Delineation of AV Conduction Pathways by Selective Surgical Transection: Effects on Antegrade and Retrograde Transmission

Introduction: The role for transitional cells as determinants of AH and HA conduction was examined in the superfused rabbit AV junction.Methods: Bipolar electrodes and microelectrodes were used to record antegrade A-H and retrograde H-A activation, before and after transection of the transitional cell input to the compact AV node.Results: During pacing from the high right atrium, inferior to the coronary sinus os, beneath the fossa ovalis, or on the anterior limbus, AV Wenckebach block (WB) was mediated by identical transitional cells grouped in close apposition to the compact AV node. Paced WB cycle lengths were shorter from the high right atrium (196 ± 12 msec) and inferior to the coronary sinus os (195 ± 8 msec) versus the fossa ovalis (217 ± 9 msec) or anterior limbus (206 ± 11 msec). With His bundle pacing, retrograde HA WB (211 ± 17 msec) was observed within the N cell region within the compact AV node. After transection of posterior and superior transitional cell input to the compact AV node, the antegrade AH WB cycle length was prolonged (245 ± 18 msec), with an increased WB incidence within the NH region (compact AV node)(5% to 41%; p = 0.014). The incidence of retrograde HA WB determined within the NH region was increased (30% to 88%), with a decrease in the stimulus-fast pathway conduction time (98 ± 7 to 49 ± 6 msec; p < 0.01).Conclusions: The data demonstrate (1) a common transitional cell population determining AH WB, independent of atrial stimulation site, and (2) a plasticity of transitional cell-compact AV node connections, with rapid AH and HA conduction favored by removal of posterior/superior AV nodal input.Supported by a grant from the American Heart Association, Oklahoma Affiliate.     

Differential interaction of adrenergic and cholinergic effects on AV junctional automaticity and AV conduction

The effects of postsynaptic autonomic interactions on atrioventricular (AV) junctional automaticity and AV conduction were studied in six canine heart in situ using direct injections of norepinephrine (NE) and physostigmine (PSM) into the AV node artery. Injection of NE (0.05 microgram/ml, 2 ml) caused an AV junctional rhythm (AVJR) in every dog. After injection of PSM (10 micrograms/ml, 2 ml), the responses of AVJR to NE were virtually identical to those observed before cholinesterase inhibition (160 +/- 13 vs 162 +/- 12 bpm). In contrast, this moderate cholinesterase inhibition still had a readily demonstrable negative dromotropic effect. In any given dog, depressed AV conduction was characterized by one of two types (I and II) of retrograde atrial capture during AVJR. Before PSM in the AV junction, onset of atrial depolarization during AVJR preceded the onset of ventricular depolarization in both type I and type II responses. After PSM, atrial depolarization occurred later with respect to ventricular depolarization (i.e., during or mostly after ventricular activation) in type I, whereas in the type II responses atrial depolarizations began much earlier than before PSM, thus being completed long before the onset of ventricular activation. Because of such differential responsiveness of AV junctional automaticity and AV conduction and because of the two types of intranodal conduction observed after administration of PSM into the AV junction, we can postulate that under appropriate autonomic imbalance retrograde or antegrade AV block could readily develop in spite of preserved AV junctional automaticity.     

Nonparoxysmal atrioventricular junctional rhythm. A clinical and electrophysiologic study

The patient, a 74-year-old man, developed a persistent nonparoxysmaljunctional accelerated rhythm at rate of 60-75 beats min^–1because of chronic depressed sinus node function. Intravenousatropine resulted in no change of junctional pacemaker ratebut i.v. isoproterenol significantly accelerated it suggestingthat autonomic neural imbalance might underlie the mechanismof nonparoxysmal junctional rhythm. Intravenous verapamil (10mg) induced no change in the junctional pacemaker rate and postpacingpauses suggesting that the slow inward current did not playan important role in the nonparoxysmal junctional rhythm.     

