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Article

Arrhythmogenic substrate and its modification by nicorandil in a murine model of long QT type 3 syndrome.

Progress in biophysics and molecular biology - 1 Jan 2000

Hothi Sandeep S, Booth Stephen W, Sabir Ian N, Killeen Matthew J, Simpson Fergus, Zhang Yanmin, Grace Andrew A, Huang Christopher L-H

Abstract excerpt

The gain-of-function Scn5a+/DeltaKPQ mutation in the cardiac Na(+) channel causes human long QT type 3 syndrome (LQT3) associated with ventricular arrhythmogenesis. The K(ATP) channel-opener nicorandil (20muM) significantly reduced arrhythmic incidence in Langendorff-perfused Scn5a+/Delta hearts during programmed electrical stimulation; wild-types (WTs) showed a total absence of arrhythmogenicity. These...

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PMID: 19351517
DOI: 10.1016/j.pbiomolbio.2009.01.006

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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