| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Treating to New Targets (TNT) Study: does lowering low-density lipoprotein cholesterol levels below currently recommended guidelines yield incremental clinical benefit? Waters, D. D., J. R. Guyton, et al. (2004), Am J Cardiol 93(2): 154-8. Abstract: The Treating to New Targets (TNT) trial is a parallel-group study that has randomized 10,003 patients from 14 countries to double-blind treatment with either atorvastatin 10 or 80 mg. During the double-blind period, low-density lipoprotein (LDL) cholesterol levels are expected to reach approximate mean values of 100 mg/dl (2.6 mmol/L) for the low-dose atorvastatin group and 75 mg/dl (1.9 mmol/L) for the high-dose group. Randomized patients are expected to be followed for an average of 5 years. The primary end point is the time to occurrence of a major cardiovascular event, defined as coronary heart disease death, nonfatal myocardial infarction, resuscitated cardiac arrest, or stroke. The large patient numbers in the TNT study and long follow-up should ensure that there is adequate power to definitively determine if reducing LDL cholesterol levels to approximately 75 mg/dl (1.9 mmol/L) can provide additional clinical benefit. |
| Treatment and prevention of coronary heart disease by lowering serum cholesterol levels; from the pioneer work of C.D. de Langen to the third "Dutch Consensus on Cholesterol" Jukema, J. W. and M. L. Simoons (1999), Acta Cardiol 54(3): 163-8. Abstract: In the beginning of this century a possible relation was observed between cholesterol-rich foods, blood cholesterol levels and atherosclerosis by "pioneers" in this field as Anitschkow and De Langen. In the second half of this century a definite link was established between serum cholesterol levels and development of coronary heart disease (CHD). In angiographic studies it has recently been shown that a decrease in total cholesterol as well as in low-density lipoprotein cholesterol level results in a retardation of the progression of vascular disease. Furthermore, clinical event intervention trials demonstrated that therapy with cholesterol synthesis inhibitors reduces not only cardiovascular and total mortality, but also other manifestations of CHD. These recent results prompted to revise, for the second time, the Dutch consensus text for lipid lowering therapy, with the following conclusions. Hypercholesterolaemia is treated with a low-saturated fat diet and normalisation of weight. For individuals, this might result in a reduction of the risk for myocardial infarction or death and for the population in a decrease of the mean serum cholesterol concentration and a reduction of the incidence of CHD. The indication for drug therapy is founded on the expected effectiveness to reduce the incidence of (new manifestations of) CHD, which is related to the level of the absolute risk of vascular disease. Treatment with cholesterol synthesis inhibitors must be considered in (a) patients with familial hypercholesterolaemia; (b) all patients with a history of myocardial infarction or other symptomatic vascular disease with a total cholesterol concentration above 5.0 mmol/l and a life expectancy of at least five years; (c) persons without known vascular disease with a combination of diabetes mellitus, hypertension, hypercholesterolaemia, cigarette smoking and high risk for development of CHD, rising from 25% per 10 years at the age of 40 years to 35-40% per 10 years at the age of 70 years, with a life expectancy of at least five years. If these guidelines are followed, the calculated cost-effectiveness is about Dfl. 40,000 per life year gained or less. The consensus committee judges this reasonable in comparison with other therapeutic interventions in the Netherlands. Thus by now, with regard to lipids and atherosclerosis, the definite link has been established between observational medicine and an effective treatment modality which is applicable in daily practise. |