Electrical ablation of junctional tachycardias showing a long RP interval

Transvenous catheter ablation of the anomalous pathway was attemptedin seven patients with drug-resistant repetitive long RF tachycardias.The patients were aged 5·5–65 years (median 20years) and had received from four to seven antiarrhythmic agentswithout effect. Electrophysiological studies confirmed the anomaloussubstrate for tachycardia in five patients but in two patientsan intranodal mechanism could not be excluded. Discharges weredelivered to the coronary sinus ostium or low right atrium closeto the ostium using conventional defibrillators (three patients)or a modified device (four patients). Transient A V block wasseen after six attempts progressing to permanent block in onepatient. In no patient could enduring block in the retrogradelimb of tachycardia be achieved, and tachycardia recurred inall patients in whom anterograde conduction remained intact.The failure of selective ablation techniques in long RP tachycardiamay reflect the diversity of substrate anatomy or particularproperties (anatomical or functional) of the pathway comparedwith the usual types of anomalous pathway.     

Manifest and concealed AV nodal reentry in wenckebach type of AV conduction with AV junctional escape rhythm

An electrocardiogram was obtained that was characterized by sinus rhythm with progressive prolongation of the PR interval not followed by a blocked sinus impulse. After a critically long PR interval, the QRS complex was followed by a premature P′ wave, representing an echo beat, a manifest reentry in the atrioventricular (AV) node. The pause, occasioned by the premature P′ wave, was at times interrupted by an AV junctional escape beat, occurring with an escape interval of 1.21–1.24 seconds. On other occasions, however, the escape beat did not manifest on schedule, even though the pause was markedly longer than the escape cycle. This suggested that the manifest reentry was followed by a further concealed reentry, resulting in inapparent discharge of the AV junctional escape pacemaker, whose firing was postponed, thereby allowing the sinus impulse to capture the ventricles.     

Combined effects of glucose and hypoxia on cardiac automaticity and conduction

The combined effects of glucose and graded hypoxia on automaticity and conduction were studied in the isolated sinoatrial (SA) node, right atrium and atrioventricular (AV) node of the rabbit heart, and in the conducting system of isolated right canine ventricles. Transmembrane action potentials were recorded simultaneously with the extracellular His bundle electrogram. At normoxia (PO₂ 460 mmHg), variations in the extracellular glucose concentration between 0 and 50 mm had no significant effect on automaticity and conduction within the different cardiac regions. At moderate hypoxia (PO₂ 130 mmHg), absence of glucose significantly prolonged the post-stimulatory sinus-node recovery time but the sinus rate and the conduction parameters were not significantly related to the extracellular glucose concentration. At severe hypoxia (PO₂ 40 mmHg), the nodal electrical activity including sinus rate, SA and AV nodal potential amplitude and conduction were markedly dependent on the extracellular glucose concentration; 50 mm glucose considerably improved the depressed nodal function. In contrast, the atrial and particularly the ventricular conduction parameters were much less sensitive to substrate-free media even at severe hypoxia. The results indicate that glucose combined with hypoxia predominantly affects the slow response activity but has only little action on the fast Na inward current.     

Selective experimental chelation of calcium in the AV node and His bundle

There are P cells in the human and canine AV (atrioventricular) node which are virtually devoid of gap junctions. All other components of myocardial cellular connections are calcium-dependent except the gap junction. Direct perfusion of disodium EDTA through the AV node artery of 16 anaesthetized dogs produced three immediate effects: complete AV block, a rapid irregular atrial rhythm and a separate rapid irregular ventricular rhythm. The atrial arrhythmia was short in duration and sinus rhythm resumed, initially with complete AV and VA block; both waned until normal AV conduction returned in each dog. In 3 of the 16 dogs there was transient complete AV block during which two independent His potentials were separately associated with the atrial and ventricular complexes. When conducted sinus rhythm resumed, there was initially A-H prolongation (but not H-V). Atropine, propranolol and reserpine had no influence on any electrophysiologic effect of EDTA. Both tachycardias probably originate in P cells of the AV node, the irregularity being attributable to varying enhancement of automaticity plus functional disaggregation of P cells. AV block is attributed to failure of conduction between disaggregated P cells, which in turn must be an obligatory pathway for normal AV conduction, because of their anatomic interposition. The findings further suggest that the AV nodal P cells are the site of the normal 40 ms delay in AV conduction, and that they may be the site of origin of the His potential.     

