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Articles by B. J Scherlag
Total Records ( 2 ) for B. J Scherlag
  G Niu , B. J Scherlag , Z Lu , M Ghias , Y Zhang , E Patterson , T. W Dasari , S Zacharias , R Lazzara , W. M Jackman and S. S. Po
 

Background— The objective of this study was to develop an acute experimental model showing both focal and macroreentrant sustained atrial fibrillation (AF).

Methods and Results— In 31 anesthetized dogs, bilateral thoracotomies allowed the attachment of electrode catheters at the right and left superior pulmonary veins, atrial free walls, and atrial appendages. Acetylcholine, 100 mmol/L, was applied topically to either appendage. Sequential radiofrequency ablation was achieved for the ganglionated plexi (GP), found adjacent to the 4 pulmonary veins. In 12 separate studies, a propafenone bolus, 2 mg/kg, was given before and after GP ablations at the start of acetylcholine-induced AF.

Acetylcholine caused abrupt onset of AF (n=22) or induced AF by burst pacing (n=9) that lasted ≥10 minutes. Rapid, regular, or fractionated atrial electrograms were consistently seen (average cycle length, 37±7 ms) at the appendages versus cycle lengths of 114±23 ms at other atrial sites. After ablations of GP, AF abruptly terminated (n=25). In 6 dogs, sustained atrial tachyarrhythmias continued. Pacing at specific atrial sites organized electrograms of one atrium or also captured the other atrium. The latter resulted in termination when pacing was stopped in 4 of these 6 experiments. Propafenone did not change the duration of focal AF before GP ablation (17±9 versus 14±8 minutes; control, P=0.6) but terminated reentrant atrial tachyarrhythmias (12±3 versus 2±1 minutes, P=0.0009).

Conclusions— Before GP ablation, acetylcholine (100 mmol/L) induced sustained AF characterized by rapid, focal firing. GP ablations were associated with loss of focal firing and regularization of electrograms in both atria before termination. Propafenone failed to terminate focal AF but rapidly terminated entrainable macroreentrant atrial tachyarrhythmias.

  S Li , B. J Scherlag , L Yu , X Sheng , Y Zhang , R Ali , Y Dong , M Ghias and S. S. Po
 

Background— We used high-frequency stimulation delivered during the refractory period of the atrium and pulmonary veins (PVs) to induce focal firing and atrial fibrillation (AF). This study was designed to demonstrate that bilateral low-level vagosympathetic nerve stimulation (LL-VNS) could suppress high-frequency stimulation-induced focal AF at atrial and PV sites.

Methods and Results— In 23 dogs anesthetized with Na-pentobarbital, electrodes in the vagosympathetic trunks allowed LL-VNS at 1 V below that which slowed the sinus rate or atrioventricular conduction. Multielectrode catheters were fixed at the right and left superior and inferior PVs and both atrial appendages. LL-VNS continued for 3 hours. At the end of each hour, the high-frequency stimulation algorithm consisting of a 40-ms train of stimuli (200 Hz; stimulus duration, 0.1 to 1.0 ms) was delivered 2 ms after the atrial pacing stimulus during the refractory period at each PV and atrial appendages site. The lowest voltage of high-frequency stimulation that induced AF was defined as the AF threshold. Five dogs without LL-VNS served as sham controls. Six dogs underwent LL-VNS after transection of bilateral vagosympathetic trunks. LL-VNS induced a progressive increase in AF threshold at all PV and atrial appendages sites, particularly significant (P<0.05) at the right superior PV, right inferior PV, left superior PV, and right atrial appendage. Bilateral vagosympathetic transection did not significantly alter the previous findings, and the 5 sham control dogs did not show changes in AF threshold at any site over a period of 3 hours.

Conclusions— LL-VNS may prevent episodic AF caused by rapid PV and non-PV firing.

 
 
 
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