| Treatment goals for low-density lipoprotein cholesterol in the secondary prevention of coronary heart disease: absolute levels or extent of lowering? Cullen, P. and G. Assmann (1997), Am J Cardiol 80(10): 1287-94. Abstract: The results of the Scandinavian Simvastatin Survival Study (4S) and the Cholesterol and Recurrent Events (CARE) study make abundantly clear the benefits of lowering low-density lipoprotein (LDL) cholesterol in patients with a history of coronary artery disease. Current guidelines in the United States and Germany recommend a treatment goal for LDL cholesterol of 100 mg/dl. However, the evidence for setting such a goal is not consistent among trials. It has even been argued that setting an absolute LDL goal may be unhelpful, per se, because the higher the patient's pretreatment LDL cholesterol, the more difficult achieving this goal becomes. It has also been recognized that measures to lower LDL cholesterol, and medications in particular, produce a relative rather than an absolute degree of reduction in circulating levels. For example, most statins produce a similar proportional decrease in LDL cholesterol irrespective of baseline LDL. Thus, if the baseline LDL is 180 mg/dl, the decrease in LDL with a particular statin dose may be 60 to 120 mg/dl, whereas if the baseline LDL is 120 mg/dl, the expected decrease in LDL with the same statin dose would be only 40 to 80 mg/dl (i.e., a 30% reduction in each case). These points have led some investigators to suggest that it may be more practicable to recommend the amount by which LDL should be lowered rather than by specifying an absolute level of LDL cholesterol which should be achieved. This report summarizes the proceedings of an international symposium held on this topic on October 4, 1996, in Berlin by the International Task Force for Prevention of Coronary Heart Disease and the Institute of Arteriosclerosis Research at the University of Munster. |
| Treatment of a low HDL cholesterol level Margolis, S. (1990), Jama 264(23): 3063. |
| Treatment of Brazilian kala-azar with a short course of amphocil (amphotericin B cholesterol dispersion) Dietze, R., E. P. Milan, et al. (1993), Clin Infect Dis 17(6): 981-6. Abstract: Amphotericin B is an effective but toxic antileishmanial agent. Lipid-encapsulated amphotericin B should have a high therapeutic index for visceral leishmaniasis because reticuloendothelial cells, the sole site in which Leishmania is found, will phagocytize and concentrate the complex. Amphotericin B cholesterol dispersion (Amphocil; 2 mg/kg.d intravenously) was administered to 10 Brazilians with kala-azar for 10 days (cohort 1) and to 10 Brazilians with kala-azar for 7 days (cohort 2). All patients were successfully treated: 19 of the 20 patients were without visible parasites in the bone marrow; the mean time to afebrility was 4.2 days; spleen size regressed by a mean of 79% 2 months after therapy; and no patient had clinical or laboratory abnormalities by the end of 6-12 months of follow-up. Side effects were fever and chills accompanied by respiratory distress, but not nephrotoxicity, in children < 3 years of age. |
| Treatment of cholesterol gallstone patients with ursodeoxycholic acid Marzio, L. (1991), Gastroenterology 101(1): 275-6. |
| Treatment of cholesterol gallstones with litholytic bile acids Salen, G., G. S. Tint, et al. (1991), Gastroenterol Clin North Am 20(1): 171-82. Abstract: Cholesterol gallstone disease is reversible and can be treated medically with either CDCA or UDCA. Both bile acids correct the hepatic metabolic defect that is responsible for hypersecretion of cholesterol into the bile, and both desaturate the bile. UDCA is preferred because it is more effective, desaturate the bile to a greater extent than CDCA, and eliminates cholesterol as stable liquid crystalline dispersions. UDCA is virtually free of side effects and does not produce toxicity. Symptoms are relieved rapidly, and the quality of life improves. Dietary restrictions can be relaxed as the stones dissolve. |
