Dual AV nodal pathways--vagal influences on AV nodal conduction

This 52-year-old male presented with syncope and demonstrated two distinct PR intervals on the electrocardiogram. Electrophysiologic studies showed dual AV nodal pathways. Right-sided carotid sinus massage induced prolonged periods of sinus arrest with no change in AH interval. Left-sided carotid sinus massage produced long AH intervals (slow pathway conduction) with some slowing of sinus rate. Whenever sinus rhythm with slow pathway conduction was observed (long AH) a 20-30 mmHg drop systolic pressure was seen. Following implantation of an AV sequential pacemaker, the patient has been asymptomatic.     

Dual AV Nodal Pathways—Vagal Influences on AV Nodal Conduction

This 52-year-old male presented with syncope and demonstrated two distinct PR intervals on the electrocar-diogram. Electrophysiologic studies showed dual A V nodal path ways. Right-sided carotid sinus massage induced prolonged periods of sinus arrest with no change in AH interval. Left-sided carotid sinus massage produced long AH intervals (slow pathway conduction) with some slowing of sinus rate. Whenever sinus rhythm with slow pathway conduction was observed (long AH) a 20-30 mmHg drop systolic pressure was seen. Following implantation of an AV sequential pacemaker, the patient has been asymptomatic.     

Effects of AV Sequential Versus Asynchronous AV Pacing on Pulmonary Hemodynamics

We studied the effects of various pacing modes on cardiac hemodynamics and pulmonary gas alterations in chronic heart blocked dogs. Changing the pacing mode from an atrioventricular interval of 100 ms (AV100) to a ventriculo-atrial interval of 100 ms (VA100) caused a significant fall in left ventricular pressure (117.64 +/- 11.91 to 95.60 +/- 16.58 mmHg) and cardiac output from 2.18 +/- 0.24 to 1.46 +/- 0.20 L/min. Following the change in pacing mode from AV100 to VA100, there was an increase in the alveolar-arterial O2 gradient from 23.28 +/- 6.97 to 28.74 +/- 8.43 mmHg and a decrease in the arterial CO2 tension from 32.42 +/- 3.22 to 29.42 +/- 3.22 mmHg. There was also a decrease in arterial CO2 tension when the AV100 pacing mode was compared to asynchronous ventricular pacing (32.42 +/- 3.22 versus 30.56 +/- 2.82 mmHg). The minute volume of O2 also decreased when the pacing mode was changed from AV100 to asynchronous ventricular pacing (0.134 +/- 0.01 versus 0.126 +/- 0.01 L/min) and decreased further at VA100 to 0.114 +/- 0.01 L/min. Other significant changes were also observed: the percent of expired CO2 decreased when the pacing mode was changed from AV100 to VA100 (3.68 +/- 0.13 versus 3.37 +/- 0.26%) or to asynchronous ventricular pacing (3.40 +/- 0.31%). The end-expiratory O2 increased and CO2 decreased when the pacing mode was changed from AV100 to VA100. The breath-by-breath correlation of end-expiratory O2 and CO2 with left ventricular systolic pressure showed an almost immediate increase in O2 and reduction in CO2 concentration associated with decreasing systolic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Permanent AV Block or Modification of AV Nodal Function by Selective AV Nodal Artery Ethanol Infusion

The acute and chronic effects of selective AV nodal artery ethanol infusion on AV nodal function was studied in 9 closed chest anesthetized dogs. Using standard percutaneous techniques of arterial catheterization, a 2.2 French infusion catheter was positioned in the AV nodal artery. Ten minute infusions into the AV nodal artery of 25%, 50%, or 100% ethanol in normal saline at rates of 0.5 mL/min acutely resulted in complete AV nodal block (AVB) in 5 dogs, 2:1 AV nodal block in 1 dog, and prolongation of AV nodal effective refractory period and/or Wenckebach cycle length in the remaining 3 dogs. One dog died with persistent complete AV block 1 week after the ethanol infusion. When restudied 4 weeks later, 7 of the 8 surviving dogs had persistent modification of AV nodal function, including complete AV block in 5 dogs and lengthening of AV nodal effective refractory period and/or Wenckebach cycle length without AV block in 2 dogs. Pathologic examination of the animals exhibiting chronic modification or ablation of AV nodal function revealed healing infarction of the AV node or its approaches. Distant myocardial necrosis was not observed and left ventricular function was normal. Slow infusion of low concentrations of ethanol into the AV nodal artery results in AV nodal modification or ablation due to localized necrosis in or around the AV node. This technique may have a role in AV nodal modification or ablation, particularly in patients who have failed DC shock or radiofrequency ablation.     

