The Dynamic Nature of Ventriculoatrial Conduction

An endless loop tachycardia starts when the atrial sensory amplifier of a dual chamber pacemaker identifies an early atrial signal originating from a ventricular or atrial premature depolarization or from myopotential noise. The tachycardia will continue as long as ventriculoatrial conduction is sustained. By selecting the appropriate atrial sensitivity setting, postventricular atrial refractory period, or upper rate limit, it is possible to eliminate sustained endless loop tachycardia. Electrophysiological data obtained at the time of dual chamber pacemaker implantation can assist the physician when selecting these settings. This report summarizes our intraoperative data on ventriculoatrial conduction obtained from 432 consecutive patients. One hundred sixty-two patients had evidence of ventriculoatrial conduction including 14% of patients with antegrade complete heart block and 32% with 2:1 AVB. The majority of patients with preserved antegrade conduction had sustained retrograde conduction. During incremental ventricular pacing, ventriculoatrial conduction prolonged in the majority of patients, and with faster ventricular pacing rates, ventriculoatrial block developed. Ventriculoatrial block developed in half of the patients at a ventricular pacing rate exceeding 120 bpm. Analysis of these data suggests that by selecting an upper rate limit of 140 bpm, a postventricular atrial refractory period of 300 msec, and an atrioventricular interval of 125 msec, approximately 90% of patients will not have sustained endless loop tachycardia.     

V-A block during atrioventricular nodal reentrant tachycardia: reentry confined to the AV node

Retrograde block during atrioventricular (AV) nodal reentrant tachycardia is considered a rare phenomenon that can potentially occur in the AV node or in the atrium. A patient with slow-fast AV nodal reentrant tachycardia and transient VA block localized in the AV node is presented. Pharmacological and stimulation maneuvers identified the site of block in the AV node and not in the atrium. Thus, AV nodal reentry can be confined to the AV node.     

Ventriculoatrial Conduction in Patients with Implantable Cardioverter Defibrillators: Implications for Tachycardia Discrimination by Dual Chamber Sensing

Incorporation of atrial electrograms in the tachycardia detection algorithm may improve tachyarrhythmia discrimination by ICDs but retrograde ventriculoatrial (VA) conduction over the AV node during ventricular tachyarrhythmia may be problematic. The present study analyzed VA conduction characteristics in 66 ICD patients who had evaluation of the VA conduction system by electrophysiological studies before implant. VA conduction was demonstrated in patients during ventricular decremental stimulation. Forty patients had inducible sustained monomorphic VT. The minimum cycle length maintaining 1:1 VA conduction during ventricular stimulation was longer than the cycle of VT in every patient (496 ±100 msec vs 320 ± 81 msec; P < 0.01). Occasional VA conduction during VT was observed in five patients and one patient had 2:1 VA conduction during induced VT. No patient had 1:1 VA conduction during VT. We conclude that brisk VA conduction is uncommon and 1:1 VA conduction during VT is rare in ICD recipients. VA conduction is unlikely to complicate the incorporation of atrial electrograms into tachyarrhythmia detection algorithms.     

Long-Term Follow-Up of Patients Treated with VVI Pacing and Sequential Pacing with Special Reference to VA Retrograde Conduction

The aim of this prospective study is comparing long-term prognosis in patients implanted with a WI pacemaker (group A) with those implanted with a sequential pacing device, AAI or DDD, (group B). Both groups of 45 patients each, were comparable as regards to age, sex, pacing indications, underlying heart disease, and technical conditions of implantation and were followed-up over 55 months. Atrial arrhythmias (A.A.) incidence was higher in group A: 24. 4% than group B: 8.8% (P < 0.05). Arterial embolisms (A.E.) occurred in group A patients only. Worsening or occurrence of exercise limitation was more frequent in group A: 35.6% as compared to group B: 13.3% (P < 0.05) and deaths related to these complications, occurred in seven cases in group A versus four cases in group B. In group A, all patients who experienced a worsening or occurrence of an A.A. or an A.E., had a ventriculoatrial condLction (VAC). No statistical difference was observed in worsening or occurrence of exercise limitation between patients with VAC and those without VAC: nine (42.8%) and seven (29.2%) but they respectively experienced at least one complication in 16 cases (76.2%) and seven cases (29.2%) (P < 0.01). In conclusion, Jong-term prognosis in patients implanted with VVI pacing as compared to patients implanted with sequential pacing is poorer. The presence of VAC in patients treated with permanent WI pacing is a major factor for complications and deaths related to A.E. and cardiac failure. Thus WI pacing should be avoided in patients with VAC.     

