Molecular basis of arrhythmias

Manish Shah, Fadi G. Akar, Gordon F. Tomaselli

Research output: Contribution to journalReview article

118 Citations (Scopus)

Abstract

The characterization of single gene disorders has provided important insights into the molecular pathogenesis of cardiac arrhythmias. Primary electricalal diseases including long-QT syndrome, short-QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia have been associated with mutations in a variety of ion channel subunit genes that promote arrhythmogenesis. Pathological remodeling of ionic currents and network properties of the heart critical for normal electrical propagation plays a critical role in the initiation and maintenance of acquired arrhythmias. This review focuses on the molecular and cellular basis of electrical activity in the heart under normal and pathophysiological conditions to provide insights into the fundamental mechanisms of inherited and acquired cardiac arrhythmias. Improved understanding of the basic biology of cardiac arrhythmias holds the promise of identifying new molecular targets for the treatment of cardiac arrhythmias.

Original languageEnglish (US)
Pages (from-to)2517-2529
Number of pages13
JournalCirculation
Volume112
Issue number16
DOIs
StatePublished - Oct 18 2005
Externally publishedYes

Fingerprint

Cardiac Arrhythmias
Brugada Syndrome
Long QT Syndrome
Ion Channels
Genes
Maintenance
Mutation

Keywords

  • Arrhythmia
  • Electrophysiology
  • Genetics
  • Ion channels
  • Molecular biology

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Molecular basis of arrhythmias. / Shah, Manish; Akar, Fadi G.; Tomaselli, Gordon F.

In: Circulation, Vol. 112, No. 16, 18.10.2005, p. 2517-2529.

Research output: Contribution to journalReview article

Shah, Manish ; Akar, Fadi G. ; Tomaselli, Gordon F. / Molecular basis of arrhythmias. In: Circulation. 2005 ; Vol. 112, No. 16. pp. 2517-2529.
@article{7f5ed07f6ed74247a399127d08d60294,
title = "Molecular basis of arrhythmias",
abstract = "The characterization of single gene disorders has provided important insights into the molecular pathogenesis of cardiac arrhythmias. Primary electricalal diseases including long-QT syndrome, short-QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia have been associated with mutations in a variety of ion channel subunit genes that promote arrhythmogenesis. Pathological remodeling of ionic currents and network properties of the heart critical for normal electrical propagation plays a critical role in the initiation and maintenance of acquired arrhythmias. This review focuses on the molecular and cellular basis of electrical activity in the heart under normal and pathophysiological conditions to provide insights into the fundamental mechanisms of inherited and acquired cardiac arrhythmias. Improved understanding of the basic biology of cardiac arrhythmias holds the promise of identifying new molecular targets for the treatment of cardiac arrhythmias.",
keywords = "Arrhythmia, Electrophysiology, Genetics, Ion channels, Molecular biology",
author = "Manish Shah and Akar, {Fadi G.} and Tomaselli, {Gordon F.}",
year = "2005",
month = "10",
day = "18",
doi = "10.1161/CIRCULATIONAHA.104.494476",
language = "English (US)",
volume = "112",
pages = "2517--2529",
journal = "Circulation",
issn = "0009-7322",
publisher = "Lippincott Williams and Wilkins",
number = "16",

}

TY - JOUR

T1 - Molecular basis of arrhythmias

AU - Shah, Manish

AU - Akar, Fadi G.

AU - Tomaselli, Gordon F.

PY - 2005/10/18

Y1 - 2005/10/18

N2 - The characterization of single gene disorders has provided important insights into the molecular pathogenesis of cardiac arrhythmias. Primary electricalal diseases including long-QT syndrome, short-QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia have been associated with mutations in a variety of ion channel subunit genes that promote arrhythmogenesis. Pathological remodeling of ionic currents and network properties of the heart critical for normal electrical propagation plays a critical role in the initiation and maintenance of acquired arrhythmias. This review focuses on the molecular and cellular basis of electrical activity in the heart under normal and pathophysiological conditions to provide insights into the fundamental mechanisms of inherited and acquired cardiac arrhythmias. Improved understanding of the basic biology of cardiac arrhythmias holds the promise of identifying new molecular targets for the treatment of cardiac arrhythmias.

AB - The characterization of single gene disorders has provided important insights into the molecular pathogenesis of cardiac arrhythmias. Primary electricalal diseases including long-QT syndrome, short-QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia have been associated with mutations in a variety of ion channel subunit genes that promote arrhythmogenesis. Pathological remodeling of ionic currents and network properties of the heart critical for normal electrical propagation plays a critical role in the initiation and maintenance of acquired arrhythmias. This review focuses on the molecular and cellular basis of electrical activity in the heart under normal and pathophysiological conditions to provide insights into the fundamental mechanisms of inherited and acquired cardiac arrhythmias. Improved understanding of the basic biology of cardiac arrhythmias holds the promise of identifying new molecular targets for the treatment of cardiac arrhythmias.

KW - Arrhythmia

KW - Electrophysiology

KW - Genetics

KW - Ion channels

KW - Molecular biology

UR - http://www.scopus.com/inward/record.url?scp=27144517158&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=27144517158&partnerID=8YFLogxK

U2 - 10.1161/CIRCULATIONAHA.104.494476

DO - 10.1161/CIRCULATIONAHA.104.494476

M3 - Review article

VL - 112

SP - 2517

EP - 2529

JO - Circulation

JF - Circulation

SN - 0009-7322

IS - 16

ER -