Search

Objectives: The objective was to assess the effect ofverapamil on atrial fibrillation (AF) cycle length and spatial dispersion of refractoriness in patients with chronic AF., Background: Previous studies have suggested that verapamil prevents acute remodeling by AF. The effects of verapamil in chronic AF are unknown., Methods: During electrophysiologic study in 15 patients with chronic AF (duration >1 year), 12 unipolar electrograms were recorded from right atrial free wall, right atrial appendage and coronary sinus, along with monophasic action potential recordings from the right atrial appendage. The mean fibrillatory interval at each atrial recording site was used as an index for local refractoriness. Dispersion of refractoriness was calculated as the standard deviation of all local mean fibrillatory intervals expressed as a percentage of the overall mean fibrillatory interval. After baseline measurements, verapamil (0.075 mg/kg intravenous in 10 min) was infused and the measurements were repeated., Results: After administration ofverapamil, mean fibrillatory intervals shortened by a mean of 16.6 +/- 3.3 ms (p < 0.001) at the right free wall, 15.0 +/- 3.5 ms (p < 0.001) at the appendage and 17.1 +/- 3.2 ms (p < 0.01) in the coronary sinus. Monophasic action potential duration decreased by 15.9 +/- 4.0 ms (p < 0.01). Dispersion of refractoriness increased in all patients from 3.8 +/- 0.8 to 5.1 +/- 1.8 (p < 0.001). A strong correlation between mean fibrillatory intervals and action potential duration was found, both before and after verapamil., Conclusions: Verapamil caused shortening of refractoriness and increase in spatial dispersion of refractoriness in patients with chronic AF. This implies that verapamil is not useful in reversing the remodeling process in these patients.

Objectives: We sought to quantify the effects of electrode-target distance and intracavitary blood flow on radiofrequency (RF) power required to induce transient conduction block, using a Langendorff-perfused canine ablation model., Background: Given the thermally mediated nature of RF catheter ablation, cooling effects of intracavitary blood flow and electrode-target distance will influence lesion extension and geometry and electrophysiologic effects., Methods: In eight Langendorff-perfused canine hearts, the right ventricular free wall was opened, and the right bundle branch (RBB) carefully localized by multielectrode activation mapping. The right atrium was paced at cycle length of 500 ms. Proximal and distal electrodes were attached at the endocardial aspect of the RBB, and the perfused heart was submerged in heparinized blood at 37 degrees C. A standard 4-mm tip ablation electrode was positioned at a constant contact pressure of 5 g between the two electrodes at the site of maximal RBB potential (0 mm) and 2 and 4 mm distant from this site along a line perpendicular to the RBB. RF pulses (500 kHz) were delivered for 30 s at 0.5-W increments until transient bundle branch block. In four hearts, intracavitary flow was simulated by directing a 30-cm/s jet of blood parallel to the septum at the ablation site, and the protocol was repeated to assess the effects on power required for block. In one heart, the effect of variable flow was assessed (0, 15 and 30 cm/s)., Results: An exponential distance-related increase was seen in power required for block, from 1.8 +/- 0.9 W (mean +/- SD) at 0 mm to 5.4 +/- 1.1 W at 4 mm. In the presence of 30-cm/s flow, an increase to 3.9 +/- 0.8 W at 0 mm and 13.1 +/- 2.4 W at 2 mm was seen. At 4 mm, coagulum formation invariably occurred before block could be induced. For 15-cm/s flow, less power was required: 3 and 7 W at 0 and 2 mm, respectively., Conclusions: Increasing the ablation electrode-target distance causes an exponential increase in power required for conduction block; this relation is profoundly influenced by intracavitary flow. Given the geometry of endomyocardial RF lesions, these findings are particularly relevant for directly subendocardial ablation targets.

Objectives: The goal of the study was to quantify the response of myocardial impulse propagation to hyperthermia and identify the temperatures required for transient and permanent block in conduction., Background: Although it is generally accepted that the effects of radiofrequency ablation are thermally mediated, the precise response of myocardial impulse conduction to heating remains to be quantified., Methods: Twenty-three preparations of ventricular myocardium from 10 beagle dogs were superfused at 36.5 to 37.5 degrees C and paced at a cycle length of 600 ms. Heating was performed for 30 s at 5-min intervals by an independent flow of heated superfusate. A 16-electrode grid was used to record extracellular electrograms directly before each heating episode (control value) and at 10, 20 and 30 s., Results: Between 38.5 and 45.4 degrees C, conduction velocity was higher than that at the directly preceding control value (p < 0.05), reaching a maximum of 114% between 41.5 and 42.5 degrees C. Above 45.4 degrees C, a gradual decrease occurred, with transient block (absence of impulse conduction for < or = 5 min) after heating to 49.5 to 51.5 degrees C. This was followed by tachycardia in 69% of all cases immediately after cessation of heating. Permanent block occurred after a significantly higher temperature of 51.7 to 54.4 degrees C had been reached. Pacing at sites allowing preferential conduction either parallel or perpendicular to fiber orientation caused no difference in reaction to heating. Repeated heating of some preparations to 47.0 to 50.5 degrees C revealed no cumulative effects on conduction velocity., Conclusions: Transient and permanent block in impulse conduction occurred at 49.5 to 51.5 degrees C and 51.7 to 54.4 degrees C, respectively, in superfused canine myocardium, the former frequently being followed directly by tachycardia. Reaction of conduction velocity to hyperthermia was independent of myocardial fiber orientation and number of preceding heating episodes. Results may contribute to a better understanding of electrophysiologic phenomena observed during radiofrequency ablation procedures.

Objectives: The objective of the study was to record the electrocardiogram (ECG) of a large whale to obtain crucial data for comparative electrophysiologic analysis., Background: The data were needed to establish the mismatch between heart size and PR interval and QRS duration in mammals., Methods: In the waters off the coast of Newfoundland, in two humpback whales (Megaptera novaeangliae) with an estimated weight of 30,000 kg a 1-lead ECG was recorded, enabling reliable assessment of P waves and QRS complexes., Results: It was found that both the PR interval (atrioventricular [AV] transmission time) and QRS duration (ventricular excitation) are extremely short for animals of this size. These findings are difficult, if not impossible, to explain on the basis of currently accepted electrophysiologic theories. However, the narrow QRS complex may be due to a very dense His-Purkinje network in the ventricular wall of whales. Alternative mechanisms that can explain the function of the mammalian AV node need to be considered and explored., Conclusions: The results of the study may be of value for the understanding of the ECG in humans.

In 13 patients with atrial fibrillation, the effect of right ventricular pacing at various rates on spontaneous RR intervals was studied. Five hundred consecutive RR intervals were recorded and measured before and during varying right ventricular pacing rates. As anticipated, all RR intervals longer than the right ventricular pacing intervals were abolished. However, RR intervals shorter than the right ventricular pacing intervals were also eliminated. It is difficult to explain the elimination of RR intervals shorter than the pacing intervals with the accepted concepts concerning the mechanisms governing the rate and rhythm of the ventricular response to atrial fibrillation. An alternative explanation may be that during atrial fibrillation the atrioventricular node behaves as a nonprotected pacemaker that is electrotonically modulated by the chaotic atrial electrical activity. The result is a random ventricular rhythm. With right ventricular pacing, the automatic focus is depolarized by the retrogradely concealed conducted ventricular impulses, the short RR intervals are not generated as a consequence and the rhythm becomes pacemaker dependent.