Dynamic Electrophysiology of Ventriculoatrial Conduction: Implications for DDD and DDDR Pacing

CAZEAU, S., ET AL.: Dynamic Electrophysiology of Ventriculoatrial Conduction: Implications for DDD and DDDR Pacing. The behavior of ventriculoatrial conduction (VAC) during exercise remains unknown. In order to determine its characteristics and the consequences it might have on dual chamber pacemaker technology and programming, 17 patients underwent an electrophysiological study (EPS) of atrioventricular conduction (AVC) and of VAC during a protocol including three steps: supine rest, upright position, and finally during cycloergometric exercise; the measurements were done at progressively increasing pacing rates. During a preimplantation EPS, Wenckebach points AVC-W and VAC-W and conduction times, AVCT and VACT (as a function of pacing rate), were measured in ten consecutive patients using temporary leads and an external device. In another study, AVCT, VACT, AVC-W, and VAC-W were measured by telemetric recordings under identical conditions in seven patients implanted earlier with a DDD pacemaker. A 1/1 VAC was observed in 7/17 patients (41%) at rest, and in 13/17 patients (76%) at the end of the protocol; VAC was never observed in 4/17 patients [23%], but occurred in six of the ten patients initially free, three standing at rest and three on exercise. For all patients, the VAC behavior remained of “nodal” type, indicated by a progressive increase in VACT as pacing rate rose up to the VAC-W point. Neither the existence of exercise-induced VAC nor the maximal VACT-W could be predicted from AVC or VAC data obtained at rest. However, at the same pacing rates, standing up and exercise induced a shortening effect on VACT, and improved the VAC-W by an average of 33%. These results suggest that the electrophysiological behavior of VAC does not obey any general rule and cannot be predicted individually. It would thus appear unwise to base pacemaker mediated tachycardia (PMT) protection solely on long postventricular atrial refractory period (PVARP) programming in DDD patients. This work also revealed the potential risks of a rate responsive auto-adaptive PVARP algorithm as proposed in certain new devices.     

Pacemaker Syndrome Evaluated by Cardiopulmonary Exercise Testing

Two patients who presented with dyspnea on effort, persisting after insertion of a fixed rate ventricular demand pacemaker (VVI) for sick sinus syndrome, were evaluated by cardiopulmonary exercise testing. During VVI pacing a heightened ventilatory response to exercise and a fluctuation of ventilation occurred. The high ventilatory equivalent for CO2 throughout exercise with VVI pacing suggests that the patients had ventilation-perfusion mismatching due to an increase in the pulmonary capillary wedge pressure caused by 1:1 ventriculoatrial conduction. Rate responsive ventricular (VVIR) pacing associated with intact 1:1 ventriculoatrial conduction exaggerated the exertional dyspnea, while rate responsive atrial (AAIR) pacing improved the ventilatory response to exercise. We suggest that a heightened ventilatory response to exercise due to ventilation-perfusion mismatching may be an important factor causing the pacemaker syndrome, and that cardiopulmonary exercise testing is useful in identifying the exercise-induced symptoms with ventricular pacing.     

Characteristics of Ventriculoatrial Conduction in Patients with Enhanced Atrioventricular Nodal Conduction

To study the characteristics of the ventriculoatrial conduction system in palienfs capable of rapid antegrade atrioventricuiar conduction, eiectrophysiologic studies were performed in 23 subjects capable of 1:1 atrioventricular conduction at atrial cycle lengths < 300 ms (Group I). and in 23 subjects with normal 1:1 atrioventricular conduction (Group II). During venfricular pacing, ventriculoatrial block at all cycle lengths was seen in 5/23 (22%) in Group I and in 7/23 (30%) in Group II patients (p = NS). In the remainder, the minimum ventricuar pacing cycle length maintaining 1:1 ventriculoatrial conduction was 359 ± 85 ms in Group I, compared to 444 ± 118 ms in Group II (p < .02). Both flat and exponential VA conduction interval curves, drawn as a function of pacing cycle length, were observed in both groups. Discontinuous ventricuioatrial conduction curves were seen in 5/18 (28%) Group I and 1/16 (6%) Group II patients (p = NS). In conclusion, retrograde ventriculoatrial conduction, when present in patients capable of rapid 1:1 atrioventricular conduction, is maintained at shorter cycle lengths than in patients with normal atrioventricular conduction. Quantitative, rather than qualitative, differences distinguish the two groups.     

