Conduction abnormalities in nonischemic dilated cardiomyopathy

Basic mechanisms and arrhythmic consequences

Fadi G. Akar, Gordon F. Tomaselli

Research output: Contribution to journalReview article

30 Citations (Scopus)

Abstract

Heart failure is associated with an increased risk of sudden death caused by ventricular tachyarrhythmias. The role of altered repolarization in the formation of arrhythmogenic substrates and triggers has been studied at multiple levels of integration, including molecular, cellular, tissue, and organ levels. Numerous studies have focused on conduction abnormalities in the context of ischemic heart disease and left ventricular dysfunction after myocardial infarction. However, ischemia alone, independent of left ventricular dysfunction, alters conduction by depressing membrane excitability and increasing tissue resistivity. In this review, we focus on the role of conduction abnormalities in the genesis of arrhythmias in nonischemic dilated cardiomyopathy and discuss their underlying cellular and molecular mechanisms, including changes in myocyte excitability, the extracellular matrix, and cell-to-cell coupling. We compare the nature of conduction slowing in ischemic and nonischemic heart failure and highlight the mechanistic differences between the two disease etiologies.

Original languageEnglish (US)
Pages (from-to)259-264
Number of pages6
JournalTrends in Cardiovascular Medicine
Volume15
Issue number7
DOIs
StatePublished - Oct 1 2005
Externally publishedYes

Fingerprint

Dilated Cardiomyopathy
Left Ventricular Dysfunction
Heart Failure
Sudden Death
Tachycardia
Muscle Cells
Myocardial Ischemia
Extracellular Matrix
Cardiac Arrhythmias
Ischemia
Myocardial Infarction
Membranes

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Conduction abnormalities in nonischemic dilated cardiomyopathy : Basic mechanisms and arrhythmic consequences. / Akar, Fadi G.; Tomaselli, Gordon F.

In: Trends in Cardiovascular Medicine, Vol. 15, No. 7, 01.10.2005, p. 259-264.

Research output: Contribution to journalReview article

@article{fdfe47223bfc40e0af7c6fddd06eb6a8,
title = "Conduction abnormalities in nonischemic dilated cardiomyopathy: Basic mechanisms and arrhythmic consequences",
abstract = "Heart failure is associated with an increased risk of sudden death caused by ventricular tachyarrhythmias. The role of altered repolarization in the formation of arrhythmogenic substrates and triggers has been studied at multiple levels of integration, including molecular, cellular, tissue, and organ levels. Numerous studies have focused on conduction abnormalities in the context of ischemic heart disease and left ventricular dysfunction after myocardial infarction. However, ischemia alone, independent of left ventricular dysfunction, alters conduction by depressing membrane excitability and increasing tissue resistivity. In this review, we focus on the role of conduction abnormalities in the genesis of arrhythmias in nonischemic dilated cardiomyopathy and discuss their underlying cellular and molecular mechanisms, including changes in myocyte excitability, the extracellular matrix, and cell-to-cell coupling. We compare the nature of conduction slowing in ischemic and nonischemic heart failure and highlight the mechanistic differences between the two disease etiologies.",
author = "Akar, {Fadi G.} and Tomaselli, {Gordon F.}",
year = "2005",
month = "10",
day = "1",
doi = "10.1016/j.tcm.2005.08.002",
language = "English (US)",
volume = "15",
pages = "259--264",
journal = "Trends in Cardiovascular Medicine",
issn = "1050-1738",
publisher = "Elsevier Inc.",
number = "7",

}

TY - JOUR

T1 - Conduction abnormalities in nonischemic dilated cardiomyopathy

T2 - Basic mechanisms and arrhythmic consequences

AU - Akar, Fadi G.

AU - Tomaselli, Gordon F.

PY - 2005/10/1

Y1 - 2005/10/1

N2 - Heart failure is associated with an increased risk of sudden death caused by ventricular tachyarrhythmias. The role of altered repolarization in the formation of arrhythmogenic substrates and triggers has been studied at multiple levels of integration, including molecular, cellular, tissue, and organ levels. Numerous studies have focused on conduction abnormalities in the context of ischemic heart disease and left ventricular dysfunction after myocardial infarction. However, ischemia alone, independent of left ventricular dysfunction, alters conduction by depressing membrane excitability and increasing tissue resistivity. In this review, we focus on the role of conduction abnormalities in the genesis of arrhythmias in nonischemic dilated cardiomyopathy and discuss their underlying cellular and molecular mechanisms, including changes in myocyte excitability, the extracellular matrix, and cell-to-cell coupling. We compare the nature of conduction slowing in ischemic and nonischemic heart failure and highlight the mechanistic differences between the two disease etiologies.

AB - Heart failure is associated with an increased risk of sudden death caused by ventricular tachyarrhythmias. The role of altered repolarization in the formation of arrhythmogenic substrates and triggers has been studied at multiple levels of integration, including molecular, cellular, tissue, and organ levels. Numerous studies have focused on conduction abnormalities in the context of ischemic heart disease and left ventricular dysfunction after myocardial infarction. However, ischemia alone, independent of left ventricular dysfunction, alters conduction by depressing membrane excitability and increasing tissue resistivity. In this review, we focus on the role of conduction abnormalities in the genesis of arrhythmias in nonischemic dilated cardiomyopathy and discuss their underlying cellular and molecular mechanisms, including changes in myocyte excitability, the extracellular matrix, and cell-to-cell coupling. We compare the nature of conduction slowing in ischemic and nonischemic heart failure and highlight the mechanistic differences between the two disease etiologies.

UR - http://www.scopus.com/inward/record.url?scp=26444500576&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=26444500576&partnerID=8YFLogxK

U2 - 10.1016/j.tcm.2005.08.002

DO - 10.1016/j.tcm.2005.08.002

M3 - Review article

VL - 15

SP - 259

EP - 264

JO - Trends in Cardiovascular Medicine

JF - Trends in Cardiovascular Medicine

SN - 1050-1738

IS - 7

ER -