| Treatment of cholesterol-fed rabbits with dietary vitamins E and C inhibits lipoprotein oxidation but not development of atherosclerosis Morel, D. W., M. de la Llera-Moya, et al. (1994), J Nutr 124(11): 2123-30. Abstract: New Zealand White rabbits were made hypercholesterolemic by feeding a high cholesterol diet (10 g/kg diet) with or without added antioxidants. The antioxidants used were either probucol (10 g/kg) or vitamin E (10 g/kg) plus vitamin C (0.6 g/kg). Serum cholesterol concentrations were monitored as a function of time. At the end of 10 wk, serum and lipoprotein vitamin E concentrations, the extent of oxidation of lipoprotein fractions (thiobarbituric acid reacting substances), the susceptibility of lipoprotein to oxidation in vitro (conjugated diene formation) and the extent of atherosclerosis (aortic area stained by Sudan IV and plaque thickness) were measured. Rabbits fed diets supplemented with vitamins E and C had markedly higher serum vitamin E concentrations, marked vitamin E enrichment in all lipoprotein fractions, less oxidation in VLDL and LDL and enhanced resistance of LDL to further in vitro oxidation, but did not have significantly less aortic atherosclerosis. Rabbits given supplemental probucol likewise exhibited reduced oxidation of lipoproteins. However, aortic atherosclerosis in these animals was significantly lower, as were serum cholesterol concentrations. Inhibition of lipoprotein oxidation itself was not sufficient to reduce atherosclerosis in cholesterol-fed New Zealand White rabbits. |
| Treatment of high blood cholesterol in patients with coronary heart disease Nagai, Y. and S. Yamashita (2003), Nippon Rinsho 61 Suppl 4: 675-81. |
| Treatment of high-risk patients with ezetimibe plus simvastatin co-administration versus simvastatin alone to attain National Cholesterol Education Program Adult Treatment Panel III low-density lipoprotein cholesterol goals Feldman, T., M. Koren, et al. (2004), Am J Cardiol 93(12): 1481-6. Abstract: This study assessed whether the co-administration of ezetimibe and simvastatin would be more effective than simvastatin monotherapy in allowing high-risk patients to achieve a low-density lipoprotein (LDL) cholesterol goal of <100 mg/dl. Men and women with LDL cholesterol >/=130 mg/dl and meeting National Cholesterol Education Program Adult Treatment Panel III criteria for coronary heart disease (CHD) or CHD risk equivalent were randomized to 1 of 4 daily treatments for 23 weeks: simvastatin 20 mg (n = 253), ezetimibe 10 mg plus simvastatin 10 mg (n = 251), ezetimibe 10 mg plus simvastatin 20 mg (n = 109), and ezetimibe 10 mg plus simvastatin 40 mg (n = 97). In all groups, patients not at goal had their simvastatin doses doubled at weeks 6, 12, and/or 18, up to a maximum of 80 mg. The primary efficacy objective was LDL cholesterol goal attainment (<100 mg/dl) after 5 weeks of treatment. Ezetimibe plus any dose of simvastatin produced greater reductions in LDL cholesterol and allowed more patients to achieve goal after 5 weeks (p <0.001) and at the end of the study (p <0.001) than simvastatin 20 mg alone. At 5 weeks, 75%, 83%, and 87% of patients receiving ezetimibe plus simvastatin 10, 20, and 40 mg had LDL cholesterol <100 mg/dl compared with 46% of patients receiving simvastatin 20 mg. In patients who started on ezetimibe plus simvastatin 10, 20 and 40 mg, 33%, 22%, and 12%, respectively, required simvastatin titration during the study compared with 68% of patients who started on simvastatin 20 mg. The corresponding median simvastatin doses used were 10, 20, 40, and 40 mg, respectively. Ezetimibe plus simvastatin was well tolerated, with an overall safety profile similar to that of simvastatin monotherapy. Thus, through the dual inhibition of cholesterol absorption and synthesis, ezetimibe plus simvastatin allowed more patients to reach LDL cholesterol <100 mg/dl at a lower simvastatin dose and with fewer dose titrations than simvastatin monotherapy. |
