Sudden cardiac death, genes, and arrhythmogenesis: Consideration of new population and mechanistic approaches from a National Heart, Lung, and Blood Institute workshop, part I

Peter M. Spooner, Christine Albert, Emelia J. Benjamin, Robin Boineau, Robert C. Elston, Alfred L. George, Xavier Jouven, Lewis H. Kuller, Jean W. MacCluer, Eduardo Marbán, James E. Muller, Peter J. Schwartz, David S. Siscovick, Russell P. Tracy, Wojciech Zareba, Douglas P. Zipes

Research output: Contribution to journalArticle

100 Citations (Scopus)

Abstract

Malignant ventricular arrhythmias are the leading mechanism of death in patients with acute and chronic cardiac pathologies. The extent to which inherited mutations and polymorphic variation in genes determining arrhythmogenic mechanisms affect these patients remains unknown, but based on recent population studies, this risk appears significant, deserving much greater investigation. This report summarizes a National Heart, Lung, and Blood Institute workshop that considered sources of genetic variation that may contribute to sudden cardiac death in common cardiac diseases. Evidence on arrhythmogenic mechanisms in recent population studies suggests a significant portion of the risk of sudden cardiac death in such broad populations may be unrelated to traditional risk factors for predisposing conditions such as atherosclerosis, hypertension, and diabetes and instead may involve unrecognized genetic and environmental interactions that influence arrhythmic susceptibility more directly. Additional population and genetic studies directed at discovering the sources of inherited molecular risk that are most directly linked to arrhythmia initiation and propagation, in addition to studies on previously well-described risk factors, would appear to have considerable potential for reducing premature cardiovascular mortality.

Original languageEnglish
Pages (from-to)2361-2364
Number of pages4
JournalCirculation
Volume103
Issue number19
StatePublished - May 15 2001

Fingerprint

National Heart, Lung, and Blood Institute (U.S.)
Sudden Cardiac Death
Education
Cardiac Arrhythmias
Population
Genes
Premature Mortality
Population Genetics
Heart Diseases
Atherosclerosis
Pathology
Hypertension
Mutation

Keywords

  • Arrhythmia
  • Death, sudden
  • Epidemiology
  • Genetics
  • Ion channels
  • Mortality
  • Tachyarrhythmias

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Spooner, P. M., Albert, C., Benjamin, E. J., Boineau, R., Elston, R. C., George, A. L., ... Zipes, D. P. (2001). Sudden cardiac death, genes, and arrhythmogenesis: Consideration of new population and mechanistic approaches from a National Heart, Lung, and Blood Institute workshop, part I. Circulation, 103(19), 2361-2364.

Sudden cardiac death, genes, and arrhythmogenesis : Consideration of new population and mechanistic approaches from a National Heart, Lung, and Blood Institute workshop, part I. / Spooner, Peter M.; Albert, Christine; Benjamin, Emelia J.; Boineau, Robin; Elston, Robert C.; George, Alfred L.; Jouven, Xavier; Kuller, Lewis H.; MacCluer, Jean W.; Marbán, Eduardo; Muller, James E.; Schwartz, Peter J.; Siscovick, David S.; Tracy, Russell P.; Zareba, Wojciech; Zipes, Douglas P.

In: Circulation, Vol. 103, No. 19, 15.05.2001, p. 2361-2364.

Research output: Contribution to journalArticle

Spooner, PM, Albert, C, Benjamin, EJ, Boineau, R, Elston, RC, George, AL, Jouven, X, Kuller, LH, MacCluer, JW, Marbán, E, Muller, JE, Schwartz, PJ, Siscovick, DS, Tracy, RP, Zareba, W & Zipes, DP 2001, 'Sudden cardiac death, genes, and arrhythmogenesis: Consideration of new population and mechanistic approaches from a National Heart, Lung, and Blood Institute workshop, part I', Circulation, vol. 103, no. 19, pp. 2361-2364.
Spooner, Peter M. ; Albert, Christine ; Benjamin, Emelia J. ; Boineau, Robin ; Elston, Robert C. ; George, Alfred L. ; Jouven, Xavier ; Kuller, Lewis H. ; MacCluer, Jean W. ; Marbán, Eduardo ; Muller, James E. ; Schwartz, Peter J. ; Siscovick, David S. ; Tracy, Russell P. ; Zareba, Wojciech ; Zipes, Douglas P. / Sudden cardiac death, genes, and arrhythmogenesis : Consideration of new population and mechanistic approaches from a National Heart, Lung, and Blood Institute workshop, part I. In: Circulation. 2001 ; Vol. 103, No. 19. pp. 2361-2364.
@article{a1bb50942f6747a6af53893274b6d61e,
title = "Sudden cardiac death, genes, and arrhythmogenesis: Consideration of new population and mechanistic approaches from a National Heart, Lung, and Blood Institute workshop, part I",
abstract = "Malignant ventricular arrhythmias are the leading mechanism of death in patients with acute and chronic cardiac pathologies. The extent to which inherited mutations and polymorphic variation in genes determining arrhythmogenic mechanisms affect these patients remains unknown, but based on recent population studies, this risk appears significant, deserving much greater investigation. This report summarizes a National Heart, Lung, and Blood Institute workshop that considered sources of genetic variation that may contribute to sudden cardiac death in common cardiac diseases. Evidence on arrhythmogenic mechanisms in recent population studies suggests a significant portion of the risk of sudden cardiac death in such broad populations may be unrelated to traditional risk factors for predisposing conditions such as atherosclerosis, hypertension, and diabetes and instead may involve unrecognized genetic and environmental interactions that influence arrhythmic susceptibility more directly. Additional population and genetic studies directed at discovering the sources of inherited molecular risk that are most directly linked to arrhythmia initiation and propagation, in addition to studies on previously well-described risk factors, would appear to have considerable potential for reducing premature cardiovascular mortality.",
keywords = "Arrhythmia, Death, sudden, Epidemiology, Genetics, Ion channels, Mortality, Tachyarrhythmias",
author = "Spooner, {Peter M.} and Christine Albert and Benjamin, {Emelia J.} and Robin Boineau and Elston, {Robert C.} and George, {Alfred L.} and Xavier Jouven and Kuller, {Lewis H.} and MacCluer, {Jean W.} and Eduardo Marb{\'a}n and Muller, {James E.} and Schwartz, {Peter J.} and Siscovick, {David S.} and Tracy, {Russell P.} and Wojciech Zareba and Zipes, {Douglas P.}",
year = "2001",
month = "5",
day = "15",
language = "English",
volume = "103",
pages = "2361--2364",
journal = "Circulation",
issn = "0009-7322",
publisher = "Lippincott Williams and Wilkins",
number = "19",

