Diagnostic performance of QT interval variables from 24-h electrocardiography in the long QT syndrome
Nathalie Neyroud,P. Maison Blanche,Isabelle Denjoy,S. Chevret,Claire Donger,Eric Dausse,J. Fayn,Fabio Badilini,N. Menhabi,Ketty Schwartz,Pascale Guicheney,Philippe Coumel +11 more
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TLDR
QT interval variables obtained from 24-h ECG recordings improve long QT syndrome diagnosis by showing an increased nocturnal ventricular repolarization rate-dependence in genotyped chromosome 11-linked patients.Abstract:
Aims The long QT syndrome is mainly defined by QT interval prolongation (QTc >0·44s). However, data obtained in genotyped patients showed that resting QTc measurement alone may be inaccurate for ascertaining the phenotype. The aim of this study was to evaluate the diagnostic performance of QT interval rate-dependence in untreated chromosome 11-linked patients. Methods The study population consisted of 25 untreated long QT patients linked to chromosome 11 and 25 age- and gender-matched controls. QTc intervals were measured on 12-lead resting ECG recordings. From 24-h Holter recordings, the slope of the relationship between ventricular repolarization and heart rate was studied separately day and night to assess neural modulation. Mean heart rates and rate-dependences of QT and Q-maximum of T (QTm) intervals were compared between long QT patients and controls for both time periods.read more
Citations
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Journal ArticleDOI
Low Penetrance in the Long-QT Syndrome Clinical Impact
TL;DR: It is no longer acceptable to exclude LQTS among family members of definitely affected patients on purely clinical grounds, and it now appears appropriate to perform molecular screening in allfamily members of genotyped patients.
Journal ArticleDOI
Evaluation of drug-induced QT interval prolongation: implications for drug approval and labelling.
Marek Malik,A. John Camm +1 more
TL;DR: Since QT interval prolongation is only an indirect surrogate of predisposition to the induction of torsade de pointes tachycardia, any conclusion that a drug is safe should be reserved until postmarketing surveillance data are reviewed, since the area of drug-related cardiac proarrhythmic toxicity is fast evolving.
Journal ArticleDOI
Impaired endothelial function following a meal rich in used cooking fat.
Michael J.A. Williams,Wayne H.F. Sutherland,Maree P. McCormick,Sylvia A. de Jong,Robert J. Walker,Gerard T. Wilkins +5 more
TL;DR: Ingestion of a meal rich in fat previously used for deep frying in a commercial fast food restaurant resulted in impaired arterial endothelial function, suggesting that intake of degradation products of heated fat contribute to endothelial dysfunction.
Journal ArticleDOI
Recommendations for the Use of Genetic Testing in the Clinical Evaluation of Inherited Cardiac Arrhythmias Associated with Sudden Cardiac Death: Canadian Cardiovascular Society/Canadian Heart Rhythm Society Joint Position Paper
Michael H. Gollob,Louis Blier,Ramon Brugada,Jean Champagne,Vijay S. Chauhan,Sean Connors,Martin Gardner,Martin S. Green,Robert M. Gow,Robert J. Hamilton,Louise Harris,Jeff S. Healey,Kathleen A. Hodgkinson,Christina Honeywell,Michael Kantoch,Joel A. Kirsh,Andrew D. Krahn,Michelle A. Mullen,Ratika Parkash,Damian P. Redfearn,Julie Rutberg,Shubhayan Sanatani,Anna Woo +22 more
TL;DR: This document represents the first ever published recommendations outlining the role of genetic testing in various clinical scenarios, the specific genes to be considered for testing, and the utility of test results in the management of patients and their families.
Journal ArticleDOI
Involvement of IsK-Associated K+ Channel in Heart Rate Control of Repolarization in a Murine Engineered Model of Jervell and Lange-Nielsen Syndrome
Milou Daniel Drici,Isabelle Arrighi,Christophe Chouabe,Jeffrey R. Mann,Michel Lazdunski,Georges Romey,Jacques Barhanin +6 more
TL;DR: It is concluded that the isk gene product and/or ISKs, when present, blunts the QT adaptation to heart rate variations and that steeper QT-RR relationships reflect a greater susceptibility to arrhythmias in patients lacking IKs.
References
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Journal ArticleDOI
A molecular basis for cardiac arrhythmia: HERG mutations cause long QT syndrome
Mark E. Curran,Igor Splawski,Katherine W. Timothy,Vincent Gm,Eric D. Green,Keating Mt,Keating Mt +6 more
TL;DR: In this article, the authors investigated patients with long QT syndrome (LQT), an inherited disorder causing sudden death from a ventricular tachyarrythmia, torsade de pointes.
Journal ArticleDOI
Positional cloning of a novel potassium channel gene: KVLQT1 mutations cause cardiac arrhythmias.
Qing Wang,Mark E. Curran,Igor Splawski,Timothy C. Burn,J. M. Millholland,T. J. VanRaay,Jiaxiang Shen,Katherine W. Timothy,Vincent Gm,Vincent Gm,T. De Jager,Peter J. Schwartz,J.A. Towbin,Arthur J. Moss,Donald L. Atkinson,Gregory M. Landes,Timothy D. Connors,M T Keating +17 more
TL;DR: In this article, positional cloning was used to establish KVLQT1 as the chromosome 11-linked LQT 1 gene responsible for the most common inherited cardiac arrhythmia.
Journal ArticleDOI
Coassembly of K(V)LQT1 and minK (IsK) proteins to form cardiac I(Ks) potassium channel.
Michael C. Sanguinetti,Mark E. Curran,Anruo Zou,Jiaxiang Shen,Peter S. Spector,Donald L. Atkinson,M T Keating +6 more
TL;DR: KVLQT1 is the subunit that coassembles with minK to form IKS channels and IKS dysfunction is a cause of cardiac arrhythmia, and is shown to encode a K+ channel with biophysical properties unlike other known cardiac currents.
Journal ArticleDOI
K v LQT1 and IsK (minK) proteins associate to form the I KS cardiac potassium current
TL;DR: It is shown that KVLQT1 associates with IsK to form the channel underlying the IKS cardiac current, which is a target of class-Ill anti-arrhythmic drugs and is involved in the L QT1 syndrome.
Journal ArticleDOI
SCN5A mutations associated with an inherited cardiac arrhythmia, long QT syndrome
Qing Kenneth Wang,Jiaxiang Shen,Jiaxiang Shen,Igor Splawski,Donald L. Atkinson,Donald L. Atkinson,Zhizhong Li,Jennifer L. Robinson,Arthur J. Moss,Jeffrey A. Towbin,Mark T. Keating +10 more
TL;DR: Genetic linkage between LQT3 and polymorphisms within SCN5A, the cardiac sodium channel gene, and single strand conformation polymorphism and DNA sequence analyses suggest that mutations in SCN 5A cause chromosome 3-linked LQt and indicate a likely cellular mechanism for this disorder.
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