AV Pacing and LV Performance

Five patients with impaired left ventricular function (LV) and implanted AV sequential pacemakers underwent serial radionuclide angiograms. The goal was a non-invasive evaluation of the rapid changes in left ventricular performance elicited by rate, pacing mode and AV interval manipulation. End diastolic volume, end systolic volume, stroke volume and cardiac output were increased by AV sequential pacing in comparison with ventricular pacing at 70 beats per minute. No significant change in ejection fraction and blood pressure were noted with changing AV sequential pacing rates at usual pacing rates. Our data suggest that a short A V interval (150 ms) improved LV performance more than a long AV interval (250 ms). A non-invasive technique to optimize left ventricular performance on an acute basis by varying heart rate, AV interval and pacing mode with the implanted AV sequential pacemaker is feasible and may be useful in selective clinical situations.     

Dual AV nodal paths leading to AV nodal reentrant tachycardia.

A 27-year-old white female with a history of paroxysmal supraventricular tachycardia presented to the emergency department complaining of intermittent palpitations. Although no tachydysrhythmia was present, she was noted to have two distinct PR intervals during normal sinus rhythm while in the emergency department. The patient was referred for electrophysiologic study. This study demonstrated dual AV nodal paths, and AV nodal reentrant tachycardia was induced and terminated. She was placed on flecainide for outpatient management of her dysrhythmia. Dual AV nodal pathways leading to AV nodal reentrant tachycardia is discussed.     

A Nodoventricular Fiber Associated with Dual AV Nodal Conduction, AV Nodal Reentrant Tachycardia, and Anterior Location of the Slow AV Nodal Pathway

We present a case of a patient with a nodoventricular tract, associated with dual AV nodal conduction and AV nodal reentrant tachycardia, and an anteroseptal location of the slow AV nodal pathway. The remarkable feature of this case is the site of successful ablation, in the anteroseptum just anterior and superior to the His bundle, where both preexcitation and dual AV nodal physiology were abolished.     

Mechanisms of AV Node Reentrant Tachycardia in Young Patients With and Without Dual AV Node Physiology

Recent advances in electrophysiological mapping and radiofrequency catheter ablation have demonstrated the participation of perinodal atrial tissue or pathways in atrioventricular node reentrant tachycardia (AVNRT). Current concepts of the role of these pathways in the genesis of the various forms of AVNRT continue to evolve. In view of these recent advances, this study investigated the electrophysiology of AVNRT in young patients, and factors potentially associated with variant forms of this arrhythmia. Detailed programmed stimulation and catheter mapping were performed in 35 consecutive young patients with AVNRT. This group consisted of 15 male and 20 female patients, with a mean age of 12.1 ± 4.2 years (range 3–18 years). Of the 35 patients, 23 demonstrated dual AV node physiology, either in response to a critically timed extrastimulus (n = 17) or to rapid pacing (n = 6). The common form (antegrade slow-retrograde fast) of AVNHT was demonstrated in 21 of these 23 patients. Antegrade fast-retrograde slow (n = 1) and antegrade slow-retrograde slow (n = 1) forms of AVNRT were identified in the 2 other patients. In contrast, only 5 of the 12 patients who did not demonstrate dual AV node physiology had the common form of AVNRT (P = 0.03). Eive of these patients also had the slow-slow form of AVNRT, while 1 patient each had a fast-slow and fast-fast form of AVNRT. Patients with dual AV node physiology were older (14.2 ± 2.0 years) and more likely to be female (16 of 23) than patients in whom dual A V node physiology was not identified, where the mean age was 10.6 ± 4.2 years and only 4 of 12 patients were female (P = 0.02 for age and P = 0.07 for gender). These observations suggest that the physiology of AV node reentry may evolve as a function of age, with slow-fast AVNRT prevalent in adolescents. However, absence of dual AV node physiology should not preclude diagnosis of AVNRT in young patients with supraventricular tachycardia, in whom atypical forms of AVNRT may be common.     

