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Acute coronary thrombosis

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. [Pg.534]

When it is suspected that there may only be small differences between active treatments, and when placebo controls are unavailable for clinical or ethical reasons, then it is often necessary to resort to large-scale studies ( mega-trials ). A good, famous example was the clinical trial known by the acronym GUSTO, where streptokinase and recombinant tissue plasminogen activator (t-PA) were compared for acute coronary thrombosis (for a commentary, see Hampton, 1996). [Pg.122]

GP Ilia Association between Pl allele and acute coronary thrombosis Unknown 112... [Pg.637]

Angina pectoris strictly translated is pain in the pectoral region of the chest. Usually this is referred to simply as angina and the typical presentation is that of a crushing pain in the upper left side of the chest which may radiate into the neck or down the left arm. The pain is usually severe and often produces significant distress in the sufferer. This is referred pain that is brought about because of insufficient blood flow to the myocardium. In severe cases, it may be a symptom of acute coronary thrombosis (heart attack). [Pg.57]

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. [Pg.309]

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. [Pg.119]

In contrast to unfractionated heparin, the factor Xa inhibitor tick anticoagulant peptide (TAP) effectively inhibited coronary arterial thrombosis in a canine electrolytic injury model (57). TAP was also effective in inhibition of the procoagulant properties of whole blood clots in vitro however, it was stated that TAP might be not optimal due to its slow binding kinetics (54). Meanwhile, several low molecular weight direct factor Xa inhibitors are in clinical development (Table I), some of them specifically for the treatment and secondary prevention of ACS. DX-9065a, ZK-807834 and otamixaban have been intensively characterized in vitro and in vivo and are in clinical investigations for the treatment of acute arterial thrombosis. [Pg.122]

Gelfand EV Cannon CR Acute coronary syndromes. In Colman RW et at, eds. Hemostasis and Thrombosis Basic Principles and Clinical Practice. Philadelphia Lippincott, Williams and Wilkins, 2006 1387-1404. [Pg.124]

The early clinical benefits observed in statin trials of acute coronary syndrome patients (MIRACL and PROVE-IT TIM 1-22) where coronary vascular inflammation, thrombosis, and unstable plaque are critical pathophysiologic elements that may be positively modified by statins compared to the more delayed benefits observed in statin trials of patients with stable coronary artery disease. [Pg.163]

Secondary endpoints Binary restenosis at 4 months follow-up (defined as > 50% diameter stenosis by QCA) Quantitative coronary angiography endpoints including late loss, loss index, late absolute MLD at 4 months Incidence of (sub)acute stent thrombosis (SAT) to 30 day follow-up, MACE at 4 and 9 months... [Pg.331]

In order to study new drugs for their antithrombotic potential in coronary arteries, Folts and Rowe (1974) developed the model of periodic acute platelet thrombosis and cyclic flow reductions (CFRs) in stenosed... [Pg.277]

Villota JN, Rubio LF, Flores JS, Peris VB, Burguera EP, Gonzalez VB, Banuls MP, Escorihuela AL. Cocaine-induced coronary thrombosis and acute myocardial infarction. Int J Cardiol 2004 96 481-2. [Pg.528]

Because of its powerfiil vasodilator action sodium nitroprusside is often used to treat vascular emergencies associated with hypertensive crisis. Since this compound shows some anti-platelet activity both in vitro and in vivo (Levin et al 1982, Hines and Barash 1989) its acute clinical effects may also be mediated, in part, through inhibition of platelet function. Recently, sodium nitroprusside was administered intrapericardially to treat experimentally induced coronary Arombosis in dogs (Willerson et al 1996). As this route of administration of sodium nitroprusside produced less vasodilatation than systemic one, localized administration of this dmg may offer new therapeutic possibilities for the treatment of the coronary thrombosis. [Pg.468]

Clinically observed effects The number of people who suffered clinically observed health effects individually attributable to radiation exposure due to the Chernobyl accident was relatively modest, given the accident s dimensions. A total of 237 persons, all of them workers dealing with the accident, were suspected of suffering clinical syndromes of radiation exposure and were hospitalized, and 134 of them were diagnosed with acute radiation syndrome. Of these, 28 died of the consequences of radiation injuries (three other persons died at the time of the accident two due to non-radiation blast injuries and one due to a coronary thrombosis). Some years after the accident, 14 additional persons in this group died however, their deaths were found to be not necessarily attributable to radiation exposure. [Pg.476]

An increased risk of thrombotic events, especially coronary thrombosis, has been reported in elderly patients taking retinoids (33). Two patients with acute promyelocytic leukemia developed thrombus in the right ventricle during induction treatment with tretinoin plus idarubicin (34). [Pg.3656]

The rupture of an atherosclerotic plaque in an epicardial coronary artery with subsequent occlusive coronary thrombosis has been established as the decisive event in the pathogenesis of acute myocardial infarction12. Other, milder forms of plaque rupture with subsequent embolization of atherosclerotic and thrombotic debris into the coronary microcirculation have also been recognized before2 5, but the clinical frequency and importance of microembolization have only recently been appreciated6-8. [Pg.127]

R. J. Frink, P. A. Rooney, J. O. Trowbridge and J. P. Rose, Coronary thrombosis and platelet/fibrin microemboli in death associated with acute myocardial infarction, Br Heart J 59, 196-200 (1988). [Pg.139]

Aberrant thrombus formation and deposition on blood vessel walls imderlies the pathogenesis of acute cardiovascular disease states which remain the principal cause of morbidity and mortality in the industrialized world [1,2,3]. Plasma proteins, proteases and specific cellular receptors that participate in hemostasis have emerged as important risk considerations in thrombosis and thromboembolic disorders. The clinical manifestations of the above disease states include acute coronary artery and cerebrovascular syndromes, peripheral arterial occlusion, deep vein thrombosis and pulmonary/renal embolism [3]. The most dilabilitating acute events precipitated by these disorders are myocardial infarction and stroke. In addition, the interplay between hemostatic factors and hypertension (4) or atherosclerosis (5) dramatically enhances the manifestation of these pathologic states. [Pg.271]

This chapter will not cover the acute coronary syndromes as readers are referred to the accompanying chapter in this text. However, it should be evident that the occurrence of acute plaque rupture and thrombosis has a significant impact on the prognosis of a patient with chronic ischemic heart disease. Cardiogenic shock... [Pg.68]

The anticlotting drugs are used in the treatment of myocardial infarction and other acute coronary syndromes, atrial fibrillation, ischemic stroke, and deep vein thrombosis (DVT). The anticoagulant and thrombolytic drugs ate effective in treatment of both venous and arterial thrombosis. Antiplatelet dmgs are used primarily for treatment of arterial disease. [Pg.304]


See other pages where Acute coronary thrombosis is mentioned: [Pg.320]    [Pg.410]    [Pg.667]    [Pg.128]    [Pg.638]    [Pg.139]    [Pg.147]    [Pg.320]    [Pg.410]    [Pg.667]    [Pg.128]    [Pg.638]    [Pg.139]    [Pg.147]    [Pg.310]    [Pg.225]    [Pg.226]    [Pg.231]    [Pg.303]    [Pg.320]    [Pg.310]    [Pg.315]    [Pg.155]    [Pg.525]    [Pg.225]    [Pg.226]    [Pg.500]    [Pg.1438]    [Pg.135]    [Pg.325]    [Pg.206]    [Pg.266]    [Pg.531]    [Pg.543]   
See also in sourсe #XX -- [ Pg.57 ]




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