Abstract
Ventricular arrhythmias in the setting of acute myocardial ischemia and infarction remain a serious health problem because of their sudden and unpredictable nature and their potentially grave results. Electrophysiological changes that may be responsible for these arrhythmias have been described in cardiac cells and in ischemic tissue. Experimental models have played a major role in elucidating the diversity of potential mechanisms for these arrhythmias. Increases in extracellular K+, the presence of toxic metabolites, and the accumulation of catecholamines in ischemic tissue all appear to have a role in arrhythmogenesis. The autonomic nervous system also appears to play a major role in these arrhythmias. With increased understanding of the pathophysiology underlying these arrhythmias, prevention can be enhanced and therapy can be better targeted.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 966-975 |
| Number of pages | 10 |
| Journal | PACE - Pacing and Clinical Electrophysiology |
| Volume | 20 |
| Issue number | 4 I |
| DOIs | |
| State | Published - Jan 1 1997 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
Cite this
Cellular and pathophysiological mechanisms of ventricular arrhythmias in acute ischemia and infarction. / Ehlert, Frederick A.; Goldberger, Jeffrey.
In: PACE - Pacing and Clinical Electrophysiology, Vol. 20, No. 4 I, 01.01.1997, p. 966-975.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Cellular and pathophysiological mechanisms of ventricular arrhythmias in acute ischemia and infarction
AU - Ehlert, Frederick A.
AU - Goldberger, Jeffrey
PY - 1997/1/1
Y1 - 1997/1/1
N2 - Ventricular arrhythmias in the setting of acute myocardial ischemia and infarction remain a serious health problem because of their sudden and unpredictable nature and their potentially grave results. Electrophysiological changes that may be responsible for these arrhythmias have been described in cardiac cells and in ischemic tissue. Experimental models have played a major role in elucidating the diversity of potential mechanisms for these arrhythmias. Increases in extracellular K+, the presence of toxic metabolites, and the accumulation of catecholamines in ischemic tissue all appear to have a role in arrhythmogenesis. The autonomic nervous system also appears to play a major role in these arrhythmias. With increased understanding of the pathophysiology underlying these arrhythmias, prevention can be enhanced and therapy can be better targeted.
AB - Ventricular arrhythmias in the setting of acute myocardial ischemia and infarction remain a serious health problem because of their sudden and unpredictable nature and their potentially grave results. Electrophysiological changes that may be responsible for these arrhythmias have been described in cardiac cells and in ischemic tissue. Experimental models have played a major role in elucidating the diversity of potential mechanisms for these arrhythmias. Increases in extracellular K+, the presence of toxic metabolites, and the accumulation of catecholamines in ischemic tissue all appear to have a role in arrhythmogenesis. The autonomic nervous system also appears to play a major role in these arrhythmias. With increased understanding of the pathophysiology underlying these arrhythmias, prevention can be enhanced and therapy can be better targeted.
UR - http://www.scopus.com/inward/record.url?scp=0030981414&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0030981414&partnerID=8YFLogxK
U2 - 10.1111/j.1540-8159.1997.tb05501.x
DO - 10.1111/j.1540-8159.1997.tb05501.x
M3 - Review article
C2 - 9127403
AN - SCOPUS:0030981414
VL - 20
SP - 966
EP - 975
JO - PACE - Pacing and Clinical Electrophysiology
JF - PACE - Pacing and Clinical Electrophysiology
SN - 0147-8389
IS - 4 I
ER -