[Ventriculo-atrial conduction in patients with Wolff-Parkinson-White syndrome].
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In order to clarify whether SNRT, CSNRT and SACT are reproducible tests, 20 patients with sick sinus syndrome underwent two successive electrophysiological studies with an interval of 24 hours; mean sinus cycle, SACT, SNRT, CSRNT were evaluated. Although no significant differences were found between the mean values of the two studies, in isolated cases remarkable variations of one or more parameters were observed. We conclude that SNRT, CSNRT and SACT are reproducible tests only if mean values in a large number of patients are considered, while they are not as useful in quantifying sinus node dysfunction in single cases. In conclusion, while SNRT, CSNRT and SACT are reproducible and useful in comparing data from relatively large number of patients, great caution should be used before drawing conclusions of potentially serious diagnostic and prognostic consequence in the single patient.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Selective coronarography, assessment of hemodynamics, sinus node function, sinoatrial and intraatrial conduction were performed in 53 coronary heart disease (CHD) patients with supraventricular arrhythmia. The severity of cardiac rhythm paroxysms was evaluated at transesophageal pacing by measurements of arrhythmia induction frequency threshold. 29 patients underwent aortocoronary shunting. No relationships were found between the pattern of arrhythmia, degree of stenosis, number of coronary lesions. Aortocoronary bypass changed neither pattern nor severity of supraventricular arrhythmia.
Explore the source record for details and available documents.
The purpose of this study was to test the assumption that the cause for postoperative atrial flutter/fibrillation after cardiopulmonary bypass is inadequate atrial myocardial protection. Dogs were subjected to cardioplegic arrest for 60 minutes without augmented atrial hypothermia (seven dogs, control group) or augmented atrial hypothermia with topical atrial cooling (seven dogs, study group). Twenty-five electrodes (15 on the right atrium and 10 on the left atrium) were fixed on the atria to measure effective refractory period and conduction time. Data were taken before bypass, immediately after bypass, and 2 hours after bypass. During cardioplegic arrest the mean temperatures measured in the atria were significantly lower (p less than 0.001) in the study group (13.5 degrees +/- 7.0 degrees C) than in the control group (23.7 degrees +/- 3.2 degrees C). There was no significant change in the mean effective refractory period after bypass in the control or study groups or in the prevalence of inducibility of atrial flutter/fibrillation by extrastimulation (3/7 dogs in the control group and 2/7 in the study group). During right atrial pacing, total conduction times were significantly longer (p less than 0.025 at cycle lengths of 300 and 350 msec) in the control group (74 +/- 5 msec and 75 +/- 7 msec, respectively) than in the study group (65 +/- 9 msec and 64 +/- 8 msec, respectively) immediately after bypass. Two hours after bypass, however, there were no significant differences under the same conditions between the two groups. There were no significant differences in conduction during left atrial pacing after bypass. Comparing those atria that were inducible with those not inducible demonstrated a significantly increased dispersion of effective refractory period (90 +/- 23 msec versus 74 +/- 18 msec, p less than 0.05) and increased conduction time in the inducible group. We concluded that augmented atrial hypothermia during cardioplegic arrest had no effect on the inducibility of fibrillation, had no effect on repolarization, and had only a small effect on conduction, which resolved within 2 hours after bypass. However, the study demonstrates that when the atria are inducible the substrates are an increased dispersion of refractoriness and a prolongation of conduction time.
Explore the source record for details and available documents.
UNLABELLED: Atrial fibrillation (AF) has been associated with premature beats and decreased atrial conduction velocities. On the other hand, prevalence of AF is increased in the elderly. The aim is to evaluate and analyze the relation between age, atrial size and a new index of dynamic interatrial conduction time (iaCT) in a homogeneous population of patients (pts) with structurally normal heart without AF. METHODS: 45 patients (pts) without structural heart disease aged 53 +/- 20 years referred for electrophysiologic study were analyzed. To examine the atrial electrophysiologic characteristics we studied interatrial conduction time (iaCT), double potentials and fragmented atrial activity during premature stimulation of high right atrium; prior to investigation, all antiarrhythmic drugs were withdrawn for an appropriate period of time. The following parameters were assessed: baseline iaCT (iaCTb) between high right atrium (HRA) and distal coronary sinus (CS), iaCT during HRA pacing S1S1 600ms (iaCTS1), maximum prolongation of iaCT during S2 and S3 delivery (iaCTS2, iaCTS3). We calculated a derived parameter: maximum prolongation iaCT/decremental index (DI)= iaCT S3-ia CTS1/iaCTS1%. The following echocardiograhic parameters were assessed: left atrial dimensions and surface (LAs), right atrial dimension and surface (RAs), total atrial surface (TAs=LAs+RAs) and left atrial volume (LAv) calculated using ellipse formula. RESULTS: iaCT ranged from 42 to 87ms; DI ranged from 16 to 52%. Simple regression analysis demonstrated a statistically significant linear correlation between the age of pts and HRA DI (r = 0.76, r2 = 0.55, p <0.0001). A trend toward a significant correlation was found between TAs and DI (r=0.64, r2=0.41, p<0.0001) LAv and DI (r=0.59, r2=0.35, p<0.0001). No significant correlation was found in this group between age and iaCT. Atrial double potentials and fragmentated electrograms were recorded using HRA stimulation in CS leads in 7 pts (15%) all aged >35 years. Pts were divided into two groups: 17 pts with normal electrophysiologic findings and 28 pts with junctional reentrant tachycardia. There were no significant differences between subgroups concerning the main studied parameters. CONCLUSIONS: This study shows a direct better correlation for age than atrial size in the relation with the dynamic behaviour interatrial conduction, suggesting that higher incidence in AF in the elderly might be also a consequence of the higher incidence of atrial conduction disturbances.