Controlled Cryothermal Injury to the AV Node: Feasibility for AV Nodal Modification

Elective subtotal injury to the AV node-His bundle region may create a negative dromotropic effect to provide a therapeutic advantage in some patients with supraventricular tachycardia without creating complete AV block. We examined the effects of cryosurgery to the AV nodal region, varying temperature and time using a 15 mm circular cryoprobe applied directly to the canine AV node-His bundle region. Twelve dogs were anesthetized and the heart was exposed through a right thoracotomy. Electrophysiological data obtained included conduction intervals, incremental pacing, and extrastimulus testing. Under inflow occlusion, the cryoprobe was positioned over the AV node-His bundle region using anatomical landmarks and a single freeze was applied (-15 degrees C to -60 degrees C, 15 to 60 seconds). Dogs were allowed to recover for 1 month, after which time electrophysiological testing was repeated under similar conditions; then the animals were sacrificed. With probe temperatures of -60 degrees C for 15 to 60 seconds, five of six dogs experienced complete heart block with dense fibrosis observed in the AV nodal-His bundle region. After freezing with higher temperatures, the remaining seven dogs had return of atrioventricular conduction postoperatively with prolongation of AH time observed in five and marked prolongation of the Wenckebach cycle length in three of the five. We conclude that controlled cryothermal injury to the AV node-His bundle region may be useful to create a desirable negative dromotropic response without creating complete AV block.     

Simultaneous AV Nodal Reentrant and Ventricular Tachycardias

Simultaneous AV nodal reentrant and ventricular tachycardias were observed during the course of an electrophysiological study in a 51-year-old patient who suffered from recurrent attacks of sustained ventricular tachycardia. Occurrence of simultaneous tachycardias was facilitated by the fact that both tachycardias had a similar cycle length. Ventricular tachycardia was most probably initiated by AV nodal tachycardia previously induced by atrial extrastimulation following the administration of atropine.     

Spontaneous Manifestation of Dual AV Nodal Pathways Resulting in Complex Patterns of AV Conduction

Dual intranodal pathways are not uncommonly demonstrated at electophysiological study¹ especially in patients with intranodal re-entrant tachycardias.^2-3 This type of tachycardia is the most common spontaneous manifestation (albeit indirect) of dual AV nodal pathways. Other forms of spontaneous expression of dual atrio-His conduction are rare,^4–6 In this report we describe a patient who exhibited complex atrioventricular conduction patterns over two intranodal pathways.     

Plasma ANP and Cyclic GMP Levels Versus Left Ventricular Performance at Different AV Delays in AV Sequential Pacing

Eleven resting patients with an implanted DDD pacemaker were studied. After 30 minutes of AV sequentiai pacing at a rate of 80 beats/min with three consecutive atrioventricular delays (AVDs; 100, 150, and 200 msec) peripheral venous blood was drawn for further analyses by specific radioimmunoassays of atrial natriuretic peptide (ANP) and the ANP second messenger, cyclic guanosine monophosphate (cGMP). Relative changes in left ventricular (LV) stroke volume following alterations of AVD were assessed by means of pulsed-Doppler echocardiography through measurement of LV outflow time-velocity integrals (TVI). The optimal AVD (oA VD) was defined in individual patients as that which was associated with the greatest TVI and with improvement over both other AVDs of more than 4%. The oA VD was found in nine patients. For these nine patients no significant differences in either plasma ANP or cGMP between various AVDs were observed. However, we found such differences with respect to values measured at oAVD; both ANP and cGMP levels were lowest at oAVD. Pooling together the data obtained in 11 patients at three AVDs, a positive correlation between ANP and cGMP levels was found (r = 0.7, P < 0.0001. n = 33). Moreover, changes of plasma ANP and cGMP induced by every A VD increment of 50 msec were also correlated (r = 0.6, P < 0.01, n = 22). It is concluded that in AV sequential pacing at rest piasma ANP reaches minimal levels at the AVD, which provides the best LV performance. Although levels of cGMP changed in parallel with those of ANP, low relative values of cGMP differences may limit the usefulness of cGMP assays in optimization of the AVD.