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PubMed1995

Use of neural networks in predicting the risk of coronary artery disease.

Artificial neural networks were created to predict the occurrence of coronary artery disease based on information from the serum lipid profile. The development of the networks involved a strategy which permitted learning from censored observations. The networks were developed with data from the Cholesterol Lowering Atherosclerosis Study, which followed serum lipoprotein levels and clinical events in 162 patients over a period of up to 10 years. Inputs consisted of seven different mean lipid values, and the desired output was the time period during which a complication of coronary artery disease was predicted to occur. Cross-validation was performed by splitting the data into separate training and testing sets, scoring the performance of the neural network strategy on the testing sets, and comparing scores with those obtained from Cox regression models developed on the same training data. Performance of the neural network strategy exceeded that of Cox regression in predicting clinical outcomes (66% vs 56%, McNemar's test P = 0.005). The network design provided an effective approach to predicting outcomes from a clinical trial with variable follow-up times.

Adult↗
PubMed1982

Reduction of exogenous oxalate in urine of rats by binding with aluminium-oxyhydrate (Andursil) and an anion-exchanger (Colestid) in the intestinal tract.

The influence of calcium carbonate, aluminium oxyhydrate (Andursil) and an anion exchanger (Colestid) on the absorption of oxalate from the intestine in rats was investigated. The animals were administered daily doses of 15mg oxalate as a 14C-sodium-oxalate solution by means of a throat probe, and the substances of interest were mixed with the food. The intake of food and the 14C-activity in the urine were measured during four urine-collecting periods of 3 days each. The quantity of the enterally administered oxalate excreted with urine has a negative correlation to the amount of the investigated test substances ingested with food.

Aluminum Hydroxide↗
PubMed1978

[Drug treatment of primary hyperlipoproteinemia (author's transl)].

Cardiovascular disease has become the major cause of death in the Western countries. There is strong evidence that elevations of serum lipids contribute to the pathogenesis of premature atherosclerosis. The classification of the hyperlipoproteinemias has been most beneficial as a guide to development of dietary and pharmacological regimens for lowering serum lipid concentrations. The results of dietary and drug prevention trials are discussed. Insight into the mechanisms involved in lipoprotein metabolism as well as the mode of action and of side-effects of hypolipidemic drugs is reviewed. Using present knowledge of heart disease research, it is reasonable to suggest dietary and drug treatments for the high risk patient.

Anion Exchange Resins↗
PubMed1986

Lipoprotein fractions and receptors: a role for probucol?

Cholesterol transport in the plasma involves several lipoprotein families. The process is remarkably ordered and is driven vectorily by apolipoproteins, which activate appropriate enzymes or serve as recognition sites for lipoprotein receptors. Of the lipoproteins in plasma, low density lipoprotein (LDL) contains most of the cholesterol and has the greatest atherogenic potential. Its plasma concentration is determined by LDL receptor activity, which serves to regulate intracellular cholesterol concentrations. LDL receptor activity in the body is not fixed, but can be stimulated by drugs that affect hepatic cholesterol content, such as inhibitors of HMG-CoA reductase or bile acid sequestrants. By stimulating LDL receptor activity, these drugs increase the fractional catabolic rate of apoLDL. HMG-CoA reductase inhibitors also appear to reduce the apoLDL synthetic rate. As a consequence, LDL cholesterol levels are reduced while high density lipoprotein (HDL) cholesterol levels remain stable or increase. Probucol is a drug that lowers both LDL and HDL cholesterol levels. It appears to lower LDL cholesterol levels by affecting LDL structure rather than by stimulating LDL receptor activity. It has no consistent effect on LDL synthetic rates. Probucol lowers plasma HDL cholesterol levels by decreasing the synthetic rates of the major HDL apolipoproteins. The biologic significance of these probucol-induced changes in HDL metabolism is unknown.

Anticholesteremic Agents↗
PubMed1986

Medical management of hyperlipidemia and the role of probucol.

Recent experimental and epidemiologic evidence has dispelled all doubts about the need to treat patients with hyperlipidemia. Therapy should focus on 3 areas: control of concomitant risk factors for atherosclerosis, reduction of lipid levels through diet and, if response to diet proves inadequate, administration of lipid-lowering agents. There are 4 categories of first-line drugs: resins, fibrates, nicotinic acid and probucol. Probucol has a sustained effect, additive to that of a lipid-lowering diet; it can reduce total serum cholesterol and cause xanthoma regression even in patients with receptor-defective homozygous familial hypercholesterolemia. It is effective when used alone and has an additive effect when combined with resins or nicotinic acid. Compared with many other lipid-lowering medications, it is well tolerated. Although the combination of probucol and clofibrate may cause a significant decrease in high density lipoproteins, there is no evidence that this decrease carries any adverse consequences for the underlying disease process.

Adult↗
PubMed1976

Drug treatment of hyperlipidemia.

