Abstract
The contribution of left (versus right) ventricular stimulation to the induction of ventricular tachyarrhythmias was studied in 37 dogs with chronic experimental myocardial infarction, and 17 dogs with normal hearts. Programmed stimulation of the endocardium at both ventricular apices employed an aggressive protocol of up to 7 extrastimuli. The right ventricle was the most successful site for induction of ventricular tachycardia after myocardial infarction (74% of dogs with ventricular tachycardia). Ten of 11 animals with slow ventricular tachycardia (≥ 140 msec) were inducible from the right ventricle. In contrast, left ventricular stimulation was required to induce rapid ventricular tachycardia (cycle length < 140 msec) in 5 of 10 dogs (P < 0.05). No animal required more than five extrastimuli from any site for induction of ventricular tachycardia. In the normal heart, ventricular fibrillation was induced most often from the right ventricle (77% of dogs) when compared with the left ventricle (47%, P < 0.05). Ventricular tachycardia was never induced in normal animals. These results show that the right ventricular apex is the most successful site for induction of "slow" ventricular tachycardia in this canine model when using five extrastimuli. Rapid ventricular tachycardia is frequently induced from the infarcted left ventricle, but this arrhythmia may not be clinically significant. The normal right ventricle is significantly more susceptible to ventricular fibrillation than is the left ventricle, but this does not interfere with induction of ventricular tachycardia in the infarcted heart.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 317-324 |
| Number of pages | 8 |
| Journal | International Journal of Cardiology |
| Volume | 28 |
| Issue number | 3 |
| DOIs | |
| State | Published - 1990 |
| Externally published | Yes |
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Keywords
- Dog
- Stimulation site
- Ventricular tachyarrhythmia
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
Cite this
Right versus left ventricular stimulation : influence on induction of ventricular tachyarrhythmias in dogs. / Hunt, Geraldine B; Ross, David L.
In: International Journal of Cardiology, Vol. 28, No. 3, 1990, p. 317-324.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Right versus left ventricular stimulation
T2 - influence on induction of ventricular tachyarrhythmias in dogs
AU - Hunt, Geraldine B
AU - Ross, David L.
PY - 1990
Y1 - 1990
N2 - The contribution of left (versus right) ventricular stimulation to the induction of ventricular tachyarrhythmias was studied in 37 dogs with chronic experimental myocardial infarction, and 17 dogs with normal hearts. Programmed stimulation of the endocardium at both ventricular apices employed an aggressive protocol of up to 7 extrastimuli. The right ventricle was the most successful site for induction of ventricular tachycardia after myocardial infarction (74% of dogs with ventricular tachycardia). Ten of 11 animals with slow ventricular tachycardia (≥ 140 msec) were inducible from the right ventricle. In contrast, left ventricular stimulation was required to induce rapid ventricular tachycardia (cycle length < 140 msec) in 5 of 10 dogs (P < 0.05). No animal required more than five extrastimuli from any site for induction of ventricular tachycardia. In the normal heart, ventricular fibrillation was induced most often from the right ventricle (77% of dogs) when compared with the left ventricle (47%, P < 0.05). Ventricular tachycardia was never induced in normal animals. These results show that the right ventricular apex is the most successful site for induction of "slow" ventricular tachycardia in this canine model when using five extrastimuli. Rapid ventricular tachycardia is frequently induced from the infarcted left ventricle, but this arrhythmia may not be clinically significant. The normal right ventricle is significantly more susceptible to ventricular fibrillation than is the left ventricle, but this does not interfere with induction of ventricular tachycardia in the infarcted heart.
AB - The contribution of left (versus right) ventricular stimulation to the induction of ventricular tachyarrhythmias was studied in 37 dogs with chronic experimental myocardial infarction, and 17 dogs with normal hearts. Programmed stimulation of the endocardium at both ventricular apices employed an aggressive protocol of up to 7 extrastimuli. The right ventricle was the most successful site for induction of ventricular tachycardia after myocardial infarction (74% of dogs with ventricular tachycardia). Ten of 11 animals with slow ventricular tachycardia (≥ 140 msec) were inducible from the right ventricle. In contrast, left ventricular stimulation was required to induce rapid ventricular tachycardia (cycle length < 140 msec) in 5 of 10 dogs (P < 0.05). No animal required more than five extrastimuli from any site for induction of ventricular tachycardia. In the normal heart, ventricular fibrillation was induced most often from the right ventricle (77% of dogs) when compared with the left ventricle (47%, P < 0.05). Ventricular tachycardia was never induced in normal animals. These results show that the right ventricular apex is the most successful site for induction of "slow" ventricular tachycardia in this canine model when using five extrastimuli. Rapid ventricular tachycardia is frequently induced from the infarcted left ventricle, but this arrhythmia may not be clinically significant. The normal right ventricle is significantly more susceptible to ventricular fibrillation than is the left ventricle, but this does not interfere with induction of ventricular tachycardia in the infarcted heart.
KW - Dog
KW - Stimulation site
KW - Ventricular tachyarrhythmia
UR - http://www.scopus.com/inward/record.url?scp=0025078180&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0025078180&partnerID=8YFLogxK
U2 - 10.1016/0167-5273(90)90314-U
DO - 10.1016/0167-5273(90)90314-U
M3 - Article
VL - 28
SP - 317
EP - 324
JO - International Journal of Cardiology
JF - International Journal of Cardiology
SN - 0167-5273
IS - 3
ER -