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At least 379 records · Page 21Linked to original sources
PubMed1982

Overview of randomized clinical trials of lipid intervention for atherosclerotic cardiovascular disease.

This paper is a review of the scientific and economic (when possible) impact of 15 randomized clinical trials of lipid intervention for atherosclerotic cardiovascular disease. No effort has been made to be all-inclusive and certain smaller and first generation studies have been omitted. No effort has been made to offer detailed analyses of protocols; we have limited discussion to summaries of the salient features of each study presented. After stating the data, we introduce certain reflections and raise some of the more obvious questions that emerge.

Arteriosclerosis↗
PubMed1994

Benefits of lipid-lowering therapy in men with elevated apolipoprotein B are not confined to those with very high low density lipoprotein cholesterol.

OBJECTIVES: Do the benefits of intensive lipid-lowering therapy extend to patients with only borderline or moderately elevated levels of low density lipoprotein (LDL) cholesterol? BACKGROUND: The merits of the present LDL cholesterol treatment goal of < or = 100 mg/dl need to be clarified for patients without high levels of LDL cholesterol, particularly for those patients previously classified as having only borderline high (130 to 159 mg/dl) or desirable (101 to 130 mg/dl) levels. METHODS: Disease change and clinical events were examined in LDL cholesterol subgroups in the Familial Atherosclerosis Treatment Study (FATS) trial, a randomized, blinded, quantitative arteriographic comparison of one conventional and two intensive lipid-lowering strategies in men with coronary artery disease, a positive family history and apolipoprotein B > or = 125 mg/dl. The primary end point, disease change per patient, was measured as the mean change in severity of stenosis (delta %SProx) among nine standard proximal segments. RESULTS: Of the 120 patients completing the 30-month protocol, 60 had a baseline LDL cholesterol < 90th percentile (mean LDL cholesterol 152 mg/dl) and 60 > 90th percentile (mean LDL cholesterol 221 mg/dl). Thirty-one patients had levels < 160 mg/dl (mean LDL cholesterol 134 mg/dl) and 89 > 160 mg/dl (mean LDL cholesterol 205 mg/dl). Patients with LDL cholesterol < 90th percentile benefited angiographically from therapy (delta %SProx = -1.5% diameter stenosis [regression] during intensive therapy vs. +2.3% diameter stenosis [progression] during conventional therapy, p < 0.01), as did patients with LDL cholesterol < 160 mg/dl (delta %SProx = -4.2% vs. +3.3% diameter stenosis, p = 0.0001). By comparison, angiographic benefit was less pronounced among those entering with very high LDL cholesterol (delta %SProx = -0.2% vs. +1.9% diameter stenosis, p = 0.07) or with LDL cholesterol > or = 160 mg/dl (delta %SProx = +0.2% vs. +1.6% diameter stenosis, p = 0.13). Intensive therapy resulted in a statistically significant reduction in clinical events only in the subgroup with baseline LDL cholesterol < 90th percentile (2 of 42 vs. 8 of 29 patients initially enrolled, p = 0.01) and a trend toward fewer events in patients with LDL cholesterol < 160 mg/dl (2 of 20 vs. 6 of 15 patients, p = 0.05). No such difference was seen in the higher LDL cholesterol subgroups. CONCLUSIONS: Treatment benefit in the FATS trial was not confined to patients with very high levels of LDL cholesterol and was in fact particularly evident in those patients with levels < 160 mg/dl. Such patients should be considered more likely, not less, to benefit from intensive lipid-lowering therapy.

Adult↗
PubMed2004

Effectiveness and tolerability of ezetimibe add-on therapy to a bile acid resin-based regimen for hypercholesterolemia.

Combination lipid-reducing therapy is increasingly used, particularly for the management of severe or combined dyslipidemia in patients at high risk for coronary heart disease. To assess the potential additive effects of combining the cholesterol absorption inhibitor ezetimibe with a bile acid resin (BAR), a prospective chart review was performed of 40 patients in whom ezetimibe 10 mg/day was added to a stable regimen that included a BAR. At an average follow-up of 107 +/- 57 days, ezetimibe coadministration significantly reduced total cholesterol by 18%, triglycerides by 14%, and low-density lipoprotein cholesterol by 19% (all p < or =0.03), without significantly changing high-density lipoprotein cholesterol, and the combination was well tolerated.

Allylamine↗
PubMed2000

The pharmacokinetics and pharmacodynamics of agents proven to raise high-density lipoprotein cholesterol.

Bile acid sequestrants, fibric acid derivatives (fibrates), hydroxy-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors ("statins"), and niacin are able to increase HDL-C serum concentrations to varying degrees. Bile acid sequestrants are the least effective, whereas niacin is the most powerful agent for increasing HDL-C levels. Because of 2 alternate metabolic pathways of niacin breakdown, flushing or hepatotoxicity can occur in patients taking niacin. These effects can be mediated in a carefully designed formulation of niacin that releases the drug at a predictable rate. Niacin has few drug interactions and is a relatively inexpensive means of increasing HDL-C. A combination formulation that combines niacin plus a statin has shown promise in ongoing clinical trials.

Biological Availability↗
PubMed1996

Drug therapy for hypercholesterolemia in patients with cardiovascular disease: factors limiting achievement of lipid goals.

