Exercise-induced distal atrioventricular block

Three patients with 1:1 atrioventricular (AV) conduction at rest developed fixed 2:1 or 3:1 AV block during treadmill exercise testing. Electrophysiologic study documented block distal to the AV node in all three patients, and suggested that the exercise-induced block occurred because of increased atrial rate and abnormal refractoriness of the His-Purkinje conduction system. The findings in these three patients suggest that high grade AV block appearing during exercise reflects conduction disease of the His-Purkinje system rather than of the AV node, even in the absence of bundle branch block. Patients with this diagnosis should be considered for permanent cardiac pacing.     

Crossed atrioventricular connections

Four cases of crossed atrioventricular connections are described. All of them were diagnosed at cardiac catheterization by angiocardiography and one was examined pathologically. Two possessed situs solitus, one with concordant connections and the other with discordant connections; the other had two situs inversus, both of them with concordant connections. Two had double-outlet right ventricle, one had transposition of the great arteries, and the other had normally related and connected great arteries. These cases have been interpreted as representing abnormal rotation of the ventricles following sepatation. A review of 36 cases previously reported on and our own cases, suggests that most patients have concordant atrioventricular connections. There are many types of ventriculo-arterial connections, the most frequent being transposition of the great arteries. There has not been any case reported with persistent truncus arteriosus. On the basis of atrioventriculo-arterial connections, we propose a classification for this malformation. We discuss the importance of the bulboventricular loop in the type of atrioventricular connections, some clinical implications for the diagnosis, and analyze the value of the rules to localize the ventricles by means of the position of the great arteries.     

Retrograde dual atrioventricular nodal pathways

Thirty-one (3.5 percent) of 887 studied patients had retrograde dual atrioventricular (A-V) nodal pathways, as manifested by discontinuous retrograde A-V nodal conduction curves (29 patients) or by two sets of ventriculoatrial (V-A) conduction intervals at the same paced cycle length (2 patients). All patients had A-V nodal reentrant ventricular echoes of the unusual variety induced with ventricular stimulation (25 patients had single, 2 patients had double and 4 patients had more than three ventricular echoes). The weak link of the reentrant circuit was always the retrograde slow pathway. Eleven of the 31 patients also had anterograde dual A-V nodal pathways (bidirectional dual pathways). Eight patients (26 percent) had spontaneous as well as inducible A-V nodal reentrant paroxysmal supraventricular tachycardia (of the unusual type in three and the usual type in five). In addition, three patients (10 percent) had only inducible supraventricular tachycardia (two of the unusual and one of the usual type).Retrograde dual A-V nodal pathways are uncommon. They are associated with the finding of at least single A-V nodal reentrant ventricular echoes (all patients), anterograde dual pathways (one third of patients) and A-V nodal reentrant paroxysmal supraventricular tachycardia of the usual or unusual variety (one third of patients).     

Alternative mechanisms of apparent supernormal atrioventricular conduction

Alternative mechanisms were found to explain several different electrocardiographic examples of apparent supernormal atrioventricular (A-V) conduction in man using programmed premature atrial and ventricular stimulation and His bundle recordings. Sudden shortening of the P-R interval during A-V nodal Wenckebach phenomenon was due to manifest or concealed reentry within the A-V node. Gap phenomena in which late atrial premature depolarizations blocked while earlier atrial premature depolarizations conducted were shown to result from delay of earlier atrial premature depolarizations in the A-V node (type I gap) or in the His-Purkinje system (type II gap). Mechanisms analogous to the latter were found in cases of apparent supernormality of intraventricular conduction: Late atrial premature depolarizations resulted in aberration whereas earlier atrial premature depolarizations conducted normally because of delay within the A-V node or His-Purkinje system. Unexpected normalization of a bundle branch block pattern also resulted from Wenckebach phenomenon in the bundle branches. Atypical Wenckebach phenomenon with the first beat of the period demonstrated that aberration was due to phase 4 depolarization. Preexcitation of the ventricle before the delivery of a previously blocked atrial premature depolarization allowed conduction through the area of block (A-V node) because of earlier depolarization of the latter with earlier recovery. In the His-Purkinje system, 2:1 A-V block was converted to 1:1 conduction when a premature ventricular depolarization shortened the refractoriness of the His-Purkinje system.     

Effects of dobutamine on atrioventricular conduction.

