Intact Ventriculoatrial Conduction Research Articles

Complete Atrioventricular Block with Intact Retrograde Conduction in Cardiac Rhythm Management Devices: Implications of the Phenomenon.

Intact retrograde ventriculoatrial (VA) conduction in the presence of complete atrioventricular (AV) heart block has been well-documented in the past. We sought to describe the prevalence and clinical significance of intact VA conduction accompanied by complete antegrade AV block in patients with implanted cardiac rhythm management (CRM) devices. During routine follow-up of CRM devices in our device clinic, 42 patients were found to be in a state of complete heart block. All patients presented in sinus rhythm. The patients’ underlying rhythms were tested with the inhibition of pacing and documented AV dissociation. Subsequently, retrograde VA conduction was tested with ventricular pacing. In the 42 patients with complete heart block as the underlying rhythm, five patients demonstrated retrograde VA conduction. In conclusion, the prevalence of intact of VA conduction was 11.9% in our study. The implications of this phenomenon can have noteworthy clinical significance. The occurrence of pacemaker-mediated tachycardia and repetitive nonreentrant VA synchrony are discussed herein. All patients, even those with a device indication of complete heart block, should be tested for retrograde conduction at implantation and during routine follow-up.

Value of physical signs in the diagnosis of ventricular tachycardia.

Although the use of physical signs for the diagnosis of ventricular tachycardia (VT) was described in the early 1900s, their value in this role has never been systematically assessed. Using a blinded, randomized protocol, we examined the ability of 26 clinicians to detect ventriculoatrial (VA) dissociation during cardiac pacing in 21 patients with both atrial and ventricular pacing wires in situ after successful ablation of accessory pathways. In protocol 1 (10 patients), pacing was randomized to either ventricular pacing alone (simulating VT) or to atrioventricular sequential pacing (simulating supraventricular tachycardia or VT with intact VA conduction) at rates of 150 or 180 beats per minute. Each patients was examined by four clinicians blinded to the pacing mode. Clinicians were asked to make a diagnosis of "VA association" or "VA dissociation" after examining the patient for variability of the arterial pulse, jugular venous pulse (JVP), and first heart sound. In protocol 2 (11 patients), randomization of pacing mode was performed between examination of each of the three physical signs so that the value of each sign was assessed individually. In protocol 1, a diagnosis of VA dissociation (VT) was made in 21 of 40 observations, with a specificity of 75%, sensitivity of 70%, and a positive predictive value (PPV) of 71%. In protocol 2, from a total of 132 observations (44 for each sign), the sensitivity, specificity, and PPV for a diagnosis of VT were as follows: arterial pulse, 61%, 71%, 70%; JVP, 96%, 75%, 82%; and first heart sound, 58%, 100%, 100%. It is concluded that, in patients with a regular tachycardia of uncertain origin, clinically detectable variations in the first heart sound and JVP are highly specific and sensitive indicators, respectively, of a diagnosis of VT. Assessment of the arterial pulse is of little value in this role.

Double blind crossover comparison of the effects of dual chamber pacing (DDD) and ventricular rate adaptive (VVIR) pacing on neuroendocrine variables, exercise performance, and symptoms in complete heart block.

To compare the effects of dual chamber pacing (DDD) and ventricular rate adaptive pacing (activity sensing) (VVIR) in patients with complete heart block. Double blind crossover comparison with one month in each pacing mode. 10 consecutive patients aged 23-74 presenting with complete anterograde atrioventricular block at rest and on exercise and with an intact atrial rate response received Synergyst I (Medtronic) pacemakers. Symptom scores, maximal exercise performance on a treadmill, and the plasma concentrations of atrial natriuretic peptide, adrenaline, and noradrenaline. No significant differences were identified between pacing modes in symptom scores for dyspnoea, fatigue, and mood disturbance; exercise time; and maximal oxygen consumption. One patient with intact ventriculoatrial conduction developed pacemaker syndrome during VVIR pacing. Resting plasma concentrations of atrial natriuretic peptide were raised in complete heart block and were restored to normal by DDD pacing but not by VVIR pacing. Resting plasma catecholamine concentrations were normal in complete heart block and in both pacing modes. During exercise the increase in the concentrations of all three hormones was similar in both pacing modes. In patients with complete anterograde and retrograde atrioventricular block, symptoms and maximal exercise performance were no better during DDD than during VVIR pacing.

