Open AccessStructural and Functional Basis for the Long QT Syndrome: Relevance to Veterinary Patients
Author(s) -
Finley Melissa R.,
Lillich James D.,
Jr Robert F. Gilmour,
Freeman Lisa C.
Publication year - 2003
Publication title -
journal of veterinary internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.356
H-Index - 103
eISSN - 1939-1676
pISSN - 0891-6640
DOI - 10.1111/j.1939-1676.2003.tb02468.x
Subject(s) - medicine , herg , qt interval , long qt syndrome , pharmacodynamics , prolongation , drug , repolarization , torsades de pointes , pharmacology , cardiology , heart block , pharmacokinetics , electrocardiography , potassium channel , electrophysiology
Long QT syndrome (LQTS) is a condition characterized by prolongation of ventricular repolarization and is manifested clinically by lengthening of the QT interval on the surface ECG. Whereas inherited forms of LQTS associated with mutations in the genes that encode ion channel proteins are identified only in humans, the acquired form of LQTS occurs in humans and companion animal species. Often, acquired LQTS is associated with drug‐induced block of the cardiac K + current designated I Kr . However, not all drugs that induce potentially fatal ventricular arrhythmias antagonize I Kr , and not all drugs that block I Kr are associated with ventricular arrhythmias. In clinical practice, the extent of QT interval prolongation and risk of ventricular arrhythmia associated with antagonism of I Kr are modulated by pharmacokinetic and pharmacodynamic variables. Veterinarians can influence some of the potential risk factors (eg, drug dosage, route of drug administration, presence or absence of concurrent drug therapy, and patient electrolyte status) but not all (eg, patient gender/genetic background). Veterinarians need to be aware of the potential for acquired LQTS during therapy with drugs identified as blockers of HERG channels and I Kr .