Superior vena cava syndrome with retropharyngeal edema as a complication of ventriculoatrial shunt

Thirty‐seven‐year old female with hydrocephalus managed by a ventriculoatrial (VA) shunt presented with upper body edema, dysphagia, and headache. Imaging demonstrated thrombosis of the superior vena cava (SVC). Direct catheter thrombolysis led to resolution of thrombus burden. Superior vena cava thrombosis is a rare consequence of VA shunting and must be managed emergently.     

Inhibition of Atrial Electrical Activity by Ventricular Pacing Mediated by Vagal Stimulation

In the absence of retrograde (VA) conduction, ventricular pacing does not exert any appreciable effect upon atrial electrical activity. We report three patients (2 with complete AV block and 1 with preserved AV conduction) in which, during EP study, no VA conduction was present and, in spite of that, excessive suppression (for more than 15 secs in the first patient) of sinus (atrial) electrical activity during RV pacing was observed. The sinus node suppression was reproducible in two patients. In all patients the suppression phenomenon was not observed after intravenous administration of atropine, which suggests that it was mediated by enhanced vagal tone.     

Paradoxical Induction of Endless Loop Tachycardia by Magnet Application Over a DDD Pacemaker

It is well known that removal of a testing magnet from a DDD pulse generator may cause endless loop tachycardia in patients with retrograde ventriculoatrial conduction; application of the magnet then terminates the tachycardia. We have observed the opposite response to the magnet and in this report we describe the paradoxical induction of endless loop tachycardia by magnet application over a DDD pulse generator and its persistence despite repeated removal and reapplication of the magnet. This unusual behavior occurred only in the "magnet off" function and is due to magnet-induced signals sensed by the atrial channel circuitry.     

Analysis of Atrioventricular Nodal Reentrant Tachycardia with Variable Ventriculoatrial Block: Characteristics of the Upper Common Pathway

Background: The precise nature of the upper turnaround part of atrioventricular nodal reentrant tachycardia (AVNRT) is not entirely understood.
Methods: In nine patients with AVNRT accompanied by variable ventriculoatrial (VA) conduction block, we examined the electrophysiologic characteristics of its upper common pathway.
Results: Tachycardia was induced by atrial burst and/or extrastimulus followed by atrial-His jump, and the earliest atrial electrogram was observed at the His bundle site in all patients. Twelve incidents of VA block: Wenckebach VA block (n = 7), 2:1 VA block (n = 4), and intermittent (n = 1) were observed. In two of seven Wenckebach VA block, the retrograde earliest atrial activation site shifted from the His bundle site to coronary sinus ostium just before VA block. Prolongation of His-His interval occurred during VA block in 11 of 12 incidents. After isoproterenol administration, 1:1 VA conduction resumed in all patients. Catheter ablation at the right inferoparaseptum eliminated antegrade slow pathway conduction and rendered AVNRT noninducible in all patients.
Conclusion: Selective elimination of the slow pathway conduction at the inferoparaseptal right atrium may suggest that the subatrial tissue linking the retrograde fast and antegrade slow pathways forms the upper common pathway in AVNRT with VA block.     