| Treatment of hypercholesterolemia in the elderly: is cholesterol a risk factor and should it be treated? Luepker, R. V. and J. P. Mo (1993), Coron Artery Dis 4(7): 605-10. |
| Treatment of hypercholesterolemia. I. Do side effects of exist when cholesterol levels are reduced? Cybulska, B., W. B. Szostak, et al. (1992), Wiad Lek 45(23-24): 934-40. |
| Treatment of hyperlipidemic kidney graft recipients with lovastatin: effect on LDL-cholesterol and lipoprotein (a) Traindl, O., S. Reading, et al. (1992), Nephron 62(4): 394-8. Abstract: An increased incidence of hyperlipidemia places kidney graft recipients at increased risk for cardiovascular disease and may contribute to a decline in graft function. A study was undertaken to evaluate the safety and efficacy of lovastatin in these patients. Twelve kidney graft recipients with stable graft function and a cholesterol (chol) level over 250 mg/dl (6.46 mmol/l) were included. The lipid-lowering treatment consisted of 20 mg lovastatin daily, and all patients received immunosuppression with ciclosporin (CS) and prednisolone. Total chol decreased by 27% (300 +/- 56 to 219 +/- 28 mg/dl; 7.76 +/- 1.45 to 5.66 +/- 0.72 mmol/l; p < 0.01), LDL-chol by 35% (220 +/- 38 to 143 +/- 17 mg/dl; 5.69 +/- 0.98 to 3.70 +/- 0.44 mmol/l; p < 0.01) and triglycerides by 33% (207 +/- 127 to 138 +/- 56 mg/dl; 2.36 +/- 1.44 to 1.57 +/- 0.64 mmol/l; p < 0.05). HDL-chol increased by 10% (57 +/- 11 to 63 +/- 13 mg/dl; 1.47 +/- 0.28 to 1.63 +/- 0.34 mmol/l; NS). The ratio of total chol/HDL-chol, a generally accepted risk predictor of atherosclerosis, fell from 5.4 +/- 1.3 to 3.3 +/- 1.2, p < 0.01. Lipoprotein (a) lp(a), an independent risk predictor for atherosclerosis, was also evaluated at baseline and after 6 months of lovastatin treatment and showed a decrease of 39% (32.9 +/- 27.6 to 19.9 +/- 22.9 mg/dl; 0.85 +/- 0.71 to 0.51 +/- 0.59 mmol/l; p < 0.05). No adverse side effects were seen at this dosage, and hepatic and renal parameters remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Treatment of kala-azar in Brazil with Amphocil (amphotericin B cholesterol dispersion) for 5 days Dietze, R., S. M. Fagundes, et al. (1995), Trans R Soc Trop Med Hyg 89(3): 309-11. Abstract: We have treated 10 patients suffering from kala-azar in Brazil with Amphocil (amphotericin B cholesterol dispersion) at a dose of 2 mg/kg/d for 5 d, following an earlier study in which this dosage for 7 d was found to cure all of 9 patients, with no relapse during 12 months. In the present study, all patients demonstrated initial resolution of disease. Parasites were absent upon bone marrow re-aspiration 2 weeks after therapy; no spleen extended beyond the costal margin 2 months after therapy; white blood cell counts, platelet counts, and serum levels of albumin rapidly returned to normal. Although one patient relapsed at 5 months, 8 of the other 9 patients had spleens of normal size (undetectable on deep palpation) at 12 months after therapy. Fever, sometimes accompanied by increased respiratory rate, occurred on the first day of drug infusion in 8 of 10 patients and was more severe in patients < 6 years old. Pre-medication with a non-steroidal anti-inflammatory agent (diclofenac potassium) before the next 4 infusions protected against this side effect in 5 of 6 patients. The results of this and our previous study suggest that the most appropriate regimen of Amphocil for kala-azar is 2 mg/kg/d for 7 d, with pre-medication each day, in patients aged > 5 years. |
| Treatment of myocardial infarction and angina. Advice on reducing cholesterol should be included Reynolds, T. and A. Wierzbicki (1995), Bmj 310(6977): 466. |
