Blood Clots
I. Causes of Blood Clots
II. Nondrug Treatment
III. Drug Treatment
GLOSSARY
acute coronary syndrome this syndrome defines patients with acute chest pain caused by myocardial infarction or unstable angina.
anticoagulants blood thinners.
atheroma same as atherosclerosis, raised plaques filled with cholesterol, calcium, and other substances on the inner wall of arteries that obstruct the lumen and the flow of blood; the plaque of atheroma hardens the artery, hence the term atherosclerosis (sclerosis ¼ hardening).
myocardial infarction death of an area of heart muscle due to blockage of a coronary artery by blood clot and atheroma, medical term for heart attack.
PCI percutaneous coronary intervention; percutaneous trans-luminal coronary angioplasty (PTCA), often involving the use of intracoronary stents.
platelets very small disk-like particles that circulate in the blood alongside red and white blood cells initiating the formation of blood clots; platelets clump and form little plugs called aggregation, thus causing bleeding to stop.
IN 90% OF CASES, THE CAUSE OF A FATAL OR A nonfatal heart attack is a blood clot in a coronary artery (coronary thrombosis). The clot often occurs on the surface of a plaque of atheroma that is partially obstructing the lumen of the coronary artery. Patients may have many large atheromatous plaques and yet not develop a clot over a 5- to 15-year period. There is no test that can tell us when and where a clot will occur. Cholesterol, hyperten¬sion, exercise, and cigarette smoking have little to do with the clotting of blood; therefore, we must look elsewhere. Reduction in fatal and nonfatal heart attacks requires the prevention and therapeutic strategies outlined below.
Страницы: 1 | 2
- I. CAUSES OF BLOOD CLOTS
Blood clots are believed to occur in the coronary arteries because of platelets that become sticky when they come in contact with the damaged lining of blood vessels, where atheroma formation has commenced. Platelets interact with the damaged surfaces, and chemicals that are produced at the site cause the platelets to clump (platelet aggregation) and form a clot. Chemicals in the body that cause platelets to clump or sludge include collagen from the damaged vessel wall, adrenaline, and a very powerful platelet-clumping chemical called thromboxane A2. - II. NONDRUG TREATMENT
As a nondrug treatment, these dietary measures are strongly advised. Eat less fatty meals, which reduces saturated fat and hydrogenated fat intake. Saturated fats form LDL (bad) cholesterol in the body. Try to increase the intake of foods that may prevent blood clotting, particularly onions, garlic, and foods containing alpha-linolenic and eicosapentaenoic acids; the latter are derived from fish and cod liver oil. The polyunsaturated acids in the diet of the fish-eating Japanese and Inuit prevent clumping of platelets and have favorable effects on the blood-clotting system. These foods decrease platelet clump¬ing as well as increase vessel wall prostacyclin (prostaglan-din), a compound that helps to keep the lining of the artery clean. Try to increase your consumption of fish, for example, mackerel and salmon, which have a high content of the polyunsaturated fatty acids. Linolenic acid has been proven valuable in the prevention of plaque (see Section VII in the chapter Cholesterol). - III. DRUG TREATMENT A. Thrombolytic Agents
Rentrop reported successful recanalization of coronary thrombotic occlusion with intracoronary infusion of strep-tokinase in patients. Streptokinase was the first throm-bolytic agent employed, and its usefulness was first documented in the Italian trial of intravenous streptoki-nase (GISSI). This drug remains in use today because it is the least expensive of the available thrombolytic agents and has a low risk for intracranial hemorrhage compared with other agents that are modestly better in dissolving clots. The internationally run British trial, the International Study of Infarct Survival (ISIS–2), showed that an intravenous infusion of 1.5 million units of streptokinase administered over 1 h is not particularly expensive or troublesome to give routinely, and it provides significant reduction in mortality and morbidity in patients seen within 3 hof onset of chest pain. Most important, intra¬venous or subcutaneous heparin is not necessary when streptokinase is used; this reduces the risk for intracranial hemorrhage. - BIBLIOGRAPHY
Abrams, J., Frishman, W. H., Bates, S. M. et al. Pharmacologic options