Observations on variability of atrioventricular nodal conduction in man and the dual-pathway response

A study was made of nodal conduction times of atrial stimuliwith fixed coupling intervals, in 23 patients divided into twogroups according to their atrial stimulus test response: GroupI (continuous AV node function curve; 17 cases) and Gruop II(dual AV node pathway; six cases). The stimulation protocolinvolved the delivery of 75 stimuli with a fixed coupling interval20 ms greater than the effective refractory period (ERP) ofthe AV node (Group I) or fast pathway (Group II). The atrialcoupling intervals (A1A2) and node conduction times (A2H2) weremeasured. An evaluation was made of the dispersion of intervalswith range (R) and of the distribution of A2H2 times (² test). In both Groups, R (A2H2) was greater than R(A1A2) (P<0.05):R(A2H2) in Group II was greater than R(A2H2) in Group I (P <0.001). In Group I the distribution of A2H2 was non-normal infour cases and bimodal in five; in Group II the distributionwas non-normal and bimodal in all cases. It is concluded that: (1) the AV node generates a dispersionin its conduction times in the vicinity of its ERP, althoughthe nodal conduction curve is continuous: and (2) the so-calleddual pathway may constitute an exaggeration of AV node responseinhomogeneity.     

Differential Effect of Esmolol on the Fast and Slow AV Nodal Pathways in Patients with AV Nodal Reentrant Tachycardia

Esmolol Effect on AV Nodal Pathways. Introduction: AV nodal reentrant tachycardia (AVNRT) usually involves anterograde conduction over a slowly conducting (“slow”) pathway and retrograde conduction over a rapidly conducting (“fast”) pathway. A variety of drugs, such as beta blockers, digitalis, and calcium channel blockers, have been reported to prolong AV nodal refractoriness in both the anterograde and retrograde limbs of the circuit. However, few data are available that address whether the fast and slow pathways respond in a quantitatively different manner to drugs such as beta-adrenergic antagonists. In addition, it is not known whether the effects of these agents on refractoriness parallel the effects on conduction in the fast and slow pathways. The present study was performed to measure the effect of the intravenous beta-adrenergic agent, esmolol, on refractoriness and conduction in both the fast and slow AV nodal pathways in patients with AVNRT. Methods and Results: Thirteen patients with discontinuous AV nodal conduction properties and typical AVNRT were studied. Anterograde and retrograde AV nodal functional assessment was performed at baseline and following steady-state drug infusion of intravenous esmolol at a dose of 500 μg/kg for 1 minute, 150 /μg/kg per minute for the next 4 minutes, followed by a continuous maintenance infusion of 50 to 100 μg/kg per minute. The anterograde effective refractory period of the fast pathway increased from 381 ± 75 msec at baseline to 453 ± 92 msec during the infusion of esmolol (P = 0.003). The anterograde effective refractory period of the slow pathway was also prolonged by esmolol, from 289 ± 26 msec to 310 ± 17 msec (P = 0.005). However, the absolute magnitude of the change in the anterograde effective refractory period of the fast pathway (+72 ± 59 msec) was significantly greater than the change in anterograde effective refractory period of the slow pathway (+21 ± 16 msec, P = 0.01). The mean retrograde effective refractory period of the fast pathway increased from 276 ± 46 msec to 376 ± 61 msec during esmolol infusion (P = 0.03). Retrograde slow pathway conduction that could not be demonstrated at baseline became manifest in three patients during esmolol infusion. In contrast to the effects of esmolol on refractoriness, the AH interval during anterograde slow pathway conduction prolonged to a far greater extent (+84 msec) than the HA interval associated with retrograde fast pathway conduction (+5 msec, P = 0.04). Conclusion: The beta-adrenergic antagonist, esmolol, has a quantitatively greater effect on anterograde refractoriness of the fast than the slow AV nodal pathway. However, the effects on conduction intervals during AVNRT are greater in the anterograde slow pathway than in the retrograde fast pathway. These observations suggest that the fast and slow pathways may have differential sensitivities to autonomic influences. This difference in the response to beta-adrenergic antagonists may be exploited as a clinically useful method for demonstrating slow pathway conduction in some individuals with AVNRT.     