"V-H-A Pattern" as a criterion for the differential diagnosis of atypical AV nodal reentrant tachycardia from AV reciprocating tachycardia

BACKGROUND: During ventricular extrastimulation, His bundle potential (H) following ventricular (V) and followed by atrial potentials (A), i.e., V-H-A, is observed in the His bundle electrogram when ventriculo-atrial (VA) conduction occurs via the normal conduction system. We examined the diagnostic value of V-H-A for atypical form of atrioventricular nodal reentrant tachycardia (AVNRT), which showed the earliest atrial activation site at the posterior paraseptal region during the tachycardia. METHODS: We prospectively examined the response of VA conduction to ventricular extrastimulation during basic drive pacing performed during sinus rhythm in 16 patients with atypical AVNRT masquerading atrioventricular reciprocating tachycardia (AVRT) utilizing a posterior paraseptal accessory pathway and 21 with AVRT utilizing a posterior paraseptal accessory pathway. Long RP' tachycardia with RP'/RR > 0.5 was excluded. The incidences of V-H-A and dual AV nodal physiology (DP) were compared between atypical AVNRT and AVRT. RESULTS: V-H-A was demonstrated in all the 16 patients (100%) in atypical AVNRT and in only 1 of the 21 (5%) in AVRT (P < 0.001). DP was demonstrated in 10 patients (63%) in atypical AVNRT and in 4 (19%) in AVRT (P < 0.05). The sensitivity of V-H-A for atypical AVNRT was higher than that of DP (P < 0.05). Positive and negative predictive values were 94% and 100%, respectively, for V-H-A and 71% and 74%, respectively, for DP. CONCLUSIONS: The appearance of V-H-A during ventricular extrastimulation is a simple criterion for differentiating atypical AVNRT masquerading AVRT from AVRT utilizing a posterior paraseptal accessory pathway.     

Left Atrial Size and Wall Motion in Patients with Permanent Ventricular and Atrial Pacing

KUBICA, J., ET AL.: Left Atrial Size and Wall Motion in Patients with Permanent Ventricular and Atrial Pacing. It is well known that during permanent ventricular pacing atrial arrhythmias and embolic complications occur much more frequently in comparison to permanent atrial or sequential pacing. He-modynamic disturbances caused by ventriculoatrial conduction (VAC) are thought to be responsible for those complications. The aim of this study was to compare the left atrial size and its wall motion in three groups of patients with sick sinus syndrome. Group 1: 58 patients with VVI pacing and VAC observed (22 males, 36 females, aged 31–86, mean 62.3). Group 2: 43 patients with primary AAI pacing (13 males, 30 females, aged 27–74, mean 57.8). Group 3: 13 patients with AAI or DDD replacing the primary VVI mode due to pacemaker syndrome and/or heart failure, all with VAC present during VVI pacing (7 males, 6 females, aged 26–80, mean 59.8). Two-dimensional/M-mode echocardiography was performed in all these patients. In group 1 mean diastolic as well as mean systolic atrial diameters were significantly greater (p < 0.005) and wall motion significantly smaller (p < 0.005) in comparison to the other groups. Left atrial wall motion amounted to only 7.4% of the mean diastolic diameter in this group. Mean left atrial diastolic and systolic diameters and wall motion in patients with pacemakers preserving atrioventricular synchrony (group 2 and group 3) were almost identical and wall motion amounted to about 22% of the diastolic diameter in both these groups. We conclude that ventriculoatrial conduction leads to significant enlargement of left atrium and to the atrial wall-motion decrease. This predisposes to arrhythmias and embolic complications. Changes in atrial size and performance seem to be reversible with restoration of the physiological atrioventricular synchrony.     

Ventricular and Dual Chamber Pacing for Treatment of Carotid Sinus Syndrome

Thirty-nine consecutive patients with recurrent syncope and either cardioinhibitory or mixed type carotid sinus syndrome were studied to determine the efficacy of ventricular (VVI) pacing in 16, and dual chamber (DDD/DVI) in 23 patients. Only those patients affected by the isolated vasodepressor form were excluded. Follow-up lasted 12 ± 5 months. Symptoms were totally eliminated in 67% of patients and ameliorated with persistence of minor symptoms in 33%. All patients underwent an initial 2-month follow-up in the VVI mode. Evaluation of the 19 patients who remained symptomatic and the 20 who became asymptomatic with VVI pacing demonstrated that factors observed prior to pacemaker implant were related to failure of the VVI mode. These included symptomatic pacemaker effect (42% vs 0%), mixed carotid sinus syndrome (95% vs 65%), orthostatic hypotension (47% vs 15%), or ventriculoatrial conduction (68% vs 38%). In the 23 patients with dual chamber pacing, random 2 month comparisons were performed between VVI and DVI/DDD pacing. The dual chamber mode was preferred by 14 patients, none preferred the VVI mode and nine noted no difference. Comparison of the two groups found that the factors linked to DVI/DDD preference were symptomatic pacemaker effect (50% vs 0%), ventriculoatrial conduction (78% vs 44%), or orthostatic hypotension (50% vs 11 %). VVI pacing is efficacious in a high proportion of patients affected by cardioinhibitory or mixed carotid sinus syndrome. The identification of causes of VVI pacing failure allows determination of those who will benefit from VVI pacing and those who should have DVI/DDD. VVI pacing is suggested for the cardioinhihitory type with no symptomatic pacemaker effect and for the mixed type with no symptomatic pacemaker effect or orthostatic hypotension or ventriculoatrial conduction. Dual chamber pacing should be used in all other instances.     

