New revelations about the long-qt syndrome

Research output: Contribution to journalReview article

27 Citations (Scopus)

Abstract

Sudden death, a devastating event for any family, strikes more than 300,000 Americans each year. Cardiac arrhythmias, particularly ventricular arrhythmias, are thought to account for about 11 percent of all sudden deaths. In some cases there appears to be a familial propensity for sudden death. One inherited condition, the Romano–Ward long-QT syndrome, is an autosomal dominant disorder of cardiac repolarization that results in ventricular arrhythmias and sudden death. The long-QT syndrome has been thought to arise from either an abnormality of ion-channel regulation (the myocellular hypothesis) or altered activity of the autonomic nervous system, but definitive proof of either hypothesis.

Original languageEnglish (US)
Pages (from-to)384-385
Number of pages2
JournalNew England Journal of Medicine
Volume333
Issue number6
DOIs
StatePublished - Aug 10 1995
Externally publishedYes

Fingerprint

Sudden Death
Cardiac Arrhythmias
Long QT Syndrome
Autonomic Nervous System
Ion Channels

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

New revelations about the long-qt syndrome. / Towbin, Jeffrey.

In: New England Journal of Medicine, Vol. 333, No. 6, 10.08.1995, p. 384-385.

Research output: Contribution to journalReview article

@article{df1d83c85d134b278c0966f7ebea9864,
title = "New revelations about the long-qt syndrome",
abstract = "Sudden death, a devastating event for any family, strikes more than 300,000 Americans each year. Cardiac arrhythmias, particularly ventricular arrhythmias, are thought to account for about 11 percent of all sudden deaths. In some cases there appears to be a familial propensity for sudden death. One inherited condition, the Romano–Ward long-QT syndrome, is an autosomal dominant disorder of cardiac repolarization that results in ventricular arrhythmias and sudden death. The long-QT syndrome has been thought to arise from either an abnormality of ion-channel regulation (the myocellular hypothesis) or altered activity of the autonomic nervous system, but definitive proof of either hypothesis.",
author = "Jeffrey Towbin",
year = "1995",
month = "8",
day = "10",
doi = "10.1056/NEJM199508103330613",
language = "English (US)",
volume = "333",
pages = "384--385",
journal = "New England Journal of Medicine",
issn = "0028-4793",
publisher = "Massachussetts Medical Society",
number = "6",

}

TY - JOUR

T1 - New revelations about the long-qt syndrome

AU - Towbin, Jeffrey

PY - 1995/8/10

Y1 - 1995/8/10

N2 - Sudden death, a devastating event for any family, strikes more than 300,000 Americans each year. Cardiac arrhythmias, particularly ventricular arrhythmias, are thought to account for about 11 percent of all sudden deaths. In some cases there appears to be a familial propensity for sudden death. One inherited condition, the Romano–Ward long-QT syndrome, is an autosomal dominant disorder of cardiac repolarization that results in ventricular arrhythmias and sudden death. The long-QT syndrome has been thought to arise from either an abnormality of ion-channel regulation (the myocellular hypothesis) or altered activity of the autonomic nervous system, but definitive proof of either hypothesis.

AB - Sudden death, a devastating event for any family, strikes more than 300,000 Americans each year. Cardiac arrhythmias, particularly ventricular arrhythmias, are thought to account for about 11 percent of all sudden deaths. In some cases there appears to be a familial propensity for sudden death. One inherited condition, the Romano–Ward long-QT syndrome, is an autosomal dominant disorder of cardiac repolarization that results in ventricular arrhythmias and sudden death. The long-QT syndrome has been thought to arise from either an abnormality of ion-channel regulation (the myocellular hypothesis) or altered activity of the autonomic nervous system, but definitive proof of either hypothesis.

UR - http://www.scopus.com/inward/record.url?scp=0029641379&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029641379&partnerID=8YFLogxK

U2 - 10.1056/NEJM199508103330613

DO - 10.1056/NEJM199508103330613

M3 - Review article

VL - 333

SP - 384

EP - 385

JO - New England Journal of Medicine

JF - New England Journal of Medicine

SN - 0028-4793

IS - 6

ER -