Laser catheter-induced atrioventricular nodal delays and atrioventricular block in dogs: acute and chronic observations.

Selective modification of atrioventricular (AV) nodal conduction, that is, induction of varying degrees of AV nodal delays or block (second or third degree), or both, was achieved with a pervenous laser catheter technique. In six adult mongrel dogs anesthetized with pentobarbital (Nembutal), 5F leads were placed through femoral and external jugular veins and placed into the right atrium and His bundle region. Through another femoral vein, a 200 micron optical fiber was inserted by way of a 7F catheter with a preformed curved tip. Guided by fluoroscopy and His bundle electrograms, the fiber's tip was positioned in the AV nodal region. After autonomic blockade was achieved with intravenous propranolol (5 mg) and atropine (1 mg), AV conduction was analyzed. An argon laser delivered 3 to 4 watts into the fiber in bursts of 10 seconds' duration until the desired degree of AV nodal delay or block (second or third degree) was manifested. Monitoring of His bundle electrograms was continued for 2 hours. Four weekly serial electrocardiograms were recorded, after which electrophysiologic studies were repeated. Acute post-lasing studies showed that: in all six dogs, the mean PR interval was prolonged from 116 ms (range 100 to 135) to 153 ms (range 120 to 185), with the prolongation being caused exclusively by AH lengthening from 68 ms (range 50 to 90) to 105 ms (range 65 to 140); the mean effective refractory period of the AV node increased from less than 185 ms (range less than 150 to less than 200) to 215 ms (range 190 to 280); and the mean atrial pacing cycle length, at which second degree AV nodal block was manifested, increased from 210 ms (range 160 to 260) to 261 ms (range 205 to 320).(ABSTRACT TRUNCATED AT 250 WORDS)

Junctional pacemakers in man. Response to overdrive suppression with and without parasympathetic blockade.

This study analyzes the response to overdrive suppression of junctional pacemakers (JP) and correlates it with symptoms in 21 patients. Junctional rhythm (JR) was seen in 5 patients with intact A-V conduction, and in 16 with complete heart block, the JPs were located proximal to or within the His bundle (BH). Junctional recovery time (JRT) was measured following atrial or ventricular pacing during control and after atropine (2-2.5 mg). Control cycle length of the JR ranged from 835-2100 msec (mean 1402) and the corrected JRT (CJRT) ranged from 75 to greater than or equal to 7510 msec (mean 2966). Following atropine, the cycle length ranged from 660 to 2000 msec (mean 1115) and the CJRT ranged from 90 to greater than 6000 msec (mean 2050). All symptomatic patients were treated with permanent ventricular demand pacemakers and followed clinically from 6-72 months (mean = 35). Symptomatic patients could not be differentiated from asymptomatic patients on the basis of control heart rates, chronotropic response to atropine, and/or the site of origin of the JP as determined with BH recordings. However, presence or absence of symptoms of syncope and dizziness were well correlated with a CJRT greater than or less than 200 msec, respectively, either following atropine or during control. The determination of CJRT both before and after parasympathetic blockade provides a simpler and more reliable method for the therapeutic evaluation of patients.