Abstract
Despite impressive advances in the therapy of a number of types of heart disease in the last two decades, sudden cardiac death remains a public health problem of staggering dimensions. Current treatment options include antiarrhythmic drugs that have higher than desired failure rates and implantable defibrillators that incur significant costs to the patient and society. The development of therapies that better suppress the cardiac arrhythmias responsible for sudden cardiac death requires a broad and comprehensive understanding of the basic mechanisms underlying electrical instability in the heart. This study explores the scientific basis for a molecular genetic approach to modify cardiac excitability and thereby to create animal models of sudden cardiac death. The availability of such models will open up new avenues of research in arrhythmogenesis and facilitate the development of novel antiarrhythmic agents.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 41-48 |
| Number of pages | 8 |
| Journal | Advances in Experimental Medicine and Biology |
| Volume | 382 |
| State | Published - 1995 |
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ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
Cite this
Prospects for genetic manipulation of cardiac excitability. / Lawrence, J. H.; Johns, D. C.; Chiamvimonvat, N.; Nuss, H. B.; Marban, E.; Ter Keurs, H.; Morad, M.; Barry, W. H.
In: Advances in Experimental Medicine and Biology, Vol. 382, 1995, p. 41-48.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Prospects for genetic manipulation of cardiac excitability
AU - Lawrence, J. H.
AU - Johns, D. C.
AU - Chiamvimonvat, N.
AU - Nuss, H. B.
AU - Marban, E.
AU - Ter Keurs, H.
AU - Morad, M.
AU - Barry, W. H.
PY - 1995
Y1 - 1995
N2 - Despite impressive advances in the therapy of a number of types of heart disease in the last two decades, sudden cardiac death remains a public health problem of staggering dimensions. Current treatment options include antiarrhythmic drugs that have higher than desired failure rates and implantable defibrillators that incur significant costs to the patient and society. The development of therapies that better suppress the cardiac arrhythmias responsible for sudden cardiac death requires a broad and comprehensive understanding of the basic mechanisms underlying electrical instability in the heart. This study explores the scientific basis for a molecular genetic approach to modify cardiac excitability and thereby to create animal models of sudden cardiac death. The availability of such models will open up new avenues of research in arrhythmogenesis and facilitate the development of novel antiarrhythmic agents.
AB - Despite impressive advances in the therapy of a number of types of heart disease in the last two decades, sudden cardiac death remains a public health problem of staggering dimensions. Current treatment options include antiarrhythmic drugs that have higher than desired failure rates and implantable defibrillators that incur significant costs to the patient and society. The development of therapies that better suppress the cardiac arrhythmias responsible for sudden cardiac death requires a broad and comprehensive understanding of the basic mechanisms underlying electrical instability in the heart. This study explores the scientific basis for a molecular genetic approach to modify cardiac excitability and thereby to create animal models of sudden cardiac death. The availability of such models will open up new avenues of research in arrhythmogenesis and facilitate the development of novel antiarrhythmic agents.
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UR - http://www.scopus.com/inward/citedby.url?scp=0029143082&partnerID=8YFLogxK
M3 - Article
C2 - 8540412
AN - SCOPUS:0029143082
VL - 382
SP - 41
EP - 48
JO - Advances in Experimental Medicine and Biology
JF - Advances in Experimental Medicine and Biology
SN - 0065-2598
ER -