Atrial Sensing to Augment Ventricular Tachycardia Detection by the Automatic Implantable Cardioverter Defibrillator: A Utility Study

The triggering of automatic implantable cardioverter defibrillator (AICD) discharges by supraventricular tachycardias, despite the presence of a probability density function algorithm, remains a limitation of an otherwise highly effective device. We systematically investigated the diagnostic utility which theroretically could derive form the addition of atrial sensing capability to the AICD in 25 patients with 30 inducible sustained monomorphic ventricular tachycardias (VTs) at clinically relevant rates (greater than or equal to 150 beats/min). Patients were included only if they were not taking medication capable of depressing ventriculoatrial (VA) conduction for at least 5 half-lives prior to electrophysiological testing. We tested the simple criterion for VT that ventricular cycle length (CL) be shorter than the atrial CL (not met in sinus or most other supraventricular tachycardias). Mean VT CL was 283 +/- 47 ms (range 210 to 370). In 25 (83%) VTs, the VT criterion was consistently satisfied. Of the five cases in which the criterion was not met, 1:1 VA conduction during VT was present in four, three of which initially manifested 2:1 VA conduction lasting from 14 to 28 s and therefore would have transiently fulfilled the VT criterion. The remaining patient who failed to satisfy the VT criterion had ongoing atrial flutter during a relatively slower sustained VT, but this circumstance could be recognized because of the varying AV interval. The absence of 1:1 VA conduction at CLS less than or equal to 400 ms during ventricular pacing accurately predicted the absence of 1:1 VA conduction during VT in 95% of patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

A 2:1 AV rhythm: an adverse effect of a long AV delay during DDI pacing and its prevention by the ventricular intrinsic preference algorithm in DDD mode

A 91-year-old woman received a dual-chamber pacemaker for sick sinus syndrome and intermittently abnormal atrioventricular (AV) conduction. The pacemaker was set in DDI mode with a 350-ms AV delay to preserve intrinsic ventricular activity. She complained of palpitation during AV sequential pacing. The electrocardiogram showed a 2:1 AV rhythm from 1:1 ventriculoatrial (VA) conduction during ventricular pacing in DDI mode with a long AV interval. After reprogramming of the pacemaker in DDD mode with a 250-ms AV interval and additional 100-ms prolongation of the AV interval by the ventricular intrinsic preference function, VA conduction disappeared and the patient's symptom were alleviated without increasing unnecessary right ventricular pacing.     

Determination of creatine kinase isoenzyme MB activity in serum using immunological inhibition of creatine kinase M subunit activity. Activity kinetics and diagnostic significance in myocardial infarction.

This is a new method for the determination of creatine kinase isoenzyme MB activity in serum. The method uses direct activity measurement of creatine kinase B subunit activity after blocking of CK-M subunit activity by inhibiting antibodies. The test takes no longer than 15 min. The method yields an intra-serial C.V. of 2.0-12.9%, and a C.V. from day to day of 5.5%. The detection limit is 3.4 U/l creatine kinase MB. In the 95 cases with proven myocardial infarction several types of creatine kinase MB activity kinetics could be determined. The percentage of creatine kinase MB of peak CK-total is 6-25%, with a mean of 11.1%. The amount of creatine kinase MB with respect to total CK activity after reinfarction is higher than the amount after initial infarction.