Introduction
Article Abstract:
On April 25, 1990 a symposium was held in Chicago to bring together researchers and clinicians interested in atherosclerosis (deposition of fatty plaque on the walls of blood vessels; ''hardening'' of the arteries) and the use of lovastatin in the treatment of high levels of cholesterol in the blood. This drug was approved for use in the United States in 1987. It is the first anti-cholesterol drug that acts by inhibiting the enzyme 3-hydroxy-3-methylglutaryl coenzyme A reductase (abbreviated HMG CoA reductase). Cholesterol was first observed to be a component of atherosclerotic plaques in the 19th century, but it was not until the early 1960s that a drug was developed to block the synthesis of cholesterol within the body, thus, hopefully, reducing the risk of atherosclerosis. Like most substances in the body, the synthesis of cholesterol involves many individual steps. This first anti-cholesterol drug, MER-29, blocked the last steps in the biosynthesis of cholesterol, but it had the side effect of causing the deposition of large amounts of a fatty substance almost like cholesterol in body tissues. This substance, called desmosterol, accumulated in tissues and caused conditions such as cataracts and baldness. A search was conducted to find a substance that would block an early stage of cholesterol synthesis rather than a late stage, and, in 1976, a fungal metabolite that performed this function was discovered. It was dubbed mevastatin, and soon thereafter lovastatin, another fungal metabolite, was isolated. HMG CoA reductase inhibitors prevent the formation of mevalonic acid, an early step in cholesterol synthesis. At this stage, the products formed are water-soluble and do not lodge in the body's tissues. The participants in the symposium discuss the effectiveness of lovastatin, its safety and side effects, and the physiological basis for the drug's actions. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1991
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Introduction
Article Abstract:
Heart failure is perhaps the most complex of all disorders of the cardiovascular system. Unlike some other conditions that involve a clear-cut failure of one part of the system or another, heart failure is the failure of the system as a whole. In heart failure, the heart simply cannot adequately perform the work of pumping the blood. The condition usually arises slowly over time and involves changes in the heart muscle as it struggles against an overload of work, changes in the peripheral blood vessels that provide too much resistance to the heart, and a host of other changes including damage to the kidneys. Since there is no single target for intervention, surgeons can do nothing, and heart failure is likely to continue to be medically treated with drugs. New drugs are being developed all the time; as more is learned about cellular receptors, it is becoming possible to design new drugs that interact with these receptors to improve the circulation of patients with heart failure. In October of 1989, researchers and physicians met in Kyoto, Japan to discuss the potential of the new drug ibopamine in the treatment of heart failure. The scientific papers that were presented at this meeting have now been published together in a special May 29, 1991 issue of The American Journal of Medicine. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1991
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Introduction
Article Abstract:
In 1895, it was shown that the enzyme thrombin, which causes blood to clot, loses its biologic activity when added to defibrinated blood, or blood lacking fibrin. It was suggested that blood contained a specific inactivator of thrombin called antithrombin. In 1916, a substance isolated from the liver was shown to have very powerful anticoagulant or anti-clotting properties, and two years later, the substance was termed heparin. However, heparin prevented blood clotting only in the presence of a blood component, termed heparin cofactor, which was later shown to be the antithrombin factor. Within the past 15 years, there has been much knowledge accumulated about antithrombin and heparin-like cofactors. In addition, studies show that congenital and acquired disorders of the blood coagulation system may contribute to the development of thrombosis, the formation of blood clots. Biochemical aspects of these blood coagulation disorders may explain the enhanced blood clotting characteristics associated with some blood vessel diseases. Finally, the effectiveness of several antithrombin agents have been determined. A symposium held in September 1988, in Boston, Massachusetts, reviewed current research on the role of antithrombin III in coagulation disorders. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1989
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