Using temporary atrial wire electrodes placed at selected atrial sites, rapid atrial pacing at rates of up to 368 beats/min was used to study atrial excitability and conduction in seven patients who underwent open heart surgery. The threshold for atrial pacing was found to be an exponential function of pacing rate (r = 0.55, p less than 0.01), increasing threefold when the fastest pacing rates were compared with the slowest pacing rates (p less than 0.005). Atrial conduction times (measured from pacing to recording sites), prolonged during rapid atrial pacing both for studies conducted before institution of cardiopulmonary bypass (p less than 0.005) and for those done 7 days postoperatively (p less than 0.05). However, prolongation of conduction times always depended on achievement of a critically rapid pacing rate. During rapid atrial pacing, we observed a high incidence of alternans of the atrial electrogram (17 of 42 studies). Thus, human atrial excitability, conduction and electrogram morphology are not constant during pacing at rapid rates. Rather, at rapid pacing rates, there is depression of atrial excitability, prolongation of atrial conduction times and alternation in electrogram morphology. These findings have clinical relevance and theoretical implications for the understanding and treatment of rapid atrial rhythms.
BACKGROUND: We assessed the effects of pacing-induced chronic atrial fibrillation (AF) on sinus node function, intra-atrial conduction, and atrial refractoriness. METHODS AND RESULTS: In 15 mongrel dogs (20 to 30 kg), AV nodal block was produced by radiofrequency catheter ablation, and a ventricular-inhibited (VVI) pacemaker (Minix 8330, Medtronic) was implanted and programmed to pace at 80 pulses per minute. In 11 of these dogs, right atrial endocardial pacing leads were connected to a pulse generator (Itrel 7432, Medtronic) and set at a rate of 20 Hz to induce AF. Corrected sinus node recovery time, P-wave duration, 24-hour Holter ECG to assess AF duration, maximal heart rate in response to isoproterenol (10 micrograms/min), intrinsic heart rate after administration of atropine (0.04 mg/kg) and propranolol (0.1 mg/kg), and atrial effective refractory periods (ERPs) were obtained at baseline (EPS-1) and after 2 to 6 weeks (EPS-2) of VVI pacing alone (n = 4) or VVI pacing and rapid atrial pacing (n = 11). At EPS-2, corrected sinus node recovery time and P-wave duration were prolonged, maximal heart rate and intrinsic heart rate were decreased, atrial ERPs were shortened, and the duration of AF was increased significantly compared with EPS-1. These changes partially reversed toward baseline 1 week after conversion to sinus rhythm. Sinus node function and AF inducibility observed in the control dogs that underwent ventricular pacing alone (n = 4) did not change. CONCLUSIONS: Pacing-induced chronic AF induces sinus node dysfunction, prolongs intra-atrial conduction time, shortens atrial refractoriness, and perpetuates AF, changes that reverse gradually after termination of AF.
BACKGROUND: We report that rapid atrial pacing interrupts atrial flutter when the orthodromic wave front from the pacing impulse is blocked in an area of slow conduction in the reentry circuit. To characterize the area of slow conduction during atrial flutter and rapid pacing, we studied 11 episodes of induced atrial flutter, mean cycle length 157 +/- 20 msec, in eight dogs with sterile pericarditis. METHODS AND RESULTS: Atrial electrograms were recorded simultaneously from 95 pairs of right atrial electrodes during the interruption of atrial flutter by rapid atrial pacing, mean cycle length 139 +/- 21 msec. Areas of slow conduction during atrial flutter were demonstrated at one to three sites in the reentry circuit. After rapid pacing captured the reentry circuit, one area of slow conduction either disappeared (10 episodes) or the degree of slow conduction in an area of slow conduction decreased (one episode). Both changes were in association with activation of the region by a wave front from the pacing impulse that arrived from a direction different than that during the induced atrial flutter. Interruption of atrial flutter during rapid pacing occurred when the orthodromic wave front from the pacing impulse blocked in an area of slow conduction that had either newly evolved during rapid pacing (seven episodes) or that was previously present (four episodes). CONCLUSIONS: Areas of slow conduction present during atrial flutter and rapid pacing of atrial flutter are functional and depend on both the atrial rate and the direction of the circulating wave fronts. Interruption of atrial flutter by rapid pacing results from block of the orthodromic wave front of the pacing impulse in an area of slow conduction in the reentry circuit.
In a 72-years-old patient with intermittent bradycardia definitive atrial pacing was considered. Surface ECG was misleading because of demonstrating 2:1 anterograde block during atrial stimulation at a rate of 100 beats per minute. Intracardiac recordings disclosed the bigeminal occurrence of premature atrial contractions. Every second stimuli fall within the premature atrial contraction's refractory period simulating impaired AV-conduction. Our report emphasizes the importance of intracardiac recordings during atrial stimulation in order to evaluate the anterograde conduction before pacemaker implantation.
Explore the source record for details and available documents.