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Coronary occlusion

William Eugene Parham, Treasurer and member of the Board of Directors and of the Advisory Board of Organic Syntheses, died May 21, 1976 of a coronary occlusion near his summer home on Deer Lake, near Deer River, Minnesota, at the age of 53. Dr. Parham joined the Board of Editors on September 7, 1958 and served as Editor-in-Chief of Volume 44 of Organic Syntheses in 1964. He became a member of the Advisory Board and was elected to the Board of Directors in 1966, and served as Vice President from 1969 to 1974, at. which time he succeeded Richard S. Schreiber as Treasurer. As Treasurer, Dr. Parham was very effective in securing competent legal counsel for Organic Syntheses and in clarifying its foundation tax status with the Internal Revenue Service. [Pg.151]

These drugs are used cautiously in patients witii hypertension, epilepsy, cardiac arrhythmias, bradycardia, recent coronary occlusion, and megacolon. The safely of diese drugs has not been established for use during pregnancy (Pregnancy Category C), lactation, or in children. [Pg.222]

Treatment of coronary occlusion, acute MI, and peripheral arterial embolism ... [Pg.425]

Maroko, P.R. and Braunwald, E. (1973). Modification of myocardial infarction size after coronary occlusion. Ann. Intern. Med. 79, 720-733. [Pg.71]

One eritical factor that has been neglected in considering mechanisms of cardiac fatalities is the timeframe for various types of toxicities. For example, a majority of cocaine-related fatalities and near fatalities reported from emergency rooms are attributed to one or more types of cardiac ischemic or hypertensive episodes (Isner et al. 1986). Thus, these studies may discount the cocaine-induced arrhythmias and conduction defects as important direct causes of fatalities. Yet, if coroner reports are used as data sources (Virmani et al. 1988 Wetli and Wright 1979 Mittleman and Wetli 1984), there are great numbers of deaths in which pulmonary effusion and lack of evidence for coronary occlusion, acute myocardial infarction, or... [Pg.328]

More recent studies continue to support the unique antifibrillatory activity of bretylium. Kowey et al. [38] have shown that bretylium prevented spontaneous VF and decreased the effects on VF threshold in a feline myocardial infarction model. They attributed this beneficial effect to a decrease in the dispersion of refractoriness between normal and ischaemic regions of the heart. In contrast, clofilium (14, see below), which had little effect on dispersion of refractoriness after coronary occlusion, was unable to prevent spontaneous VF. Similar results were seen in isolated tissue studies with canine subendocardial Purkinje fibres and ventricular muscle which contained both normal and ischaemic regions [39]. In these studies bretylium caused a smaller increase in dispersion of refractoriness in subendocardial Purkinje fibres than either sotalol or clofilium. In ventricular muscle tissue, bretylium decreased dispersion while sotalol and clofilium increased dispersion of refractoriness. [Pg.73]

Unlabeled uses As an adjunct in treatment of coronary occlusion with acute Ml. Although there is some controversy regarding the efficacy of heparin therapy with concurrent antiplatelet therapy (eg, aspirin) in the prevention of rethrombosis/reocclusion after primary thrombolysis with thrombolytics during acute Ml, it is recommended by the American College of Cardiology and the American Heart Association. Generally, administer heparin IV immediately after thrombolytic... [Pg.127]

Severe myocardial disease or coronary occlusion psychoses hypersensitivity to disulfiram or to other thiuram derivatives used in pesticides and rubber vulcanization patients receiving or who have recently received metronidazole, paraldehyde, alcohol, or alcohol-containing preparations. [Pg.1324]

The paradigm shift in 1980 on the causation of acute myocardial infarction to acute coronary occlusion by a thrombus created the rationale for thrombolytic therapy of this common lethal disease. At that time—and for the first time-intravenous thrombolytic therapy for acute myocardial infarction in the European Cooperative Study Group trial was found to reduce mortality significantly. Later studies, with thousands of patients in each trial, provided enough statistical power for the 20% reduction in mortality to be considered statistically significant. Although the standard of care in areas with adequate facilities and experience in percutaneous coronary intervention (PCI) now favors catheterization and placement of a stent, thrombolytic therapy is still very important where PCI is not readily available. [Pg.765]

Hirche HJ, Franz C, Bos L, Bissig R, Lang R, Schramm M Myocardial extracellular K+ and H + increase and noradrenaline release as possible cause of early arrhythmias following acute coronary occlusion in pigs. J Mol Cell Cardiol 1980 12 579-593. [Pg.128]

Patients without ST-segment elevation usually do not have an acute coronary occlusion. Therefore, they will not benefit by thrombolytic therapy, but do have the risk of its complications. [Pg.136]

DeWood MA, Spores J, Notske R, et al. Prevalence of total coronary occlusion during the early hours of transmural myocardial infarction. N EnglJ Med 1980 303 897-902. [Pg.137]

Alfonso F Goicolea J, Hernandez R, et al. Angioscopic findings during coronary angioplasty of coronary occlusions. J Am Coll Cardiol 1995 26(1) 135-141. [Pg.277]

Costa MA, Sabate M, van der Giessen JM, et al. Late coronary occlusion after intracoronary brachytherapy. Circulation 1999 IOO(8) 789-792. [Pg.287]

In pigs, high dose of VEGF delivered extraluminally after coronary occlusion caused higher blood flow in the ischemic territory (31). In a canine model of chronic coronary ischemia, VEGF showed enhanced collateral vessel density and blood flow when delivered as a local infusion, although not when administered systemically (32). [Pg.358]

Christofferson RD, Lehmann KG, Martin GV et al. Effect of chronic total coronary occlusion on treatment strategy. Am J Cardiol 2005 95 1088-1091. [Pg.541]

Srivatsa SS, Edwards WD, Boos CM, et al. Histologic correlates of angiographic chronic total coronary occlusion, JACC 1995 29 955-963,... [Pg.542]

Migliorini A, Moschi G, Vergara R, et al. Drug-eluting stent supported percutaneous coronary intervention for chronic total coronary occlusion. Catheter Cardiovasc Interv 2006 67 344-348. [Pg.542]

Rahel BM, Laarmen GJ, Suttorp MJ, et al. Primary stenting of occluded native coronary arteries II—rationale and design of the PRISON II study a randomized comparison of bare metal stent implantation with Sirolimus-eluting stent implantation for the treatment of chronic total coronary occlusions. Am Heart J 2005 I49 el-e3. [Pg.542]

Ajluni SC, Jones D, Zidar FJ, et al. Prolonged urokinase infusion for chronic total native coronary occlusions clinical, angiographic, and treatment observations. Cathter Cardiovasc Diagn 1995 34 106-1 10. [Pg.542]

De Oliveira et al. explained the effects of hyaluronidase in terms of a reduction of the water content of the ischemic myocardium [107]. Hyaluronidase would reduce the edema during the acute phase following coronary occlusion and thereby reduce the injury. Intramyocardial edema occurs after the occlusion of coronary arteries, resulting in an increased water content of the myocardial tissues. Hyaluronidase produces a faster diffusion of fluids and thereby reduces edema in the damaged area. To examine the effects of hvaluronidase on in fere-... [Pg.169]


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See also in sourсe #XX -- [ Pg.164 ]




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Arterial occlusion coronary

Atherosclerosis Coronary occlusion

Cardiovascular disease coronary occlusions

Chronic coronary arterial occlusions

Coronary arteries occlusion

Coronary artery disease chronic occlusions

Coronary sinus occlusive

Left anterior descending coronary artery occlusion

Myocardial infarction coronary occlusion

Occlusion

Right coronary artery occlusion

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