Modifications of the delta wave on the surface ECG during an exercise stress test were compared to electrophysiological variations in accessory pathway (AP) refractoriness and in AV node conduction, during intravenous isoproterenol infusion in ten patients with WPW syndrome. In one patient, the delta wave persisted unchanged at the end of exercise and, with isoproterenol, there was a greater reduction in the AP anterograde effective refractory period (AERP) than in AV node conduction time. In three patients, the delta wave became less and less apparent but without completely disappearing; in these patients, the slight reduction of the AERP in the accessory pathway with isoproterenol was comparable to the reduction in AV node conduction time, explaining the progressive fusion between the two activation fronts. In the six other patients, the delta wave completely disappeared during exercise: in two cases, suddenly from one cycle to the next with strong concordance between the measured (isoproterenol) and the estimated (exercise test) AERP in the AP; in four cases, the disappearance was progressive with a significantly greater reduction in the AV node conduction time than in the measured AERP of AP which was nonetheless very short, 190 to 225 ms, during isoproterenol infusion. These findings confirm the limitations of the exercise test to predict the AERP of the AP. In addition, they demonstrate that modifications in the delta wave during exercise result from a balance between the relative effects of sympathetic stimulation on refractoriness of AP and normal AV conduction.
Introduction The influence of the autonomic nervous system on the pathogenesis of complex fractionated atrial electrograms (CFAE) during atrial fibrillation (AF) is incompletely understood. This study evaluated the impact of pharmacological autonomic blockade on CFAE characteristics. Methods Autonomic blockade was achieved with propanolol and atropine in 29 patients during AF. Three-dimensional maps of the fractionation degree were made before and after autonomic blockade using the Ensite Navx® system. In 2 patients, AF terminated following autonomic blockade. In the remaining 27 patients, 20113 electrogram samples of 5 seconds duration were collected randomly throughout the left atrium (10054 at baseline and 10059 after autonomic blockade). The impact of autonomic blockade on fractionation was assessed by blinded investigators and related to the type of AF and AF cycle length. Results Globally, CFAE as a proportion of all atrial electrogram samples were reduced after autonomic blockade: 61.6±20.3% vs. 57.9±23.7%, p=0.027. This was true/significant for paroxysmal AF (47±23% vs. 40±22%, p=0.003), but not for persistent AF (65±22% vs. 62±25% respectively, p=0.166). Left atrial AF cycle length prolonged with autonomic blockade from 170±33 ms to. 180±40 ms (p=0.001). Fractionation decreases only in the 14/27 patients with a significant (>6ms) prolongation of the AF cycle length (64±20% vs. 59±24%, p=0.027), while fractionation did not reduce when autonomic blockade did not affect the AF cycle length (58±21% vs. 56±25%, p=0.419). Conclusions Pharmacological autonomic blockade reduces CFAE in paroxysmal AF, but not persistent AF. This effect appears to be mediated by prolongation of the AF cycle length.
In dual chamber pacing, an improvement of exercise capacity is expected when the atrial refractory period is shortened, because the 2/1 point is increased. This objective can be achieved by greatly reducing atrioventricular delay (AVD) on exercise. Are such variations (up to 100-120 ms) detrimental from a haemodynamic standpoint? This study was performed to analyse this particular aspect of DDD pacing. Three DDD pacing modes, differing by their AVDs (fixed 200 ms AVD, fixed 150 ms AVD, and rate-adapted AVD) were tested in random order, with a haemodynamic protocol including ten patients with chronic atrio-ventricular (A-V) block. For the rate-adapted AVD pacing mode, AVD was reduced by 20 ms every 10 beats min-1 increment (from 220 ms at 90 beats min-1 to 100 ms at 150 beats min-1). Pacing rate was increased from 90 to 150 beats min-1 by increments of 10 beats min-1 every 5 min. Cardiac performance was significantly improved with the rate-adapted AVD above the two fixed AVDs, despite a large AVD variation. When AVD was rate adapted, cardiac index, stroke volume index and left ventricular systolic work index were generally higher and pulmonary capillary wedge pressure, pulmonary arterial pressure and systemic vascular resistances were generally lower, especially at 120, 130 and 140 beats min-1. Comparing the two fixed AVDs, 200 AVD improved cardiac function more at lower heart rates, whereas 150 AVD improved cardiac function more at higher heart rates. Despite its limitations, this study demonstrates that the potential benefits of reducing AVD with increasing heart rates should be twofold in dual chamber pacing: (a) haemodynamic, optimizing cardiac performance on exercise for all heart rates, especially in cases of organic heart disease; (b) electrophysiologic, permitting a sufficiently rapid maximal tracking rate in cases with long post-ventricular atrial refractory periods, allowing a satisfactory level of exercise.
The correlation between heart rate (HR) and three respiratory parameters, minute ventilation (VE), tidal volume (Vt), and respiratory rate (RR), were studied. Four healthy subjects performed four exercise tests (duration 30 seconds at 50, 100, 150, or 200 W), in random order. Cardio-respiratory parameters were recorded respiratory cycle by respiratory cycle. The results of these low level exercise tests showed that oxygen consumption (VO2) was strongly correlated with VE (r = 0.91 +/- 0.10; P less than 0.01) (except in one test) and Vt (r = 0.91 +/- 0.07; P less than 0.001) (except in one test). There was no significant correlation between VO2 and RR. At exercise onset HR, VE, and Vt were modified in a matter of a few heart beats while RR varied depending on the subject and the level of exercise. During exercise average HR, VE, and Vt were significantly higher than at rest in most cases; but RR was not significantly changed by exercise. The correlations between HR and VE, Vt and RR varied from one individual to another. Nevertheless, the correlation coefficients were positive for VE and Vt, while they were negative for RR. Sensing respiratory rate thus appears to be insufficient for responsive pacing at exercise onset, but sensing respiratory volumes (Vt, VE) should give satisfactory results.
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