KCNQ1 G219E and TRPM4 T160M polymorphisms are involved in the pathogenesis of long QT syndrome: A case report

Medicine (Baltimore). 2021 Jan 15;100(2):e24032. doi: 10.1097/MD.0000000000024032.

Abstract

Rationale: Long QT syndrome (LQTS) is an inheritable disease characterized by prolonged QT interval on the electrocardiogram. The pathogenesis of LQTS is related to mutations in LQTS-susceptible genes encoding cardiac ion channel proteins or subunits.

Patient concerns: Here, we reported a 37-year-old female Uygur patient with palpitation and loss of consciousness.

Diagnoses: At the time of admission, a 12-lead electrocardiogram showed a QTc interval of 514 ms. Genetic analysis revealed KCNQ1 G219E and TRPM4 T160M mutations.

Interventions: Although beta-blockers remain the mainstay in treating LQTS, the patient underwent implantation of an automatic cardioverter defibrillator due to life-threatening arrhythmias.

Outcomes: To explore the effect of the calcium ion antagonist verapamil on ion channels, we generated human induced pluripotent stem cell cardiomyocytes (hiPSC-CMs) from the peripheral blood mononuclear cells of the patient. The changes of action potential duration in response to verapamil were observed.

Lessons: Our results showed that patient-derived hiPSC-CMs could recapitulate the electrophysiological features of LQTS and display pharmaceutical responses to verapamil.

Publication types

  • Case Reports

MeSH terms

  • Adult
  • Calcium Channel Blockers / pharmacology
  • Defibrillators, Implantable
  • Female
  • Humans
  • Induced Pluripotent Stem Cells / drug effects
  • KCNQ1 Potassium Channel / genetics*
  • Long QT Syndrome / genetics*
  • Long QT Syndrome / surgery
  • TRPM Cation Channels / genetics*
  • Verapamil / pharmacology

Substances

  • Calcium Channel Blockers
  • KCNQ1 Potassium Channel
  • TRPM Cation Channels
  • TRPM4 protein, human
  • Verapamil