Coronary thrombosis

Indications for treatment with streptokinase include acute occlusion of arteries, deep vein thrombosis, and pulmonary embolism. Streptokinase therapy in coronary thrombosis, which is the usual cause of myocardial infarction (54,71,72), has proved to be valuable. In this frequently fatal condition, the enzyme is adrninistered intravenously at a dose of 1.5 million units over 60 min, or given by intracoronary infusion at a 20,000- to 50,000-unit bolus dose followed by 2000 to 4000 units/min for 60 min therapy must be instituted as soon as practicable after the diagnosis of heart attack is made. For deep vein thrombosis, pulmonary embolism, or arterial occlusion, streptokinase is infused at a loading dose of 250,000 units given over 30 min, followed by a maintenance dose of 100,000 units over a 60-min period. 

SuccessM treatment of PEA and asystole depends almost entirely on diagnosis of the underlying cause. Potentially reversible causes include (1) hypovolemia, (2) hypoxia, (3) preexisting acidosis, (4) hyperkalemia, (5) hypothermia, (6) hypoglycemia, (7) drug overdose, (8) cardiac tamponade, (9) tension pneumothorax, (10) coronary thrombosis, (11) pulmonary thrombosis, and (12) trauma. 

Repeated injury and repair within an atherosclerotic plaque eventually lead to a fibrous cap protecting the underlying core of lipids, collagen, calcium, and inflammatory cells such as T lymphocytes. Maintenance of the fibrous plaque is critical to prevent plaque rupture and subsequent coronary thrombosis. 

Sir, scant attention seems to be paid by the medical profession and by food administrators to a very important change in the dietaries of the more civilised countries that has been occurring over recent decades with increasing intensity. I refer to the chronic relative deficiency of the polyethenoid essential fatty acids (E.F.A.).. . . The causes of death that have increased in most recent years are lung cancer, coronary thrombosis and leukaemia I believe that in all three groups deficiency of E.F.A. may be important. Your readers with stereotyped minds should stop reading at this point.. . ... 

McDunn, S., Hartz, W, Jr., Ts Ao, C., etal, Coronary thrombosis in a patient with May-Hegglin anamoly A case report. Am. J. Clin. Pathol. 95, 715-718 (1991). 

Warfarin (Fig. 10-22c) is a synthetic compound that inhibits the formation of active prothrombin. It is particularly poisonous to rats, causing death by internal bleeding. Ironically, this potent rodenticide is also an invaluable anticoagulant drug for treating humans at risk for excessive blood clotting, such as surgical patients and those with coronary thrombosis. ... 

ASPIRIN. [CAS 50-78-2]. A drug used for nearly a century to relieve headaches and geneial aches and pains and to leduce the swelling and pain associated with joints (gout, ague, rheumatoid arthritis). In recent years, attention to aspirin for its apparent role m reducing heart attacks (coronary thrombosis) and strokes has increased, Trial studies also are underway for its use in reducing the risk of fatal colon cancer. 

Hudson was succeeded at the National Bureau of Standards by his former coworker, H. S. Isbell. At the National Institutes of Health, the carbohydrate investigations are now being actively continued by his former associates H. G. Fletcher, Jr., R. K. Ness, J. W. Pratt, N. K. Richtmyer, Laura C. Stewart, H. B. Wood, Jr., and E. Zissis. Hudson died suddenly of a coronary thrombosis on December 27, 1952, in his Washington apartment. He is survived by his widow, Erin Gilmer Jones Hudson, and by two daughters, Mrs. A. G. (Alice) Hughes and Mrs. S. (Sally) Socatell, both of Trenton. 

Acute coronary syndromes (ACS) are a major cause of morbidity and mortality. They are characterized by intracoronary thrombus formation at the site of atherosclerotic plaques. Coronary thrombosis is the underlying mechanism in the transition from stable angina to the unstable angina (UA) syndrome, characterized by embolization of the developed thrombus and atherosclerotic plaque rupture. 

New small molecule FXa inhibitors currently in development are able to enter the clot/prothrombinase complex and inhibit free and bound factor Xa regarded as the key enzyme in ACS. Although direct FXa inhibitors do not inhibit platelet aggregation, they abolish platelet-dependent thrombus formation in canine coronary thrombosis. Thus, direct inhibition of FXa may have higher efficacy and better risk/benefit profile than existing antithrombotic therapies in the treatment and prevention of ACS. 

Falk E, Unstable angina with fatal outcome dynamic coronary thrombosis leading to infarction and/or sudden death autopsy evidence of recurrent mural thrombosis with peripheral embolization culminating in total vascular occlusion, Circulation 1985 71 699-708. 

Just M, Lorenz M, Skrzipczyk HJ, et al. Otamixaban, a direct factor Xa inhibitor, more potently inhibits experimental coronary thrombosis than bivalirudin, a direct thrombin inhibitor. J Thromb Haemost 2005 3(suppl I ) P01 15. 

Solandt DY and Best CH. Heparin and coronary thrombosis in experimental animals, Lancet I 938 ii 130-132,... 

Gawaz M. Role of platelets in coronary thrombosis and reperfusion of ischemic myocardium. Cardiovasc Res 2004 61 498-51 I. 

Virmani R, Guagliumi G, Farb A, et al. Localized Hypersensitivity and late coronary thrombosis secondary to a sirolimus-eluting stent. Should we be cautious Circulation 2004 109 701-705. 

Aspirin All PCI 75-325 mg Reduced incidence of coronary thrombosis (2) and Q-wave infarct (3)... 

Barnathan ES, Schwartz JS, Taylor L, et al. Aspirin and dipyridamole in the prevention of acute coronary thrombosis complicating coronary angioplasty. Circulation 1987 76(1) 125-134. 

Cardiovascular The most serious side effect of oral contraceptives is cardiovascular disease, including thromboembolism, thrombophlebitis, hypertension, and increased incidences of myocardial infarction and cerebral and coronary thrombosis. These adverse effects are most common among women who smoke and who are over 35 years of age, although they may affect women of any age. 

Stenosis- and Mechanical Injury-Induced Coronary Thrombosis (Folts-Model)... 

Five different protocols are described in the following section for the induction of coronary thrombosis. 

In this preparation, coronary thrombosis is induced by delivery of low amperage electrical current to the intimal surface of the artery according to the method described by Romson et al. (1980a). In contrast to the stenosis protocols, an occluding thrombosis is formed gradually without embolism after some hours (protocol 5). As a consequence of this time course, the thrombi formed are of the mixed type and contain more fibrin than the platelet thrombi with critical stenosis. 

The following parameters are determined to quantify electrically induced coronary thrombosis ... 

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