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Stanley Nattel

Researcher at Montreal Heart Institute

Publications -  802
Citations -  72437

Stanley Nattel is an academic researcher from Montreal Heart Institute. The author has contributed to research in topics: Atrial fibrillation & Heart failure. The author has an hindex of 132, co-authored 778 publications receiving 65700 citations. Previous affiliations of Stanley Nattel include Mayo Clinic & Brigham and Women's Hospital.

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T-Type Calcium Current Contributes to Escape Automaticity and Governs the Occurrence of Lethal Arrhythmias After Atrioventricular Block in Mice

TL;DR: This study suggests that T-type Ca2+ channels play an important role in infranodal escape automaticity and worsens bradycardia-related mortality, increases brady Cardia-associated adverse remodeling, and enhances the risk of malignant ventricular tachyarrhythmias complicating AVB.
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Acquired delayed rectifier channelopathies: how heart disease and antiarrhythmic drugs mimic potentially-lethal congenital cardiac disorders

TL;DR: An important novel contribution of the Tsuji paper is the convincing demonstration that ventricular I K is downregulation, which points to acquired conditions that may predispose to potentially lethal ventricular tachyarrhythmias while recreating ionic abnormalities associated with congenital LQTSs.
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Atrial Fibrillation and Body Composition: Is it Fat or Lean That Ultimately Determines the Risk?

TL;DR: There is evidence that adipocytes produce biologically active molecules that directly promote the development of Atrial Fibrillation (AF), and there are suggestions that weight loss as part of a structured risk-factor intervention program or as a result of bariatric surgery reduces AF risk.
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Regional Ion Channel Gene Expression Heterogeneity and Ventricular Fibrillation Dynamics in Human Hearts

TL;DR: Ion channel expression profile in myopathic human hearts is significantly altered compared to normal hearts, and multi-channel ion changes influence VF dynamic in a complex manner not predicted by known single channel linear relationships.