PubMed · 1692120
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R Sutton. 1990. DDDR pacing.. https://doi.org/10.1111/j.1540-8159.1990.tb02051.x
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It has been shown that dual chamber pacing with preservation of AV synchrony (DDD) is superior to fixed rate ventricular (VVI) or rate responsive ventricular (VVIR) pacing modes, as evaluated by ventilatory response to exercise. Previous studies have focused on the benefits of maintained AV synchrony at maximal exercise. However, there are limited data comparing O2 kinetics in different pacing modes during low intensity exercise, representing the majority of daily activities. This study aimed to provide an evaluation of different pacing modes using O2 kinetics during low intensity exercise. Nineteen patients (age 61 +/- 18 years) with complete AV block underwent low intensity treadmill exercise (35 W) with simultaneous evaluation of symptoms and O2 kinetics in three pacing modes. The first test was performed in DDD mode followed by a second test in VVIR mode with a programmed heart rate corresponding to the sinus rate during the first test. After 6 minutes of each test, the mode was switched from DDD to VVIR and vice versa. The third test was performed in VVI mode at 70 beats/min. O2 kinetics were defined as O2 deficit (time [rest to steady state] x delta VO2-sigma VO2 [rest to steady state]) and mean response time (MRT) of oxygen consumption (O2 deficit/delta VO2). The O2 deficit was 551 +/- 134 mL in DDD pacing, 634 +/- 139 mL in VVIR pacing, and 648 +/- 179 mL in VVI pacing (P = 0.001). MRT was 49 +/- 7.8 seconds in DDD pacing, 54.7 +/- 9.5 seconds in VVIR pacing, and 57.4 +/- 11.0 seconds in VVI pacing (P = 0.002). Ten (53%) patients developed symptoms during switch from DDD to VVIR mode whereas the switch from VVIR to DDD mode was not perceived by any patient (P < 0.001). In conclusion, our study shows an impact of AV synchronous pacing and heart rate adaptation on O2 kinetics during low intensity exercise that correspond to casual daily life activities. Our observations may have clinical implications for the management of patients with complete AV block.
We describe a patient in whom two tachycardias with AV dissociation were inducible by ventricular extrastimulation. The first tachycardia was characterized by a narrow QRS preceded by a His deflection with an HV interval identical to that recorded in sinus rhythm (40 ms). Premature ventricular depolarization delivered when the His bundle was refractory advanced the next His deflection. These findings suggest the presence of a nodoventricular bypass tract involved in an orthodromic tachycardia. The second tachycardia was induced after propafenone infusion and exhibited a wide QRS complex with left bundle branch block morphology; each ventricular complex was consistently associated with a His deflection with a HV interval of -15 ms. The second tachycardia may be considered to represent an antidromic tachycardia through the nodoventricular tract. However, a ventricular tachycardia cannot be excluded.
OBJECTIVE: To review the anatomical structure of the right atrioventricular junction, including the specialised atrioventricular conduction system, in hearts with Ebstein's malformation, to identify potential substrates for the abnormalities in conduction. METHODS: Five heart specimens representing the morphological spectrum of Ebstein malformation were examined grossly and histologically. RESULTS: On the endocardial surface, the atrioventricular junction was marked by a faint line in two hearts, and by a small ridge in the other three. Analysis of the right parietal junction in four hearts revealed only two accessory muscular atrioventricular connections. A plane of fibrofatty tissue separated atrial from ventricular myocardium in the right parietal junction in all hearts. The compact atrioventricular node was closer to the coronary sinus than usual. Accessory nodoventricular connections were present in four hearts, while accessory fasciculo-ventricular connections were found in one. The right bundle branch was hypoplastic or absent in four hearts. CONCLUSIONS: In this small series, the parietal atrioventricular junction was better developed than previously thought. Structural abnormalities of the atrioventricular conduction system, however, were present. These may account for some of the conduction abnormalities frequently observed with the Ebstein malformation.