Electrophysiologic characteristics of manifest and latent retrograde conduction in dogs

Atrioventricular (AV) nodal reentry requires intact retrograde ventriculoatrial (VA) conduction. The purpose of this study was to assess the contribution of various pacing and pharmacologic techniques to uncover VA conduction during apparent unidirectional VA block, and to evaluate the role of several biologic and electrophysiologic factors in concealment of retrograde conduction. Forty healthy dogs underwent catheter-electrophysiologic studies of AV and VA conduction. Group I (20 animals) had intact VA conduction. Group II (six animals) had VA dissociation with ventricular pacing initiated during sinus rhythm, but the presence of VA conduction was confirmed by isoproterenol infusion or by premature ventricular stimulation. In group III (14 animals), the above techniques failed to uncover VA conduction. Eight of 14 group III animals underwent thoracotomy and crushing or freezing of the sinoatrial (SA) node. Ventricular pacing initiated during sinus standstill was associated with 1:1 VA conduction in each experiment. VA conduction time and retrograde Wenckebach cycle length, both in the baseline state and during isoproterenol infusion, were significantly longer in the eight animals in group III than in those in group I. Age, gender, weight, breed, sinus cycle length, and anterograde AV conduction properties were not significantly different between groups I, II, and III. The data suggest that (1) in normal dogs, complete unidirectional VA block probably does not exist; (2) in the presence of anterograde input to the AV node, even sophisticated pacing and pharmacologic maneuvers may fail to uncover the presence of VA conduction; (3) although anterograde input is essential for concealment of VA conduction, the phenomenon is more closely associated with depressed retrograde than with anterograde AV nodal characteristics. These data may be important when analyzing the effects of various AV nodal modification procedures on the apparent elimination of VA conduction.

Electrophysiological determinants of antidromic reentry induced during atrial extrastimulation. Insights from a pacing model of Wolff-Parkinson-White syndrome.

The electrophysiology of antidromic reentry, a less common phenomenon than orthodromic reentry, remains a poorly understood aspect of the Wolff-Parkinson-White (WPW) syndrome. We used a pacing model of ventricular preexcitation in patients without WPW, so that electrophysiological events in the normal pathway during atrial extrastimulation (A1-A2 technique) could be precisely delineated without the obscuring effect of an actual accessory pathway. Ventricular preexcitation was simulated by an A1-V1 sequential basic drive with A2-V2 extrastimulation at progressively shorter A1-A2 (equal to V1-V2) coupling intervals. At each coupling interval tested within the zone of atrioventricular (A-V) nodal effective refractory period (since anterograde block of A2 was considered mandatory for manifestation of antidromic reentry), responses were assessed after A2 alone (method I), V2 alone (method II), and A2 plus V2 (method III, the complete preexcitation model). The entire pacing protocol was performed at two A-V intervals, short (50 msec) and long (150-180 msec), thereby simulating different proximities between the A pacing site and "accessory pathway" location. Of 47 consecutive unmedicated patients screened for the study protocol, 38 failed to meet minimal prerequisites for possible initiation of antidromic reentry because of failure in 18 (38% of total) to achieve anterograde A-V nodal block of A2, even though 1:1 ventriculoatrial conduction to cycle lengths less than or equal to 500 msec (less than or equal to 400 msec in 12) was present; and poor or absent ventriculoatrial conduction in the others. The nine remaining candidates underwent the full pacing protocol. Antidromic reentry (retrograde atrial response following V2 in method III) was observed in only two cases (4% of total), and both were associated with retrograde His-Purkinje system delays (documented by method II) occurring in tandem with a long A-V interval, thereby allowing for completion of retrograde A-V nodal recovery after penetration by A2. Indeed, such a prolonged recovery time prevented initiation of antidromic reentry in six of the nine patients (proven by intact ventriculoatrial conduction in method II). Retrograde A-V nodal block of V2, independent of A2, prevented an antidromic echo in one case. Findings in our model help to clarify the various factors, including specific anterograde and retrograde A-V nodal properties; anatomic relation between the accessory and normal pathways; and the retrograde His-Purkinje system delays, that must prevail in a concerted fashion to permit the initiation of antidromic reentry during the A1-A2 technique in patients with the WPW syndrome.