The most frequent indication for treatment of hyperlipidemia is for prevention of arteriosclerosis, a suspected but unproved benefit. The cornerstone of treatment of primary hyperlipidemia is diet; drugs may be added to, but do not replace, diet. When a drug is used with any patient, its potential benefits and hazards must be carefully weighed for the given subject. The subjects should be carefully followed and observed for side effects. Plasma lipids should be monitored during the course of treatment. Five drugs have been approved by the U.S. Food and Drug Administration for the treatment of hyperlipidemia: cholestyramine, clofibrate, nicotinic acid, sodium dextrothyroxine and beta-sitosterol. The use, the actions and the side effects of each and of several nonapproved agents are discussed.

Aminosalicylic Acids↗
PubMed1987

Hypertriglyceridemia: a contraindication to the use of bile acid binding resins.

Bile acid binding resins are indicated for treatment of elevated plasma low-density lipoprotein cholesterol concentrations. In normoglyceridemic patients, plasma concentrations of low-density lipoprotein cholesterol and total cholesterol are closely linked, and for this reason resin treatment of elevated total cholesterol levels in these patients is rational and warranted. Hypertriglyceridemic patients may also have elevated total cholesterol concentrations, and several such patients have been treated with resin. However, resin therapy in these patients is hazardous, since the elevated cholesterol level mainly results from increased plasma concentrations of very-low-density lipoproteins or chylomicrons rather than low-density lipoproteins. In these patients, resin treatment has either no effect or an adverse effect on plasma triglyceride and cholesterol concentrations. The data presented show that fewer than 5 percent of patients whose total plasma triglyceride concentration exceeded 500 mg/dl had elevated low-density lipoprotein cholesterol concentrations, irrespective of total plasma cholesterol concentrations, and no patient whose plasma triglyceride concentration exceeded 1,000 mg/dl had elevated low-density lipoprotein cholesterol levels. Treatment with bile acid binding resins in hypercholesterolemic patients is contraindicated in the presence of hypertriglyceridemia.

Cholesterol↗
PubMed1983

The peripheral circulation and treatment of hyperlipoproteinemias.

Forty patients with hyperlipoproteinemia were followed 4-9.3 years by non-invasive tests of their lower extremity circulation. Twenty-eight patients were treated by diet and/or drugs, and 12 patients were controls. Although all patients had abnormal non-invasive tests, only 15 patients had intermittent claudication. Seven patients had improved circulation tests while 13 showed a deterioration in the tests; 20 patients had no changes. The patients who showed improvement in tests had the highest incidence of intermittent claudication and the lowest average ankle to brachial artery systolic blood pressure index. Although treatment patients had a significant decrease in total cholesterol, triglycerides, and VLDL, no significant differences were found when the results of the circulation tests were analyzed according to treatment or control status of the patients, to abnormal lipid patterns, or, ignoring treatment status, to a decrease in lipids. The patients who showed a deterioration in tests had a significantly higher total cholesterol level at the beginning of, but not during, the study and did not significantly decrease their triglycerides. No significant changes occurred in HDL, LDL, or VLDL. This study presents a methodology for the long-term, non-invasive assessment of peripheral arterial disease and a pilot study for its application. Despite the small number of patients studied, the failure to demonstrate benefit would discourage a larger clinical trial of this treatment protocol.

Adult↗
PubMedDate not supplied

Treatment of common lipoprotein disorders.

The pathogenesis of arteriosclerosis is not yet fully understood. The growing body of scientific information strongly indicates that the plasma lipoproteins are playing a crucial role in the development of this disease. We now have conclusive information that dietary cholesterol can produce arteriosclerosis in animals and its removal from the diet can result in regression of these lesions. Most importantly, we know that reducing plasma cholesterol in humans will prevent mortality and morbidity related to the clinical sequelae of arteriosclerosis. A diet can be prescribed that can produce profound reductions in lipoprotein levels in many individuals. The rate of success in achieving modifications that reduce plasma cholesterol is very high. Most patients over time find a diet with reduced cholesterol and saturated fat to be quite palatable. As food suppliers become more active in emphasizing low fat, low cholesterol products, and as restaurants see a demand for healthier entrees, the task for the physician and nutritionist will become much easier. Achieving sustained weight reduction is a much more difficult problem, but this too can be accomplished in many patients if the health professionals maintain a hopeful supportive approach. Ultimately, it is the patient's responsibility to bring about these lifestyle changes. It is the physician's and nutritionist's job to monitor the process and provide sound information and encouragement. For individuals with severe lipoprotein disorders such as familial hypercholesterolemia where diet therapy is helpful but not adequate, the use of medications is now indicated (bile acid binding resins and nicotinic acid). Other medications that promise additional effectiveness and safety are under development (Compactin, Mevinolin). It is our belief that control of coronary heart disease and stroke requires appropriate treatment of lipoprotein disorders and the methods for a strong beginning in this endeavor are at hand.

Adult↗