Publications by authors named "Thom Stams"

Background: Accurate breast density evaluation allows for more precise risk estimation but suffers from high inter-observer variability.

Purpose: To evaluate the feasibility of reducing inter-observer variability of breast density assessment through artificial intelligence (AI) assisted interpretation.

Study Type: Retrospective.

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Aims: Altered ventricular activation (AVA) causes intraventricular mechanical dyssynchrony (MD) and impedes contraction, promoting pro-arrhythmic electrical remodelling in the chronic atrioventricular block (CAVB) dog. We aimed to study arrhythmogenic and electromechanical outcomes of different degrees of AVA.

Methods And Results: Following atrioventricular block, AVA was established through idioventricular rhythm (IVR; n = 29), right ventricular apex (RVA; n = 12) pacing or biventricular pacing [cardiac resynchronization therapy (CRT); n = 10].

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Article Synopsis
  • - The study investigates how chronic complete atrioventricular block (CAVB) dogs are sensitive to drug-induced torsade de pointes (TdP) arrhythmias by examining the differences in repolarization times (RT) within the heart's ventricles.
  • - Researchers inserted multiple electrodes into the ventricles of 8 CAVB dogs to monitor electrical activity before and after administering dofetilide, which triggered TdP in five of the dogs, highlighting changes in repolarization patterns.
  • - Findings suggest that TdP is initiated in areas of the heart with significant repolarization differences, indicating that a certain level of electrical gradient is necessary for TdP to occur.
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Background: Beat-to-beat variability in ventricular repolarization (BVR) associates with increased arrhythmic risk. Proarrhythmic remodeling in the dog with chronic AV-block (CAVB) compromises repolarization reserve and associates with increased BVR, which further increases upon dofetilide infusion and correlates with Torsade de Pointes (TdP) arrhythmias. It was hypothesized that these pro-arrhythmia-associated increases in BVR are induced by beat-to-beat variability in preload.

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Repolarization-dependent cardiac arrhythmias only arise in hearts facing multiple 'challenges' affecting its so-called repolarization reserve. Congestive heart failure (CHF) is one such challenge frequently observed in humans and is accompanied by altered calcium handling within the contractile heart cell. This raises the question as to whether or not the well-known calcium channel antagonist verapamil acts as an antiarrhythmic drug in this setting, as seen in arrhythmia models without CHF.

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The novel antiarrhythmic drug K201 (4-[3-{1-(4-benzyl)piperidinyl}propionyl]-7-methoxy-2,3,4,5-tetrahydro-1,4-benzothiazepine monohydrochloride) is currently in development for treatment of atrial fibrillation. K201 not only controls intracellular calcium release by the ryanodine receptors, but also possesses a ventricular action that might predispose to torsade de pointes arrhythmias. The anti- and proarrhythmic effects of K201 were investigated in the anesthetized canine chronic atrioventricular block model.

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