose of streptozotocin and the age and strain of rat influence the diabetic state. Furthermore, these data do not suggest a direct correlation between diabetes-induced alterations in myocardial inotropic sensitivity and associated changes in plasma lipid or thyroid hormone concentrations.
Can J Cardiol 1990 Mar
PMID:Myocardial and metabolic abnormalities in streptozotocin-diabetic Wistar and Wistar-Kyoto rats. 215 89

Obesity is known to be associated with diabetes, hypertension and hyperlipidemia in the majority of the patients. There could be inaccuracy in measuring the blood pressure in obesity, therefore a cuff of sufficient size is important in blood pressure measurement. All parameters of obesity have been found to have a correlation with hypertension and it has been suggested that change in weight would cause a change in blood pressure. A weight reduction of 12 kg results in a blood pressure fall of 21/13 mm Hg. Such changes in blood pressures have been noted in untreated hypertensives. A few studies have negated the role of change in weight to have any influence on hypertension. Obesity causes a higher cardiac output and higher blood volume leading to hypertension. There may be increased intracellular sodium and reduced sodium-potassium-ATPase activity in obesity which causes increased sodium loading in hypertension. Abnormalities related to the insulin-carbohydrate metabolism and the renin-angiotensin aldosteron system have also been demonstrated in obese patients. Weight reduction also causes reduced dietary salt intake and diminished sympathetic activity. The benefits of weight reduction appear to be directly related to the amount of weight lost.
Acta Cardiol 1990
PMID:Effect of obesity and weight reduction in hypertension. 218 Feb 41

The control of coronary artery disease depends primarily on its prevention at an early stage. Researchers generally agree that early prevention depends on the elimination or treatment of known risk factors, among which hyperlipidemia occupies a central position. Two European Consensus Conferences have concluded that therapy of hyperlipidemia should always start with dietary counseling. First, subjects with body mass indexes (weight/height) greater than 27 should lose weight. Second, the lipid-lowering diet should provide 55% of calories from carbohydrates; 10 to 15% from protein; and up to 30% from fat comprising 10% each of saturated, monounsaturated and polyunsaturated fatty acids; less than 300 mg/day cholesterol; 35 g/day of fiber derived largely from legumes and other vegetables; and fruit. Further reduction of fat consumption (to 20 to 25% of total energy) and of cholesterol (to less than 150 mg/day) may be attempted when patients respond inadequately to the standard diet. The goal of treatment is to minimize the risk of coronary artery disease and of pancreatitis. Where possible, a low-density lipoprotein cholesterol level of 135 mg/dl (3.5 mmol/liter) should be the goal in hypercholesterolemic patients with multiple or severe risk factors and a level of 155 mg/dl (4 mmol/liter) in the absence of other risk factors. Also, high-density lipoprotein cholesterol greater than 35 mg/dl and triglycerides less than 200 mg/dl are considered important goals of treatment. Some patients with hyperlipidemia do not respond adequately to diet and correction of underlying causes; drug treatment should then be instituted, but careful attention to diet should be continued.
Am J Cardiol 1990 Mar 20
PMID:At what levels of total low- or high-density lipoprotein cholesterol should diet/drug therapy be initiated? European guidelines. 218 Feb 66

Nephron loss is a common progression of a diverse range of kidney diseases. Recent experimental models of chronic renal disease have suggested that hemodynamic and nonhemodynamic mechanisms play key roles in progressive renal injury. Extensive renal ablation in the rat was followed by development of altered glomerular hemodynamics. Albuminuria and histologic damage leading to focal glomerulosclerosis were preceded by the development of increased glomerular pressures and were prevented by interventions such as severe dietary protein restriction and angiotensin-converting enzyme (ACE) inhibitor therapy. Both experimental interventions ameliorated glomerular hypertension. It was therefore concluded that these interventions ameliorated injury by glomerular hemodynamic effect. Similar findings were obtained in a rat model of type I diabetes mellitus induced by streptozotocin in which glomerular hemodynamic factors appeared important to the development of progressive renal disease. Recent studies have suggested that nonhemodynamic factors have important roles in the progression of glomerular injury. For example, although the predominant effects of ACE inhibitor therapy appear to be hemodynamically mediated, data are emerging which suggest that these agents may also influence growth/proliferation of glomerular cells. Because hyperplasia/hypertrophy may influence glomerular susceptibility to injury, this may also be a potential mechanism whereby ACE inhibitor therapy influences glomerular damage. In addition, a variety of studies have suggested that hyperlipidemia, which is frequent accompaniment of glomerular disease, is an important modulator of glomerular injury independent of glomerular hemodynamic effects. Coagulation factors, calcium phosphorus balance, as well as the genetic susceptibility of the glomerulus to injury, all appear to contribute to progressive nephron destruction.
Am J Cardiol 1990 May 22
PMID:Renal protective effects of angiotensin-converting enzyme inhibition. 218 11

The inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase are highly effective in treating severe elevations of serum cholesterol, and are being widely used for this purpose. In our laboratory, these drugs have been used for the treatment of other forms of dyslipidemia including primary moderate hypercholesterolemia, primary mixed hyperlipidemia, diabetic dyslipidemia, hyperlipidemia of the nephrotic syndrome, and primary hypoalphalipoproteinemia. In these conditions, the HMG CoA reductase inhibitors proved effective in substantially decreasing levels of both low-density lipoproteins and very low density lipoproteins, as well as apolipoprotein B. In some patients, they may even increase levels of high-density lipoproteins. The primary mode of action of HMG CoA reductase inhibitors appears to be to increase the synthesis of hepatic receptors for lipoproteins containing apolipoprotein B, although a reduction in synthesis of these lipoproteins has not been ruled out with certainty. Regardless of mechanisms, drugs of this type appear to have the potential for effective therapy of various forms of dyslipidemia beyond primary severe hypercholesterolemia.
Am J Cardiol 1990 Sep 18
PMID:Use of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors in various forms of dyslipidemia. 220 34

To determine the prevalence, time course and factors responsible for hyperlipidemia after heart transplantation, 83 consecutive 1-year survivors were studied. By 1 year, 83% of patients had serum total cholesterol levels greater than 5.2 mmol/liter (200 mg/dl) and 28% of the patients had serum total cholesterol higher than the age- and sex-matched ninety-fifth percentile. At the end of 1-year follow-up, serum total cholesterol correlated with the recipient age (p less than 0.0001), the preoperative cholesterol level (p less than 0.001), the actual dose of maintenance prednisone at 1 year (p less than 0.02) and the cumulative 1-year steroid dose (p less than 0.03). Similarly, the serum triglyceride level at 1 year correlated with the pretransplant level of serum triglycerides (p less than 0.0001), recipient age (p less than 0.03) and cumulative 1-year steroid dose (p less than 0.03). Patients with a pretransplant diagnosis of coronary artery disease had a significantly higher level of serum total cholesterol and triglyceride levels at 1 year (p less than 0.02 and p less than 0.03, respectively). Heart transplant recipients with body mass index greater than or equal to 25 kg/m2 also presented with significantly elevated serum total cholesterol and triglyceride levels at 1 year compared with nonobese patients (p less than 0.01 and p less than 0.002, respectively). Hyperlipidemia occurs frequently and is detected within the first month after heart transplantation. Optimal management of this problem requires further study.
Am J Cardiol 1990 Nov 01
PMID:Serial evaluation of lipid profiles and risk factors for development of hyperlipidemia after cardiac transplantation. 187 95

Treatment of hypertension aims at preventing strokes and coronary events although diuretics and beta-blockers lowered blood pressure effectively and allowed prevention of strokes in large-scale trials, they did not reduce the incidence of myocardial infarction or coronary death. The failure of diuretics and beta-blockers to afford cardiac protection may be due in part to the unfavorable effects of these agents on associated risk factors like hyperlipidemia and smoking. Hyperlipidemia is more prevalent in hypertensive patients than in matched normotensive controls, and the combination of hyperlipidemia and smoking is more frequent than can be expected to occur by chance. Diuretics and beta-blockers affect lipid metabolism negatively. Unlike these agents, alpha-blockers do not alter serum lipids and might reduce triglyceride and cholesterol levels. Several trials have shown that the outcome of treatment with beta-blockers was less favorable in smokers than in non-smokers in terms of blood pressure control and prevention of coronary events. A possible explanation is provided by acute experiments in which beta-blockade enhanced the systemic and coronary vasocontriction elicited by smoking, while alpha-blockade had the opposite effect. Although there is reason to believe that alpha-blockers may be preferable to diuretics and beta-blockers for the treatment of high risk hypertensive patients who smoke and/or exhibit high levels of serum lipids, there is a need for larger and longer trials to test their ability to reduce cardiovascular risk.
Ann Cardiol Angeiol (Paris) 1989 Dec 15
PMID:[Effect of alpha inhibitors on risk cofactors in patients with hypertension]. 257 48


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