• Open Access

Structural and Functional Basis for the Long QT Syndrome: Relevance to Veterinary Patients

Authors

  • Melissa R.1 Finley,

    1. Departments of Anatomy and Physiology, College of Veterinary Medicine, Kansas State University, Manhattan, KS
    2. Salk Institute, La Jolla, CA
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  • James D. Lillich,

    1. Departments of Clinical Sciences, College of Veterinary Medicine, Kansas State University, Manhattan, KS
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  • Robert F. Gilmour Jr,

    1. Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY
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  • Lisa C. Freeman

    1. Departments of Anatomy and Physiology, College of Veterinary Medicine, Kansas State University, Manhattan, KS
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    • 5

      DVM, PhD, Department of Anatomy and Physiology, College of Veterinary Medicine, Kansas State University, 228 Coles Hall, Manhattan, KS 66506-5802; E-mail: freeman@vet.ksu.edu


Abstract

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 IKr. However, not all drugs that induce potentially fatal ventricular arrhythmias antagonize IKr, and not all drugs that block IKr are associated with ventricular arrhythmias. In clinical practice, the extent of QT interval prolongation and risk of ventricular arrhythmia associated with antagonism of IKr 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 IKr.

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