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ventricular fibrillation/protease
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8 resultater
HIV protease inhibitors induced prolongation of the QT Interval: electrophysiology and clinical implications.
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In recent years, there have been considerable advancements in our understanding of the role of ionic channels in mediating cardiac repolarization. Advances in ion channel cloning have generated great interest in the diagnosis and understanding of electrophysiological processes involved in
Antifibrillatory effects of class III antiarrhythmic drugs: comparative study with flecainide.
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The antifibrillatory effects of flecainide 1 mg/kg + 0.05 mg/kg/min intravenously (i.v.), bretylium 6 mg/kg i.v., D-sotalol 2 mg/kg + 0.1 mg/kg/min i.v., and E-4031, a new class III drug, 50 micrograms/kg + 5 micrograms/kg/min i.v. were compared with three different methods of determining
Markers of progenitor cell recruitment and differentiation rise early during ischemia and continue during resuscitation in a porcine acute ischemia model.
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Clinical administration of bone marrow-derived stem cells in the setting of acute myocardial infarction (AMI) leads to improved left ventricular ejection fraction. Thymosin beta-4 (TB4) and vascular endothelial growth factor (VEGF) are linked to adult epicardial progenitor cell mobilization and
Sudden unexpected death as a consequence of indinavir-induced nephropathy. A case report.
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A 60-year-old male had tested in 1986, at age 46, positive for human immunodeficiency virus (HIV). In mid-1996 he was started on a protease inhibitor regimen, which included indinavir, lamivudine and stavudine, and remained on this therapy until his death. In April 1999 he was hospitalized after a
Ankyrin-B protein in heart failure: identification of a new component of metazoan cardioprotection.
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Ankyrins (ankyrin-R, -B, and -G) are adapter proteins linked with defects in metazoan physiology. Ankyrin-B (encoded by ANK2) loss-of-function mutations are directly associated with human cardiovascular phenotypes including sinus node disease, atrial fibrillation, ventricular tachycardia, and sudden
SCH 79797, a selective PAR1 antagonist, protects against ischemia/reperfusion-induced arrhythmias in the rat hearts.
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Thrombin is implicated in the genesis of arrhythmias and activation of thrombin receptors exacerbated ventricular arrhythmias following coronary artery ligation. The present study was designed to investigate the possible protective effect of the protease-activated receptor-1 antagonist, SCH79797
COVID-19 and the cardiovascular system: implications for risk assessment, diagnosis, and treatment options.
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The novel coronavirus disease (COVID-19) outbreak, caused by SARS-CoV-2, represents the greatest medical challenge in decades. We provide a comprehensive review of the clinical course of COVID-19, its comorbidities, and mechanistic considerations for future therapies. While COVID-19 primarily
Targeting cardiac mast cells: pharmacological modulation of the local renin-angiotensin system.
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Enhanced production of angiotensin II and excessive release of norepinephrine in the ischemic heart are major causes of arrhythmias and sudden cardiac death. Mast cell-dependent mechanisms are pivotal in the local formation of angiotensin II and modulation of norepinephrine release in cardiac
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