Dobutamine, a new beta-stimulating catecholamine, has been investigated in terms of its effect upon atrioventricular conduction. Bundle of His recordings were obtained on six patients in basal conditions and with right atrial pacing at rates of 100, 120, and 140 per minute. Recordings were repeated following intravenous administration of Dobutamine in doses of 5, 10, and 15 mug per kilogram per minute. Dose-response curves were thus obtained for A-H and H-V intervals. Heart rate increased only moderately with progressive concentrations of the drug. Very significant facilitation of A-H conduction was demonstrated with doses of 10 and 15 mug per kilogram per minute, with no effect upon H-V times. Dobutamine may be a clinically useful inotropic agent in conditions associated with A-V conduction disturbances.     

Dual atrioventricular nodal pathways associated with a gap phenomenon in atrioventricular nodal conduction

A 67 year old man underwent electrophysiologic study for evaluation of syncope. During atrial pacing at a basic cycle length of 600 ms, atrial premature stimuli were introduced at progressively shorter coupling intervals. The graph of atrial coupling intervals versus corresponding His bundle responses revealed an abrupt increase in atrioventricular (AV) nodal conduction time with coupling intervals from 320 to 340 ms. In an atrial coupling interval of less than 320 ms, conduction was again rapid until the effective refractory period of the atrium was reached. These unique findings are compatible with dual pathways and a gap phenomenon within the AV node.     

Echocardiographic classification of complete atrioventricular canal defects

M-mode echocardiographic records of 26 patients with surgically proven complete atrioventricular canal defect were reviewed. Fragmentation of the interventricular septum and anterior displacement of the mitral annulus into the left ventricular outflow tract were noted in all patients. In 25 of 26 a common atrioventricular valve leaflet echo could be identified in the left ventricular outflow tract at the area of the crest of the interventricular septum. Recordings of echographic scans performed in the area of the left ventricle demonstrated separate “mitral” and “tricuspid” contributions to atrioventricular valve echoes in all 13 patients with type A defect, and a single common atrioventricular valve leaflet in 10 of 11 patients with type C complete atrioventricular canal. Two patients with type B defect had findings intermediate between these two patterns. M-mode echocardiography presumptively diagnosed complete atrioventricular canal in all 26 patients and diagnosis was definitive in 25 of 26. In addition, echocardiographic atrioventricular valve patterns permitted anatomic classification in the large majority of cases.     

Demonstration of dual atrioventricular nodal pathways in man

Electrophysiologic studies in a patient manifesting two P-R intervals revealed two ranges of atrioventricular (A-V) nodal conduction time (A-H intervals) and two A-V nodal effective and functional refractory periods. Similar demonstrations in patients with paroxysmal supraventricular tachycardia would strongly support the presence of longitudinal A-V nodal dissociation with reentry as a causative mechanism.     

Wolff-Parkinson-White syndrome with 1:2 atrioventricular conduction

The QRS complex of the Wolff-Parkinson-White syndrome is thought to represent a fusion beat resulting from conduction over the normal pathway and an anomalous pathway. This report demonstrates utilization of both of these pathways resulting in two ventricular responses from a single supraventricular impulse. The presence of “1:2” atrioventricular conduction in this case firmly supports the fusion beat theory of the Wolff-Parkinson-White syndrome.     

Patterns of atrioventricular conduction in children.

In this study, intracardiac electrograms were performed in 20 children--ranging in age from eight months to 18 years and without evidence of conduction disturbances on the scalar electrocardiogram--to determine the normal conduction patterns, response to atrial pacing, and values of refractory periods. Atrial pacing--18 cases--induced a prolongation al AH on increasing heart rates in all; 11 developed Wenckebach block proximal to the bundle of His at the mean pacing rate of 224 per minute +/- 45 (1 S.D.). Refractory periods were shorter than in adults. Study of the pattern of A-V conduction revealed three types of response: (1) the atrium was the limiting structure in 11 cases; (2) the delay occurred in the A-V node only in four cases; and (3) the delay occurred both in the A-V node and His-Purkinje system. This response was observed in one case only.     

Effects of digoxin on atrioventricular conduction patterns in man

Digoxin was acutely administered to 17 patients, and its effects on atrioventricular (A-V) conduction were assessed. In the control state, before administration of digoxin, progressively premature atrial depolarization showed conduction delay and block confined solely to the A-V node in eight patients and to both the A-V node and the more distal His-Purkinje tissue in nine patients. His-Purkinje conduction delay was manifested on the surface electrocardiogram by ventricular aberration. After administration of digoxin, an early atrial premature impulse either was blocked in the A-V node or reached the distal intraventricular conduction system so late that block or conduction delay below the His bundle was reduced or no longer occurred. Ventricular aberration on the surface electrocardiogram was thus reduced or eliminated. These effects of digoxin on A-V conduction were due to its effect on the A-V node of slowing conduction of a premature impulse. Such action on the A-V node may abolish aberrant ventricular conduction in atrial fibrillation.     

