Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Cardiac Arrest Following Torsades de Pointes Caused by Hypokalemia and Catecholamines in a Patient with Congenital Long QT Syndrome Type 1 After Surgical Aortic Valve Replacement: A Case Report.
Am J Case Rep
December 2022
Department of Anesthesiology, Kindai University Faculty of Medicine, Osaka-Sayama, Osaka, Japan.
BACKGROUND Prevention of lethal arrhythmias in congenital long QT syndrome type 1 (LQT1) requires avoidance of sympathoexcitation, drugs that prolong QT, and electrolyte abnormalities. However, it is often difficult to avoid all these risks in the perioperative period of open heart surgery. Herein, we report hypokalemia-induced cardiac arrest in a postoperative cardiac patient with LQT1 on catecholamine.
View Article and Find Full Text PDFCompound Heterozygous Mutations Causing Recessive Romano-Ward Syndrome: Functional Characterization by Mutant Co-expression.
Front Cardiovasc Med
February 2021
Laboratorio de Genómica de Enfermedades Cardiovasculares, Instituto Nacional de Medicina Genómica, Mexico City, Mexico.
Next Generation Sequencing has identified many genetic variants associated with type 1 long QT or Romano-Ward syndrome, most frequently inherited in an autosomal dominant fashion, although recessive forms have been reported. Particularly in the case of missense variants, functional studies of mutants are of aid to establish variant pathogenicity and to understand the mechanistic basis of disease. Two compound heterozygous mutations (p.
View Article and Find Full Text PDFA computational analysis of the effect of sevoflurane in a human ventricular cell model of long QT syndrome: Importance of repolarization reserve in the QT-prolonging effect of sevoflurane.
Eur J Pharmacol
September 2020
Department of Physiology, Shiga University of Medical Science, Otsu, Shiga, 520-2192, Japan.
The slowly and rapidly activating delayed rectifier K channels (I and I, respectively) contribute to the repolarization of ventricular action potential in human heart and thereby determine QT interval on an electrocardiogram. Loss-of-function mutations in genes encoding I and I cause type 1 and type 2 long QT syndrome (LQT1 and LQT2, respectively), accompanied by a high risk of malignant ventricular arrhythmias and sudden cardiac death. This study was designed to investigate which cardiac electrophysiological conditions exaggerate QT-prolonging and arrhythmogenic effects of sevoflurane.
View Article and Find Full Text PDFIdentification of a Novel KCNQ1 Frameshift Mutation and Review of the Literature among Iranian Long QT Families.
Iran Biomed J
May 2019
Department of Molecular Medicine, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran.
Article Synopsis
- Long QT syndrome (LQTS) is a heart condition that can cause fainting and sudden death, primarily due to a prolonged QT interval, with the KCNQ1 gene being the most commonly associated.
- A study conducted on Iranian families identified a new homozygous KCNQ1 mutation (c.1426_1429delATGC) through DNA sequencing and examined existing cases of LQTS.
- This novel mutation is reported for the first time in the Iranian population, highlighting the significance of genetic research in identifying LQTS carriers.
Recurrent Torsades with Refractory QT Prolongation in a 54-Year-Old Man.
Am J Case Rep
December 2018
Critical Care Services, Tripler Army Medical Center, Honolulu, HI, USA.
BACKGROUND QT prolongation is a common, easily overlooked clinical problem with potentially dire consequences. Drug-induced and congenital forms are not mutually exclusive, but are treated differently. Here, we present a case of cryptogenic underlying congenital long QT syndrome (cLQTS) successfully treated with isoproterenol, a drug contraindicated in most congenital forms of this condition.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!