| Treatment of the cholesterol biosynthetic defect in Smith-Lemli-Opitz syndrome reproduced in rats by BM 15.766 Xu, G., G. Salen, et al. (1995), Gastroenterology 109(4): 1301-7. Abstract: BACKGROUND & AIMS: The Smith-Lemli-Opitz syndrome is a recessive inherited disorder characterized by neurological developmental defects and dysmorphic features with a defect in cholesterol synthesis at the conversion of 7-dehydrocholesterol to cholesterol. BM 15.766 inhibits 7-dehydrocholesterol-delta 7-reductase and reproduces the biochemical defect. The aim of this study was to investigate the effects of cholesterol, cholic acid, and lovastatin feeding on rats fed BM 15.766. METHODS: Plasma cholesterol and 7-dehydrocholesterol concentrations were related to the hepatic 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. RESULTS: With the inhibitor treatment, plasma cholesterol concentrations decreased 67%; 7-dehydrocholesterol concentrations increased from trace to 17 mg/dL; and hepatic HMG-CoA reductase activity and messenger RNA levels were stimulated 74% and two times, respectively. In inhibitor-treated rats, feeding cholesterol increased plasma cholesterol concentrations 3.7 times, decreased 7-dehydrocholesterol concentrations 88%, and reduced elevated HMG-CoA reductase activity and messenger RNA levels 74% and 49%. Feeding cholic acid increased plasma cholesterol without reducing 7-dehydrocholesterol concentrations. The combination of cholic acid and cholesterol enhanced plasma cholesterol 9.5 times without decreasing 7-dehydrocholesterol levels. Feeding lovastatin depressed plasma cholesterol further without reducing 7-dehydrocholesterol levels. CONCLUSIONS: Cholesterol is essential to correct abnormal cholesterol synthesis induced by BM 15.766 in rats by expanding the pool and inhibiting HMG-CoA reductase. Neither cholic acid nor lovastatin are effective separately, but cholic acid plus cholesterol may offer some additional benefit. |
| Treatment of the patient with ideal LDL cholesterol Mendoza Perez, E. (2003), Arch Cardiol Mex 73 Suppl 1: S98-102. Abstract: Coronary heart disease (CHD) is the leading cause of death worldwide. Low-density lipoprotein-cholesterol (LDL-C) reduction is the corner-stone in both primary and secondary cardiovascular prevention. Use of 3-hydroxy-3-methyl-glutaryl coenzyme A reductase inhibitors (statins) has proved to reduce LDL-C levels and major coronary event risks. The benefit on cardiovascular risk reduction is greater as LDL-C lowering is greater. Cardiovascular risk remains unacceptably high, even in patients with on-target LDL-C. This paper presents a review of alternatives for both approach and therapy in patients with on-target LDL-C. |
| Treatment of unstable angina with cholesterol embolization as a complication of left heart catheterization Oda, H., T. Miida, et al. (1990), Jpn Circ J 54(5): 487-92. Abstract: We describe 3 patients with cholesterol embolization after left heart catheterization via the femoral route. The left catheterizations were performed via the femoral route in all reported cases in which cholesterol embolization occurred as a complication of left catheterization. Postmortem examinations reveal that PTCA, using the right brachial approach, is the safest method for treatment of intractable angina in patients with evidence of cholesterol embolization. |
| Treatment patterns and distribution of low-density lipoprotein cholesterol levels in treatment-eligible United States adults Hoerger, T. J., M. V. Bala, et al. (1998), Am J Cardiol 82(1): 61-5. Abstract: To estimate the fraction of United States (U.S.) adults who are eligible for treatment to reduce elevated low-density lipoprotein (LDL) cholesterol levels based on Adult Treatment Panel II (ATP II) guidelines and the percent reduction in LDL cholesterol required by those who qualify for treatment, we analyzed data on 7,423 respondents to Phase 2 of the third National Health and Nutrition Examination Survey (NHANES III) administered between 1991 and 1994. Approximately 28% of the U.S. adult population aged > or = 20 years is eligible for treatment based on ATP II guidelines. Eighty-two percent of adults with coronary heart disease are not at their