}

TY - JOUR

T1 - Sudden cardiac death, genes, and arrhythmogenesis

T2 - Consideration of new population and mechanistic approaches from a National Heart, Lung, and Blood Institute workshop, part I

AU - Spooner, Peter M.

AU - Albert, Christine

AU - Benjamin, Emelia J.

AU - Boineau, Robin

AU - Elston, Robert C.

AU - George, Alfred L.

AU - Jouven, Xavier

AU - Kuller, Lewis H.

AU - MacCluer, Jean W.

AU - Marbán, Eduardo

AU - Muller, James E.

AU - Schwartz, Peter J.

AU - Siscovick, David S.

AU - Tracy, Russell P.

AU - Zareba, Wojciech

AU - Zipes, Douglas P.

PY - 2001/5/15

Y1 - 2001/5/15

N2 - Malignant ventricular arrhythmias are the leading mechanism of death in patients with acute and chronic cardiac pathologies. The extent to which inherited mutations and polymorphic variation in genes determining arrhythmogenic mechanisms affect these patients remains unknown, but based on recent population studies, this risk appears significant, deserving much greater investigation. This report summarizes a National Heart, Lung, and Blood Institute workshop that considered sources of genetic variation that may contribute to sudden cardiac death in common cardiac diseases. Evidence on arrhythmogenic mechanisms in recent population studies suggests a significant portion of the risk of sudden cardiac death in such broad populations may be unrelated to traditional risk factors for predisposing conditions such as atherosclerosis, hypertension, and diabetes and instead may involve unrecognized genetic and environmental interactions that influence arrhythmic susceptibility more directly. Additional population and genetic studies directed at discovering the sources of inherited molecular risk that are most directly linked to arrhythmia initiation and propagation, in addition to studies on previously well-described risk factors, would appear to have considerable potential for reducing premature cardiovascular mortality.

AB - Malignant ventricular arrhythmias are the leading mechanism of death in patients with acute and chronic cardiac pathologies. The extent to which inherited mutations and polymorphic variation in genes determining arrhythmogenic mechanisms affect these patients remains unknown, but based on recent population studies, this risk appears significant, deserving much greater investigation. This report summarizes a National Heart, Lung, and Blood Institute workshop that considered sources of genetic variation that may contribute to sudden cardiac death in common cardiac diseases. Evidence on arrhythmogenic mechanisms in recent population studies suggests a significant portion of the risk of sudden cardiac death in such broad populations may be unrelated to traditional risk factors for predisposing conditions such as atherosclerosis, hypertension, and diabetes and instead may involve unrecognized genetic and environmental interactions that influence arrhythmic susceptibility more directly. Additional population and genetic studies directed at discovering the sources of inherited molecular risk that are most directly linked to arrhythmia initiation and propagation, in addition to studies on previously well-described risk factors, would appear to have considerable potential for reducing premature cardiovascular mortality.

KW - Arrhythmia

KW - Death, sudden

KW - Epidemiology

KW - Genetics

KW - Ion channels

KW - Mortality

KW - Tachyarrhythmias

UR - http://www.scopus.com/inward/record.url?scp=14344280445&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=14344280445&partnerID=8YFLogxK

M3 - Article

C2 - 11352884

AN - SCOPUS:14344280445

VL - 103

SP - 2361

EP - 2364

JO - Circulation

JF - Circulation

SN - 0009-7322

IS - 19

ER -