Hereditary progressive atrioventricular conduction defect.

New data on genetics, including an extensive pedigree and certain aspects of natural history, have been compiled on Family S, which is characterized by a hereditary progressive atrioventricular (A-V) conduction defect. Concordance analysis of heart block in affected parents and their offspring suggests as a working hypothesis transmission of diathesis for the defect by means of a Mendelian autosomal dominant factor. Regression of the defect in several relatives, including reversion from first degree heart block to normal A-V conduction, defies explanation at this time. However, rapport established with the unusually large (1,067 members) and cooperative kindred will permit longitudinal evaluation of these findings.     

Electrophysiologic effects of tolamolol on atrioventricular conduction in man

The electrophysiologic effects of tolamolol (UK-6558-01), a beta-adrenergic blocking agent, were studied in 13 patients by means of intracardiac electrograms and the extrastimulus method. Tolamolol (4 to 30 mg. intravenously) resulted in : (1) prolongation of sinus cycle length (SCL) in all patients (p less than 0.01); (2) prolongation of sinus escape time (SET) in 11 of 13 patients (p less than 0.001); (3) prolongation of A-V nodal conduction time during sinus rhythm in 1i of 13 patients (p less than 0.001); (4) onset of A-V nodal Wenckebach block at longer paced cycle lengths in 10 of 11 patients (p less than 0.001); (5) prolongation of the functional refractory period (FRP) of the A-V node in 11 of 11 patients (p less than 0.001); and (6) prolongation of the effective refractory period (ERP) of the A-V node in 10 of 10 patients (P less than 0.001). Tolamolol had no effect on His-Purkinje system (HPS) conduction time in any patient, including 3 patients with abnormal H-V intervals. Because of the marked increase in A-V nodal conduction time encountered by premature atrial depolarizations, the relative and effective refractory periods of the HPS could not be determined in any patient after tolamolol. Atropine (0.5 or 1.0 mg. intravenously) significantly reversed the effects of tolamolol on: sinus cycle length (4 of 5 patients); sinus escape time (3 of 3 patients); A-V nodal conduction time (4 of 5 patients); and A-V nodal refractioriness (5 of 5 patients).     

Distal end of the atrioventricular nodal artery predicts the risk of atrioventricular block during slow pathway catheter ablation of atrioventricular nodal re-entrant tachycardia

OBJECTIVE—To search for a reliable anatomical landmark within Koch's triangle to predict the risk of atrioventricular (AV) block during radiofrequency slow pathway catheter ablation of AV nodal re-entrant tachycardia (AVNRT).
PATIENTS AND METHODS—To test the hypothesis that the distal end of the AV nodal artery represents the anatomical location of the AV node, and thus could be a useful landmark for predicting the risk of AV block, 128 consecutive patients with AVNRT receiving slow pathway catheter ablation were prospectively studied in two phases. In phase I (77 patients), angiographic demonstration of the AV nodal artery and its ending was performed at the end of the ablation procedure, whereas in the subsequent phase II study (51 patients), the angiography was performed immediately before catheter ablation to assess the value of identifying this new landmark in reducing the risk of AV block. Multiple electrophysiologic and anatomical parameters were analysed. The former included the atrial activation sequence between the His bundle recording site (HBE) and the coronary sinus orifice or the catheter ablation site, either during AVNRT or during sinus rhythm. The latter included the spatial distances between the distal end of the AV nodal artery and the HBE and the final catheter ablation site, and the distance between the HBE and the tricuspid border at the coronary sinus orifice floor.
RESULTS—In phase I, nine of the 77 patients had complications of transient (seven patients) or permanent (two patients) complete AV block during stepwise, anatomy guided slow pathway catheter ablation. These nine patients had a wider distance between the HBE and the distal end of the AV nodal artery, and a closer approximation of the catheter ablation site to the distal end of the AV nodal artery, which independently predicted the risk of AV block. In contrast, none of the available electrophysiologic parameters were shown to be reliable. When the distance between the distal end of the AV nodal artery and the ablation target site was more than 2 mm, the complication of AV block virtually never occurred. In phase II, all 51 patients had successful elimination of the slow pathways without complication when the ablation procedure was guided by preceding angiography with identification of the distal end of the AV nodal artery.
CONCLUSIONS—The distal end of the AV nodal artery shown by angiography serves as a useful landmark for the prediction of the risk of AV block during slow pathway catheter ablation of AVNRT.


Keywords: atrioventricular nodal artery; atrioventricular nodal re-entrant tachycardia; catheter ablation; heart block.