Key result
The escape rhythm following AVJ ablation was responsive to sympathetic stimulation and vagal blockade, and was prolonged by lidocaine (1,462 to 1,715 ms, P<0.001) but not verapamil or adenosine.
Why the study?
Does pharmacological modulation affect the cycle length of the escape rhythm in patients undergoing AVJ ablation for refractory atrial fibrillation?
Observational (n=48)
Does pharmacological modulation affect the cycle length of the escape rhythm in patients undergoing AVJ ablation for refractory atrial fibrillation?
The escape rhythm following AVJ ablation is responsive to sympathetic stimulation, vagal blockade, and sodium channel blockade, but not calcium channel blockade, suggesting an origin in the distal compact AV node or proximal His bundle.
Answers are grounded in this paper and cite their sources.
May inform peri-procedural drug selection after AVJ ablation; leaves open whether modulating escape rhythm improves outcomes in refractory AF.
The physiology of the escape rhythm (ER) and its response to pharmacological modulation under varying autonomic conditions were studied 48 patients undergoing radiofrequency ablation of the atrioventricular junction (AVJ) for refractory atrial fibrillation. The QRS morphology and cycle length (CL) of the baseline ER were measured 15 minutes postablation. The CL of the ER was measured in response to doses of isoproterenol, atropine, adenosine, lidocaine, and verapamil. The ER QRS was narrow (QRS < 120 ms) in 20 patients and wide (QRS > 120 ms) in 28 patients. Of the 28 patients with wide QRS ER, 11 patients had a new bundle branch block (8 patients new right bundle branch block [RBBB] and 2 patients new left bundle branch block [LBBB]). The ERCL was similar in both narrow and wide ERs (1,593 +/- 376 ms and 1,516 +/- 296 ms, P = 0.44). In 23 patients receiving isoproterenol infusion, the ER CL decreased with increasing doses from 1 mcg/min to 2 mcg/min (1,378 +/- 200 to 1,240 +/- 229 ms, P < 0.001), but did not decrease further at 3 mcg/min (1,201 +/- 192 ms, P = 0.48 vs 2 mg/min). Seven patients received 0.02 mg/kg of atropine, and ER decreased significantly (1,572 +/- 408 ms to 1,319 +/- 333 ms, P = 0.028). In 30 patients who received intravenous boluses of adenosine (6-18 mg), the ER did not change significantly. In 28 patients who received 150 mg of lidocaine, the ER increased from 1,462 +/- 286 ms to 1,715 +/- 467 ms (P < 0.001), and one patient developed transient asystole. Nineteen patients received 7.5 mg of verapamil, and the ER did not change (1,488 +/- 313 ms to 1,513 +/- 666 ms, P = 0.80). There was no significant difference in response to isoproterenol, adenosine, lidocaine, or verapamil between the patients with wide and narrow QRS ERs. We conclude that patients may have stable ERs immediately following AVJ ablation even when a wide complex ER results. The ER is responsive to sympathetic stimulation and vagal blockade. The ER is prolonged after lidocaine but not after verapamil, suggesting response to sodium but not to calcium channel blockade. These data are consistent with an ER originating in the distal compact AV node or proximal His bundle.
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Shepard et al. (1998) conducted an observational in Refractory atrial fibrillation (n=48). Pharmacological modulation (isoproterenol, atropine, adenosine, lidocaine, verapamil) vs. Baseline was evaluated on Cycle length of the escape rhythm. The escape rhythm following AVJ ablation was responsive to sympathetic stimulation and vagal blockade, and was prolonged by lidocaine (1,462 to 1,715 ms, P<0.001) but not verapamil or adenosine.
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