Pacemaker syndrome in activity-responsive VVI pacing

The “pacemaker syndrome” refers to a wide variety of clinical presentations of intolerance to ventricular pacing ranging from mild light-headedness to frank syncope. 1 These problems are thought to result from the loss of atrioventricular synchrony with consequent loss of the atrial contribution to left ventricular filling, and, in some cases, intact ventriculoatrial conduction with inappropriate atrial-ventricular systole, increased systemic and pulmonary venous pressure and consequent reflex drop in systemic arterial pressure. 2 Some studies have suggested that it is the loss of chronotropic response during VVI pacing that leads to symptoms in many patients; this response can be improved by activity-responsive VVI pacing. 3 We report a case of pacemaker syndrome that resulted from the use of an activity-responsive VVI pacing system.

Linking by collision initiated in the absence of preexisting reentrant tachycardia

Dynamic functional block in 1 limb of a reentrant circuit (“linking”) can be maintained by either repetitive interference or collision of successive impulses entering the circuit. Occurrence of linking by collision during attempted overdrive pacing of reentrant tachycardias accounts for the entrainment phenomenon. To investigate whether linking by collision can be initiated in the absence of preexisting tachycardia, a human reentrant circuit model was studied. The model consisted of the atrioventricular node and His-Purkinje system as anterograde limb and an electronic stimulator that served as “retrograde limb” by initiating a paced atrial impulse at a predetermined ventriculoatrial interval following each sensed ventricular depolarization. In 3 patients with intact ventriculoatrial conduction, “reentrant tachycardia” was initiated by a ventricular extrastimulus (V 2), which retrogradely blocked bilaterally below the His bundle. When this same V 2 was followed, instead, by a paced V 2V 2 train at a cycle length equal to the programmed ventriculoatrial interval of the “tachycardia,” it could be shown that each beat of the train not only “traversed” the simulated “retrograde limb” but also retrogradely collided with a prior circulating impulse in the anterograde limb of the circuit, thereby constituting linking by collision at a supra-Hisian level with inability of even a single “reentrant cycle” to be completed; “tachycardia” became manifest only after termination of the V 2V 2 train. The findings suggest the existence of a unique mechanism for initiation of certain clinical reentrant tachycardias during incremental pacing.

A new method for assessing ventriculoatrial conduction in the human heart.

The presence or absence of ventriculoatrial (VA) conduction in the human heart is assessed by investigating whether 1:1 retrograde atrial capture is observed during constant cycle length ventricular pacing. In this study, a new pacing protocol for assessing VA conduction was designed in which the ventricular extrastimulus was delivered during basic ventricular and atrial simultaneous pacing (VE-VASP method). The effect of this pacing protocol on VA conduction was investigated in 12 patients who showed no evidence of VA conduction with the constant cycle length ventricular pacing method. In 5 of 12 patients, intact VA conduction was demonstrated with the VE-VASP method, while VA conduction was not observed in the remaining 7 patients. These results suggest that VE-VASP method sometimes demonstrates the presence of intact VA conduction in patients who show no evidence of VA conduction during constant cycle length ventricular pacing.