PURPOSE: To determine the extent that goal lipid levels derived from the National Cholesterol Education Program (NCEP) are achievable in clinical practice, and to identify factors associated with the achievement of these goals. PATIENTS AND METHODS: We conducted a retrospective cohort study consisting of a consecutive sample of 244 patients with either coronary artery disease or peripheral vascular disease treated for hypercholesterolemia at a large Veterans Affairs medical center. Primary outcomes, recorded prospectively, were lipid levels and lipoprotein cholesterol response, and tolerance and compliance to drug therapy. Goal lipid levels were defined as low-density lipoprotein cholesterol (LDL-C) < or = 130 mg/dL and triglyceride (TG) < or = 200 mg/dL. RESULTS: Lipid-lowering drug therapy reduced LDL-C from 25% to 42% below baseline in patients with hypercholesterolemia varying from mild (130 to 160 mg/dL) to severe ( > 220 mg/dL), respectively. Approximately 75% of patients with LDL-C < or = 160 mg/dL ultimately achieved their lipid goal with drug therapy; however, less than half of patients with baseline LDL-C > 160 mg/dL achieved target lipid values. Multivariate analysis indicated that lower baseline LDL-C and triglycerides, use of combinations of drug therapy rather than monotherapy, and patient adherence to treatment predicted the achievement of goal lipid levels. CONCLUSIONS: Successful implementation of NCEP guidelines, frequently requires combination drug therapies, and is limited by poor patient tolerance and acceptance of niacin and the sequestrants.

Aged↗
PubMedDate not supplied

Resin residue.

Explore the source record for details and available documents.

Colestipol↗
PubMed1998

Influence of genotype at the low density lipoprotein (LDL) receptor gene locus on the clinical phenotype and response to lipid-lowering drug therapy in heterozygous familial hypercholesterolaemia. The Familial Hypercholesterolaemia Regression Study Group.

The relationship between molecular defect and clinical phenotype has been examined in 42 patients with heterozygous familial hypercholesterolaemia (FH) and premature coronary heart disease. The defined defects included mutations in the low density lipoprotein (LDL)-receptor gene (23/42) or the apolipoprotein B Arg3500Gln mutation (5/42). Mean LDL-cholesterol was higher, both before and during treatment with simvastatin and bile acid sequestrants, in patients predicted as having a 'severe' mutation than in those with a 'mild' mutation (8.72 +/- 2.02 mmol/l vs 6.63 +/- 1.8, P = 0.05 before and 4.51 +/- 0.90 mmol/l vs 3.19 +/- 0.58, P = 0.05 during treatment). Maximum inducible LDL-receptor activity in cultured lymphoblasts was inversely correlated with LDL-cholesterol before (r2 = 0.499, P = 0.002) and during (r2 = 0.478, P = 0.004) treatment in patients with a defined mutation in the LDL-receptor gene, but not in the 14 patients with no detectable molecular defect. LDL-cholesterol concentrations before and during treatment were significantly correlated in patients with a defined LDL-receptor gene mutation (r2 = 0.548, P = 0.0001), but not in those with no detectable genetic defect. All these correlations were weak, however and there were no differences in the response to treatment in terms of either relative reduction or absolute decrease in LDL-cholesterol concentration between patients with different LDL-receptor defects. We conclude that only part of the variable phenotype of heterozygous FH patients is explained by different LDL-receptor defects and that other factors determine the severity of their hypercholesterolaemia and the onset of coronary disease.

Adult↗
PubMed1993

Familial combined hyperlipidemia in children: clinical expression, metabolic defects, and management.

Familial combined hyperlipidemia (FCHL) is a dominantly inherited hyperlipidemia that occurs in at least 1% of the adult population and is responsible for 10% of premature coronary artery disease. In families referred for evaluation because of primary hyperlipidemia in a child, FCHL is expressed three times more commonly than familial hypercholesterolemia and half of the siblings are affected. Several metabolic defects apparently are associated with the FCHL phenotype. Most commonly, excess production of very low density lipoprotein apolipoprotein B can be demonstrated. In other families, reduced lipoprotein lipase activity is associated. One allele at a locus influencing apolipoprotein B levels predicts FCHL in a large proportion of families ascertained through affected children. Whether this allele is responsible for the excess of very low density lipoprotein apolipoprotein B detected in metabolic studies has not been elucidated. Management of FCHL in children begins with dietary modification. A bile acid sequestrant may be considered as well if diet cannot reduce the plasma low-density lipoprotein cholesterol level to less than 4.13 mmol/L (160 mg/dl) after the age of 10 years. Although the hydroxymethylglutaryl-coenzyme A reductase inhibitors are not currently recommended for children younger than 19 years of age, we speculate that they will be increasingly utilized for the management of FCHL in teenage boys who continue to have low density lipoprotein cholesterol levels greater than 4.13 mmol/L (160 mg/dl) after dietary modification.

Adolescent↗
PubMed1982

Treatment of hypercholesterolemia.

After discussing the indications for treatment of familial hypercholesterolemia and the importance of a differential diagnosis, the authors describe drug therapy for the disorder with special attention to combined drug regimens. The surgical treatment of hypercholesterolemia and the treatment of homozygous and other forms of hypercholesterolemia are also detailed.

Cholestyramine Resin↗