A Novel Form of Short QT Syndrome (SQT3) Is Caused by a Mutation in the KCNJ2 Gene
By S. Priori, S. Pandit, I. Rivolta, O. Berenfeld, E. Ronchetti, Amit S Dhamoon, C. Napolitano, J. Anumonwo, M. R. di Barletta, Smitha Gudapakkam and 3 more. Circulation Research, 2005
642 citations recorded by the source corpus.
Subfields: Cardiology and Cardiovascular Medicine, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/23475e36234ebbfe6a48fcf1ad5aad036c0ccb6f
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In Cardiology and Cardiovascular Medicine
- Bernard R. Chaitman
- Rick A. Nishimura
- J. Halperin
- Jose Luis Zamorano
- M. Creager
- Douglas P. Zipes
- C. Yancy
In Molecular Biology
Citations in the corpus
- ACC/AHA/HRS 2008 Guidelines for device-based therapy of cardiac rhythm abnormalities. (2008, background): “VF has been reported in patients with abnormal repolarization due to ion channel mutations that result in a markedly shortened QT interval (432).”
- Functions of Polyamines in Mammals* (2016, background): “1 channel due to an inherited mutation at one of the spermine-binding sites (Asp-172) caused short QT syndrome, which predisposes patients to life-threatening arrhythmias (85).”
- ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: A report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (2006, background): “Shortly thereafter, a novel form of SQTS in patients with a QTc up to 320 ms was identified.(812) At present, it is still undefined whether the diagnosis of SQTS should be based on QT or QTc and which is the sensitivity and specificity of different QT/QTc interval cutoff values.”
- Inwardly rectifying potassium channels: their structure, function, and physiological roles. (2010, background): “1 mutation produces an abrupt increase in the rate of final repolarization of the ventricular action potential and shortens its duration (628).”