Changing experience with dual chamber (DDD) pacemakers

Dual chamber (DDD) or "universal" pacemakers have had a significant impact on the advancement of artificial pacemakers by providing a more physiologic approach to cardiac pacing. However, with the early generation of DDD pacemakers (pacemakers that sense and pace in both the atrium and the ventricle), a significant number of patients experienced pacemaker-mediated tachycardia because intact ventriculoatrial conduction was sensed in the atrium and a reentrant tachycardia was induced. Newer generation DDD pacemakers have provided longer atrial refractory periods, which should correct this problem. In this study the first and second years of a 2 year experience with DDD pacemakers were compared to determine if the newer generation devices have allowed maintenance of pacing in the DDD mode as opposed to reprogramming to some alternate mode because of pacemaker-mediated tachycardia or other pacing problems. The results showed a significant decrease in pacemaker-mediated tachycardia during the second year and continuation of pacing in the DDD mode in a higher percent of patients. This improvement is attributed to improvement in the pulse generator as well as better patient selection.

Retrograde concealed conduction in the atrioventricular node: differential manifestations related to level of intranodal penetration.

Although concealed conduction in the atrioventricular node (AVN) has been the focus of numerous experimental and clinical studies, little is known about the differential effects on AVN functional behavior of prior concealed retrograde impulse penetration alone vs prior anterograde or dual AVN activation. This study was undertaken specifically to investigate this aspect of human AVN physiology in patients without intact ventriculoatrial conduction to provide a model with which to analyze concealed retrograde AVN conduction. In 13 such patients AVN behavior during a subsequent anterograde input was characterized for each of three different manners of prior AVN activation: anterograde alone (method I), simultaneous anterograde and retrograde excitation (method II), or equivalently timed retrograde concealed AVN penetration alone (method III). In all patients evidence for retrograde AVN concealment was documented by longer anterograde conduction in the AVN during method III than that observed when the retrograde impulse was omitted (method IV). Furthermore, in these patients lacking intact ventriculoatrial conduction, anterograde conduction in the AVN was facilitated and refractoriness was decreased during dual excitation vs anterograde activation alone (method II vs method I). However, when each of methods I and II were compared with concealed retrograde AVN penetration alone (method III), two patterns of AVN responses were observed: In 11 of 13 patients (group A) conduction in the AVN was "worse" and refractoriness was greater both in methods I and II compared with method III; in the remaining two patients (group B) the opposite relationships were observed. The results suggest that among patients with no ventriculoatrial AVN conduction there exist at least two subpopulations whose AVN functional characteristics differ markedly when the effects of anterograde and dual excitation are compared with equivalently timed concealed retrograde activation alone. These findings may be related to differences in level of retrograde AVN concealment in groups A and B, which can be unmasked by the outlined pacing techniques.

Demonstration of intact ventriculo-atrial conduction in man with a new method: Ventricular extrastimulus testing during basic ventricular and atrial simultaneous pacing

Demonstration of intact ventriculo-atrial conduction in man with a new method: Ventricular extrastimulus testing during basic ventricular and atrial simultaneous pacing

Hemodynamic and symptomatic consequences of ventricular pacing.

After implantation of a ventricular demand pacemaker (VVI), occasional patients continue to have dizziness, syncope, or near syncope ("pacemaker syndrome"). To identify patients in whom VVI pacing may have deleterious effects, we compared cuff blood pressure responses to VVI pacing with blood pressure responses to atrioventricular sequential pacing (DVI) or sinus rhythm in 50 consecutive patients. Patients with intact ventriculoatrial conduction had a much greater decrease in systolic blood pressure with VVI pacing (24 +/- 11 mm Hg) than those with ventriculoatrial dissociation (-4 +/- 15 mm Hg) (P less than 0.005). Patients who were in heart failure had a lesser decrease in blood pressure with VVI pacing than did those without failure (P less than 0.05); 13 of the 14 heart failure patients lacked ventriculoatrial conduction. Ten patients had symptomatic dizziness after VVI pacing; the incidence of symptoms was higher in patients with ventriculoatrial conduction (9 of 23) than in those without ventriculoatrial conduction (1 of 27) (P less than 0.003). We conclude that the presence of intact ventriculoatrial conduction appears to be a crucial determinant of the hemodynamic response to VVI pacing, and its presence may identify patients who are at risk for "pacemaker syndrome."