"Nov. 5, 2012 (Los Angeles) -- An IV infusion of "good" HDL cholesterol seems to rapidly remove cholesterol out of plaque-clogged arteries following a heart attack, a small, early study suggests.
The goal of the new treatment is to red"...
Cholesterol is probably the sole precursor of bile acids. During normal digestion, bile acids are secreted into the intestines. A major portion of the bile acids is absorbed from the intestinal tract and returned to the liver via the enterohepatic circulation. Only very small amounts of bile acids are found in normal serum.
QUESTRAN (cholestyramine) resin adsorbs and combines with the bile acids in the intestine to form an insoluble complex which is excreted in the feces. This results in a partial removal of bile acids from the enterohepatic circulation by preventing their absorption.
The increased fecal loss of bile acids due to QUESTRAN (cholestyramine) administration leads to an increased oxidation of cholesterol to bile acids, a decrease in beta lipoprotein or low density lipoprotein plasma levels and a decrease in serum cholesterol levels. Although in man, QUESTRAN (cholestyramine) produces an increase in hepatic synthesis of cholesterol, plasma cholesterol levels fall. In patients with partial biliary obstruction, the reduction of serum bile acid levels by QUES-TRAN reduces excess bile acids deposited in the dermal tissue with resultant decrease in pruritus.
In a large, placebo-controlled, multi-clinic study, LRC-CPPT1, hypercholesterolemic subjects treated with QUESTRAN (cholestyramine) had mean reductions in total and low-density lipoprotein cholesterol (LDL-C) which exceeded those for diet and placebo treatment by 7.2% and 10.4%, respec-tively. Over the seven-year study period the QUESTRAN (cholestyramine) group experienced a 19% reduction (relative to the incidence in the placebo group) in the combined rate of coronary heart disease death plus non-fatal myocardial infarction (cumulative incidences of 7% QUESTRAN (cholestyramine) and 8.6% placebo). The subjects included in the study were men aged 35-59 with serum cholesterol levels above 265 mg/dL and no previous history of heart disease. It is not clear to what extent these findings can be extrapolated to females and other segments of the hypercholesterolemic population. (See also PRECAUTIONS: Carcinogenesis, Mutagenesis, Impairment of Fertility.)
Two controlled clinical trials have examined the effects of QUESTRAN (cholestyramine) monotherapy upon coronary atherosclerotic lesions using coronary arteriography. In the NHLBI Type II Coronary Intervention Trial2, 116 patients (80% male) with coronary artery disease (CAD) documented by arteriography were randomized to QUESTRAN (cholestyramine) or placebo for five years of treatment. Final study arteriography revealed progression of coronary artery disease in 49% of placebo patients compared to 32% of the QUESTRAN (cholestyramine) group (p < 0.05).
In the St.Thomas Atherosclerosis Regression Study (STARS)3, 90 hypercholesterolemic men with CAD were randomized to three blinded treatments: usual care, lipid-lowering diet, and lipid-lowering diet plus QUESTRAN (cholestyramine) . After 36 months, follow-up coronary arteriography revealed progression of disease in 46% of usual care patients, 15% of patients on lipid-lowering diet and 12% of those receiving diet plus QUESTRAN (cholestyramine) (p < 0.02). The mean absolute width of coronary segments decreased in the usual care group, increased slightly (0.003mm) in the diet group and increased by 0.103mm in the diet plus QUESTRAN (cholestyramine) group (p < 0.05). Thus in these randomized controlled clinical trials using coronary arteriography, QUESTRAN (cholestyramine) monotherapy has been demonstrated to slow progression2, 3 and promote regression3 of atherosclerotic lesions in the coronary arteries of patients with coronary artery disease.
The effect of intensive lipid-lowering therapy on coronary atherosclerosis has been assessed by arteriography in hyperlipidemic patients. In these randomized, controlled clinical trials, patients were treated for two to four years by either conventional measures (diet, placebo, or in some cases low dose resin), or intensive combination therapy using diet plus colestipol (an anion exchange resin with a mechanism of action and an effect on serum lipids similar to that of QUESTRAN (cholestyramine) and QUESTRAN (cholestyramine) LIGHT) plus either nicotinic acid or lovastatin. When compared to conventional measures, intensive lipid-lowering combination therapy significantly reduced the frequency of progression and increased the frequency of regression of coronary atherosclerotic lesions in patients with or at risk for coronary artery disease.
1. The Lipid Research Clinics Coronary Primary Prevention Trials Results: (l) Reduction in Incidence of Coronary Heart Disease; (ll) The Relationship of Reduction in Incidence of Coronary Heart Disease to Cholesterol Lowering. JAMA 1984; 251:351-374.
2. Brensike JF, Levy RI, Kelsey SF, et al.Effects of therapy with cholestyramine on progression of coronary arteriosclerosis: results of the NHLBI type II coronary intervention study. Circulation 1984;69:313-24.
3. Watts, GF, Lewis B, Brunt JNH Lewis ES, et al.Effects on coronary artery disease of lipid-lowering diet, or diet plus cholestyramine. In the St. Thomas Atherosclerosis Regression Study (STARS). Lancet 1992;339:563-69.
Last reviewed on RxList: 6/2/2008
This monograph has been modified to include the generic and brand name in many instances.
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