Control of supraventricular tachycardia by VVI pacing in a patient with drug-induced enhanced atrioventricular conduction

A 56-year-old male with atrial fibrillation developed rapid ventricular response up to 200 beats/min or more in the postoperative stage of emergency aortocoronary bypass surgery. Resuscitation for cardiac arrest triggered this rapid ventricular rate. The idea that retrograde conduction into atrioventricular node may prevent ventricular capture of atrial fibrillation was tested. The ventricle was then paced at rapid rate followed by a gradual decrease in the pacing rate to 120 beats/min. By this method, ventricular rate was controlled and hemodynamics stabilized, with more efficiency of intra-aortic balloon counterpulsation. VVI pacing may be used in this manner to control irregular and rapid ventricular response of atrial fibrillation.     

Electrophysiological effects of quinidine alone and of the combination quinidine-verapamil on av conduction in humans

The influence of 320 mg quinidine administered intravenously (i.v.), as well as subsequent administration of 5 mg verapamil i.v. on atrioventricular conduction was studied in 8 patients during sinus rhythm and atrial stimulation with the aid of His bundle electrography. Among the electrophysiologic parameters of the atrium the sinus rate increased significantly after quinidine and again increased slightly after subsequent administration of verapamil. During sinus rhythm the PA interval was not influenced by either substance. Conversely, during atrial stimulation the STA interval increased significantly under the effect of quinidine, while verapamil had no further influence. As an indicator of conduction time in the AV node, the AH interval was decreased significantly by quinidine during sinus rhythm and atrial stimulation. This effect was significantly counteracted by the additional administration of verapamil. The HV interval as a measure of the His-Purkinje conduction was not significantly affected. The QRS duration was increased significantly by quinidine and was not further influenced by verapamil. The QT_C and QT intervals increased significantly after administration of quinidine and were again slightly, but significantly shortened by verapamil. Our investigations show that the combination of quinidine and verapamil, which has clinically been found to have a higher conversion rate than quinidine alone, is well justified from an electrophysiologic point of view and that undesirable quinidine-related effects, such as rapid AV conduction in cases of atrial fibrillation and flutter, can be avoided by the subsequent administration of verapamil.     

Quality of life and exercise capacity in patients with prolonged PQ interval and dual chamber pacemakers: a randomized comparison of permanent ventricular stimulation vs intrinsic AV conduction.

AIMS: The aim of this study was to assess quality of life (QoL) and exercise capacity during permanent ventricular stimulation (PVS) compared with intrinsic atrioventricular conduction (IAVC) in patients with dual chamber pacemakers (PMs) and an intrinsic PQ interval >210 ms. Dual chamber PMs in patients with atrioventricular (AV) block are usually programmed to PVS in VDD or DDD mode, although IAVC is preserved, but prolonged. This results in PVS, although long periods of IAVC may occur. METHODS AND RESULTS: Fourteen consecutive patients (age 76 +/- 6 years; intermittent high degree AV block in six patients, binodal disease in eight patients) were enroled in a prospective, randomized, single blind, crossover study of IAVC vs PVC. To permit IAVC, programmed AV delays were prolonged. At the end of each phase, QoL scores were assessed using a questionnaire and echocardiography and cardiopulmonary stress tests were performed. During the study period with IAVC, 95 +/- 10% of the beats were conducted intrinsically. QoL scores (28.3 +/- 11 vs 29.3 +/- 13; P = 0.68), peak exercise capacity (5.4 +/- 2.4 vs 5.2 +/- 2.9 METs; P = 0.35) and peak oxygen uptake (19.8 +/- 4.5 vs 18.8 +/- 5.2 ml/kg/min; P = 0.16) were comparable during IAVC and PVS, respectively. Similar echocardiographic values were found for left ventricular (LV) ejection fraction (50 +/- 9% vs 51 +/- 10%; P = 0.67) and velocity time integral at the left ventricular outflow tract (24 +/- 5 vs 22 +/- 6 cm; P = 0.20), respectively. CONCLUSIONS: We conclude that in patients with dual chamber PMs and intermittent high degree AV block neither PVS nor IAVC is superior with respect to QoL or exercise capacity. Therefore, pulse generators may be programmed to IAVC to extend their longevity.     

