Abstract
The incidence of dual atrioventricular (AV) nodal physiology was evaluated in 22 patients (14 males, 8 females, age 52 ± 18 years) undergoing electrophysiology studies for evaluation of ventricular tachycardia/honsustained ventricular tachycardia (n = 11), supraventricular tachycardia (n = 5), and syncope (n = 6). Patients with AV node reentrant tachycardia were excluded. Thirteen patients had riormal left ventricular function and nine patients (seven with coronary artery disease, two with dilated cardiomyopathy) had depressed left ventricular function. Single atrial extrastimuli (A2) were introduced after eight‐beat drives at paced cycle lengths of 550 msec and 400 or 450 msec beginning at coupling intervals of 650 and 500 or 550 msec, respectively. The coupling interval was decreased at 10‐msec intervals until AV node or atrial refractoriness. A second atrial extrastimulus (A3) was then added. A2 was fixed at 50 msec greater than the atrial or AV nodal refractory period. A3 was coupled to A2 at 650 and 500 or 550 msec and decremented as with single extrastimulation. Dual AV nodal physiology was defined by a 50‐msec increase in A2H2 or A3H3 with a 10‐msec decrement in the coupling interval or a discontinuous H1H2 versus A1A2 or H2H3 versus A2A3 curve. Using a single extrastimulus, 1 of 22 patients demonstrated dual AV nodal physiology. Using double extrastimuli, an additional four patients with dual AV nodal physiology were identified. The occurrence of dual AV nodal physiology determined using double extrastimuli is increased compared to using only a single extrastimulus (P = 0.03). In conclusion, dual AV nodal physiology can be demonstrated with greater frequency using an extended rather than a standard protocol.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 277-284 |
| Number of pages | 8 |
| Journal | Pacing and Clinical Electrophysiology |
| Volume | 16 |
| Issue number | 2 |
| DOIs | |
| State | Published - Jan 1 1993 |
| Externally published | Yes |
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Keywords
- AV node
- dual AV nodal physiology
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
Cite this
Extended Protocol for Demonstration of Dual AV Nodal Physiology. / BROOKS, RODNEY; Goldberger, Jeffrey; KADISH, ALAN.
In: Pacing and Clinical Electrophysiology, Vol. 16, No. 2, 01.01.1993, p. 277-284.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Extended Protocol for Demonstration of Dual AV Nodal Physiology
AU - BROOKS, RODNEY
AU - Goldberger, Jeffrey
AU - KADISH, ALAN
PY - 1993/1/1
Y1 - 1993/1/1
N2 - The incidence of dual atrioventricular (AV) nodal physiology was evaluated in 22 patients (14 males, 8 females, age 52 ± 18 years) undergoing electrophysiology studies for evaluation of ventricular tachycardia/honsustained ventricular tachycardia (n = 11), supraventricular tachycardia (n = 5), and syncope (n = 6). Patients with AV node reentrant tachycardia were excluded. Thirteen patients had riormal left ventricular function and nine patients (seven with coronary artery disease, two with dilated cardiomyopathy) had depressed left ventricular function. Single atrial extrastimuli (A2) were introduced after eight‐beat drives at paced cycle lengths of 550 msec and 400 or 450 msec beginning at coupling intervals of 650 and 500 or 550 msec, respectively. The coupling interval was decreased at 10‐msec intervals until AV node or atrial refractoriness. A second atrial extrastimulus (A3) was then added. A2 was fixed at 50 msec greater than the atrial or AV nodal refractory period. A3 was coupled to A2 at 650 and 500 or 550 msec and decremented as with single extrastimulation. Dual AV nodal physiology was defined by a 50‐msec increase in A2H2 or A3H3 with a 10‐msec decrement in the coupling interval or a discontinuous H1H2 versus A1A2 or H2H3 versus A2A3 curve. Using a single extrastimulus, 1 of 22 patients demonstrated dual AV nodal physiology. Using double extrastimuli, an additional four patients with dual AV nodal physiology were identified. The occurrence of dual AV nodal physiology determined using double extrastimuli is increased compared to using only a single extrastimulus (P = 0.03). In conclusion, dual AV nodal physiology can be demonstrated with greater frequency using an extended rather than a standard protocol.
AB - The incidence of dual atrioventricular (AV) nodal physiology was evaluated in 22 patients (14 males, 8 females, age 52 ± 18 years) undergoing electrophysiology studies for evaluation of ventricular tachycardia/honsustained ventricular tachycardia (n = 11), supraventricular tachycardia (n = 5), and syncope (n = 6). Patients with AV node reentrant tachycardia were excluded. Thirteen patients had riormal left ventricular function and nine patients (seven with coronary artery disease, two with dilated cardiomyopathy) had depressed left ventricular function. Single atrial extrastimuli (A2) were introduced after eight‐beat drives at paced cycle lengths of 550 msec and 400 or 450 msec beginning at coupling intervals of 650 and 500 or 550 msec, respectively. The coupling interval was decreased at 10‐msec intervals until AV node or atrial refractoriness. A second atrial extrastimulus (A3) was then added. A2 was fixed at 50 msec greater than the atrial or AV nodal refractory period. A3 was coupled to A2 at 650 and 500 or 550 msec and decremented as with single extrastimulation. Dual AV nodal physiology was defined by a 50‐msec increase in A2H2 or A3H3 with a 10‐msec decrement in the coupling interval or a discontinuous H1H2 versus A1A2 or H2H3 versus A2A3 curve. Using a single extrastimulus, 1 of 22 patients demonstrated dual AV nodal physiology. Using double extrastimuli, an additional four patients with dual AV nodal physiology were identified. The occurrence of dual AV nodal physiology determined using double extrastimuli is increased compared to using only a single extrastimulus (P = 0.03). In conclusion, dual AV nodal physiology can be demonstrated with greater frequency using an extended rather than a standard protocol.
KW - AV node
KW - dual AV nodal physiology
UR - http://www.scopus.com/inward/record.url?scp=0027537031&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0027537031&partnerID=8YFLogxK
U2 - 10.1111/j.1540-8159.1993.tb01577.x
DO - 10.1111/j.1540-8159.1993.tb01577.x
M3 - Article
C2 - 7680456
AN - SCOPUS:0027537031
VL - 16
SP - 277
EP - 284
JO - PACE - Pacing and Clinical Electrophysiology
JF - PACE - Pacing and Clinical Electrophysiology
SN - 0147-8389
IS - 2
ER -