target LDL cholesterol level of 100 mg/dl. Of those eligible for treatment, 65% report that they receive no treatment. Overall, 40% of people who qualify for drug therapy require an LDL cholesterol reduction of > 30% to meet their ATP II treatment goal. Approximately 75% of those with coronary heart disease who qualify for drug therapy require an LDL cholesterol reduction of >30%. Although elevated LDL cholesterol levels can be treated, prevalence rates in the U.S. adult population remain high. Several recent studies indicate that a considerable percentage of people treated with drug therapy do not reach their treatment goals. The findings in this study provide at least a partial explanation for why many patients receiving therapy do not reach their treatment goals: they require a larger reduction in LDL cholesterol than many therapies can provide. |
| Treatment with atorvastatin to the National Cholesterol Educational Program goal versus 'usual' care in secondary coronary heart disease prevention. The GREek Atorvastatin and Coronary-heart-disease Evaluation (GREACE) study Athyros, V. G., A. A. Papageorgiou, et al. (2002), Curr Med Res Opin 18(4): 220-8. Abstract: BACKGROUND: Atorvastatin is very effective in reducing plasma low-density lipoprotein cholesterol (LDL-C) levels. However, there is no long-term survival study that evaluated this statin. PATIENTS-METHODS: To assess the effect of atorvastatin on morbidity and mortality (total and coronary) of patients with established coronary heart disease (CHD), 1600 consecutive patients were randomised either to atorvastatin or to 'usual' medical care. The dose of atorvastatin was titrated from 10 to 80 mg/day, in order to reach the National Cholesterol Education Program (NCEP) goal of LDL-C <100 mg/dl (2.6 mmol/l). All patients were followed up for a mean period of 3 years. MAIN OUTCOME MEASURES: Primary endpoints of the study were defined as death, non-fatal myocardial infarction, unstable angina, congestive heart failure, revascularisation (coronary morbidity) and stroke. Secondary endpoints were the safety and efficacy of the hypolipidaemic drugs as well as the cost-effectiveness of atorvastatin. RESULTS: The mean dosage of atorvastatin was 24 mg/day. This statin reduced total chlesterol by 36%, LDL-C by 46%, triglycerides by 31%, and non-high-density lipoprotein cholesterol (non-HDL-C) by 44%, while it increased HDL-C by 7%; all these changes were significant. The NCEP LDL-C and non-HDL-C treatment goals were reached by 95% (n = 759) and 97% (n = 776), respectively, of patients on atorvastatin. Only 14% of the 'usual' care patients received any hypolipidaemic drugs throughout the study and 3% of them reached the NCEP LDL-C treatment goal. The cost per quaility-adjusted life-year gained with atorvastatin was estimated at $US 8350. During this study 196 (24.5%) CHD patients on 'usual' care had a CHD recurrent event or died vs. 96 (12%) CHD patients on atorvastatin; risk ratio (RR) 0.49, confidence interval (CI) 0.27-0.73, p < 0.0001. In detail, atorvastatin reduced, in comparison to 'usual' care, total mortality (RR 0.57, CI 0.39-0.78, p = 0.0021), coronary mortality (RR 0.53, CI 0.29-0.74, p = 0.0017), coronary morbidity (RR 0.46, CI 0.25-0.71, p < 0.0001), and stroke (RR 0.53, CI 0.30-0.82, p = 0.034). All subgroups of patients (women, those with diabetes mellitus, arterial hypertension, age 60 to 75 years, congestive heart failure, recent unstable angina or prior revascularisation) benefited from treatment with atorvastatin. Withdrawal of patients because of side-effects from the atorvastatin group was low (0.75%) and similar to that of the 'usual' care group (0.4%). CONCLUSIONS: Long-term treatment of CHD patients with atorvastatin to achieve NCEP lipid targets significantly reduces total and coronary mortality, coronary morbidity and stroke, in comparison to patients receiving 'usual' medical care. Treatment with atorvastatin is well tolerated and cost-effective. |