Titlebook: Reperfusion and Revascularization in Acute Myocardial Infarction; Gotthard Schettler (Leiter, Präsident),Robert B. J Conference proceeding

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Prehospital Thrombolysis in Acute Myocardial Infarction: The Jerusalem Experienceupt occlusion of the coronary artery and spreads as a wave front from endocardium to epicardium. Irreversible damage is complete after 6 h, but most of the necrosis has occurred within 1 h [5, 6]. Thrombolytic therapy can reopen 40% – 90% of obstructed arteries [7 – 9]. If thrombolytic therapy is to

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Very Early Urokinase Treatment in Acute Myocardial Infarctionfter a 3-h coronary artery ligation myocardial infarction had developed completely [6]. A similar relationship between myocardial salvage and the time interval from symptom onset to start of thrombolytic therapy could be found in patients with acute myocardial infarction [4]. For estimation of myoca

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Prourokinase in Acute Myocardial Infarction: Is it Effective?tended by significant problems. Urokinase and streptokinase lack fibrin selectivity and promote generalized fibrinogenolysis, at times resulting in severe bleeding [2]. Tissue-type plasminogen activator (TPA) and single-chain urokinase-type plasminogen activator (prourokinase) are both reported to b

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Recombinant Tissue-Type Plasminogen Activator in the Treatment of Myocardial Infarctiononary artery occlusion than the conventional non-fibrin-specific thrombolytic agents such as streptokinase and urokinase [1 – 3]. Reliable data on the efficacy of thrombolytics with respect to reopening occluded coronary arteries can only be obtained from randomized trials, which are listed in Table

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Thrombolytic Agents in Early Myocardial Infarction — An Overview in 1987d technician was admitted at night with a 2-h history of persisting chest pain at rest associated with nausea and perspiration. He had been entirely well until 5 months previously, when he developed angina on effort. Despite 200 mg atenolol, 80 mg isosorbide dinitrate, and 40 mg nifedipine daily, an

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The No-Reflow Phenomenoneflow. Likewise, the kidney is encapsulated in a fibrous sheath, and reflow may be limited by extrinsic compression. However, the heart has no constricting external capsule, and no-reflow must occur by mechanisms other than extrinsic compression of the organ.

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Conference proceedings 1988s for their everyday work. Critical standards for the indications and risks of the recommended procedures are given. Particular emphasis is laid on the possibilities for revascularization by means of dissolution of blood thrombi. The book aims to present top-level guidance to the pros and cons of reconstructive measures in coronary disorders.