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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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Effects of verapamil on atrial fibrillation and its electrophysiological determinants in dogs

TL;DR: Verapamil promotes AF in normal dogs by promoting multiple circuit reentry, an effect dependent on intact autonomic tone and not shared by diltiazem.
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Effects of flecainide and quinidine on Kv4.2 currents: voltage dependence and role of S6 valines.

TL;DR: Results point to an important role for S6 valines at positions 402 and 404 in mediating voltage‐dependent block by quinidine and flecainide in mediation of voltage dependence in Kv4.2WT channels.
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Diltiazem at reperfusion reduces neutrophil accumulation and infarct size in dogs with ischaemic myocardium

TL;DR: Diltiazem given during reperfusion reduces infarct size by a mechanism that includes an inhibition of neutrophil accumulation in the post-ischaemic myocardium, and to establish if an interaction with neutrophils is implied.
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Is There a Future for Antiarrhythmic Drug Therapy

TL;DR: In the future, antiarrhythmic agents will continue to be used acutely to terminate a broad range of sustained arrhythmias, and the development of molecular electrophysiology will allow for the identification of agents with selected ion channel blocking profiles which may prove efficacious with a lower risk of complications.
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Single-channel recordings of a rapid delayed rectifier current in adult mouse ventricular myocytes: basic properties and effects of divalent cations

TL;DR: Despite the abundant expression of mikr, single‐channel events were rarely observed during action‐potential clamp and 5 μm E‐4031 had no detectable effect on the action potential parameters, confirming that mIKr plays at best a minor role in repolarization of adult mouse cardiomyocytes, probably because the modulatory effects of divalent cations prevent significant mIKR opening under physiological conditions.