tachycardia/protease

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Monomorphic ventricular tachycardia due to protease inhibitor intoxication by atazanavir.

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Přihlášení Registrace

Atazanavir is a protease inhibitor approved for use in combination with other antiretroviral drugs for the treatment of human immunodeficiency virus infection. Atazanavir and other protease inhibitors can sometimes induce corrected QT prolongation and ventricular arrhythmia. A 40-year-old man with

The effects of the protease inhibitor, aprotinin, on the course of shock induced by endotoxin in cats.

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Přihlášení Registrace

The administration of endotoxin derived from Escherichia coli to anaesthetized cats resulted, within the first 5 min, in an initial increase in right atrial pressure and a reduction in systemic arterial blood pressure. Over the next 2 h shock was characterized by a reduced cardiac output,

Atazanavir induced first degree atrioventricular block and ventricular tachycardia: a case report.

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Atazanavir is one highly active antiretroviral therapy for naïve patients or patients with previous regimen failure. However, it seems that the protease inhibitor induces hyperlipidemia. Hyperbillirubinemia is the most common clinical adverse events but reports of cardiotoxicity due to atazanavir

HIV protease inhibitors induced prolongation of the QT Interval: electrophysiology and clinical implications.

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Přihlášení Registrace

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

Cathepsin A mediates susceptibility to atrial tachyarrhythmia and impairment of atrial emptying function in Zucker diabetic fatty rats.

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Přihlášení Registrace

Type 2 diabetes (T2D) is an independent risk factor for atrial fibrillation (AF) and stroke. The serine protease cathepsin A (CatA) is up-regulated in diabetes and plays an important role in the degradation of extracellular peptides. This study sought to delineate the role of CatA for the

Coagulation factor Xa induces an inflammatory signalling by activation of protease-activated receptors in human atrial tissue.

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Activated factor X (FXa) is an important player in the coagulation cascade responsible for thrombin generation, which is activated during atrial fibrillation. Increasing evidence suggests that FXa influences cell signalling in various cell types by activating protease-activated receptors (PARs). It

Systemic inflammatory response syndrome is reduced by preoperative plasma-thrombo-leukocyte aphaeresis in a pig model of cardiopulmonary bypass.

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OBJECTIVE The systemic inflammatory response syndrome (SIRS) after cardiac surgery with cardiopulmonary bypass (CPB) exacerbates organ dysfunction and increases postoperative mortality. The aim of this study was to reduce SIRS after CPB in a pig model by profoundly decreasing all blood defence

The calsequestrin mutation CASQ2D307H does not affect protein stability and targeting to the junctional sarcoplasmic reticulum but compromises its dynamic regulation of calcium buffering.

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Mutations in cardiac ryanodine receptor (RYR2) and cardiac calsequestrin (CASQ2) genes are linked to catecholaminergic polymorphic ventricular tachycardia, a life-threatening genetic disease. They predispose young individuals to cardiac arrhythmia in the absence of structural abnormalities. One such

Severe cardiac arrythmia on cisapride.

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Přihlášení Registrace

(1) Cisapride prolongs the QT interval and can cause torsades de pointes and ventricular tachycardia. (2) Cases of cardiac arrhythmia and death have occurred, even in the absence of underlying factors such as high doses and interactions with enzyme-inhibiting drugs (especially macrolide antibiotics,

Etiopathogenesis of acute pancreatitis.

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Přihlášení Registrace

Acute pancreatitis is a disease that has many causes. Each cause seems to affect the acinar cell in some way that results in the premature activation and retention of potent proteolytic enzymes. These activated enzymes then injure the acinar cell and cause the immediate release of cytokines and

A case of levofloxacin-induced anaphylaxis with elevated serum tryptase levels.

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Přihlášení Registrace

Levofloxacin, a fluoroquinolone and L-isomer of the racemate ofloxacin, has been approved for the treatment of acute and chronic bacterial infections. Gastrointestinal complaints are the most frequently reported adverse drug reactions to fluoroquinolones. Other adverse events include headache,

Pathophysiology of septic shock and implications for therapy.

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Přihlášení Registrace

Current knowledge about the pathophysiology of septic shock is reviewed, and biotechnology-based therapies under development are discussed. Patients with septic shock begin their clinical course with leukocytosis, fever, tachycardia, tachypnea, and organ hypoperfusion; shock ensues as immunologic

Ankyrin-B protein in heart failure: identification of a new component of metazoan cardioprotection.

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Přihlášení Registrace

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

Differential protein kinase C isoform regulation and increased constitutive activity of acetylcholine-regulated potassium channels in atrial remodeling.

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Přihlášení Registrace

BACKGROUND Atrial fibrillation (AF) causes atrial-tachycardia remodeling (ATR), with enhanced constitutive acetylcholine-regulated K+ current (I(KAChC)) contributing to action potential duration shortening and AF promotion. The underlying mechanisms are unknown. OBJECTIVE To evaluate the role of

SCH 79797, a selective PAR1 antagonist, protects against ischemia/reperfusion-induced arrhythmias in the rat hearts.

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Přihlášení Registrace

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

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