Effect of site, summation and asynchronism of inputs on atrioventricular nodal conduction and refractoriness

The impulses coming from the sinus node synchronically penetratethe A V node via the crista terminalis and inter-atrial septum.Studies in superfused rabbit AV preparations suggest that thecrista terminalis is a more effective input than the inter-atrialseptum, and that the summation of both inputs facilitates AVnodal conduction. The aim of this study was to verify the hypothesisin a more physiological model, such as the whole rabbit heartperfused by a Langendorff system. Fifteen rabbit hearts were studied in a Langendorff perfusionsystem with six bipolar extracellular electrodes: two for stimulating(crista terminalis and inter-atrial septum) and four for recording(crista terminalis, inter-atrial septum, His bundle electrogramand right ventricle). Seven hearts (Group I) were consecutivelypaced at the crista terminalis, inter-atrial septum and bothsites simultaneously, to determine the AV nodal Wenckebach cyclelength and effective refractory period under basal conditionsand after acetylcholine (0.75 x 10^–6 M). In eight heartsunder 0.75 x 10^–6 M acetylcholine (Group II), the cristaterminalis and inter-atrial septum were simultaneously (delay= 0 ms) or sequentially (delay = 2,4, 6,8,10,12,14,and 16 ms)stimulated to calculate the AV nodal effective refractory periodand the AH interval at an atrial coupling interval 5 ms longerthan the AV nodal effective refractory period, for each delaytested. There were no basal differences in AV nodal parameters duringcrista terminalis pacing, inter-atrial septum pacing or simultaneousstimulation in both sites in Group I; after acetylcholine, theAV nodal Wenckebach cycle length and effective refractory periodtended to be shorter during crista terminalis pacing (cristaterminalis = 188 ±33 and 147±34; inter-atrialseptum = 195±35 and 158±35; both sites = 195±34and 154±36; values expressed in cycle length of pacing-ms),although the differences did not reach statistical significance.In Group II, the AH interval tended to prolong slightly on increasingthe delay between crista terminalis and inter-atrial septumstimulation (delay 0 = 119±31, 2 = 125±29, 4 =129±33,6 = 129±29,8 = 128±30,10 = 134±34,12= 132±35,14 = 129±32,and 16 = 131 ±31 ms),butagain the differences did not reach statistical significance;the A V nodal effective refractory period did not change whenthe delay was varied. Conclusions: (1) Neither the input site nor the synchronoussummation of inputs plays an important role in A V nodal conduction.(2) These results suggest that A Vnodal response during atrialtachyarrythymias depends more on atrial rate than on shiftingsin site and time coupling of inputs.     

三磷酸腺苷对室房传导的电生理作用

目的　探讨三磷酸腺苷 (adenosine triphosphate,ATP)对房室结双径路参与的房室交界区折返性心动过速和旁路参与的房室折返性心动过速患者的室房传导的电生理作用。　方法　 39例房室交界区折返性心动过速和 6 7例房室折返性心动过速患者在右心室起搏 (频率 140次 / m in)时 ,经股静脉快速注射 ATP 2 0 mg,连续记录体表心电图和心内电图 ,观察室房传导变化。　结果　房室交界区折返性心动过速组 33例 (84.6 % )在注射 ATP后出现室房阻滞 ,其余 6例无变化。6 7例房室旁路患者在消融前 ,6 1例 (91% )室房传导无变化 ,另 6例出现室房阻滞 ,其中 2例具递减性传导 ;而在消融后 2 4例右心室起搏频率超过 16 0次 / m in,仍为 1∶ 1逆传 ,注射 ATP后 2 3例出现室房阻滞 ,仅 1例不受影响。　结论　 ATP对房室结及旁路的电生理作用不同 ,注射 ATP后出现室房阻滞对鉴别经房室结或旁路逆传有一定价值 ,是旁路消融成功的一个判别指标 ,但并不一定完全可靠     

Complete AV Block Following Mediastinal Radiation Therapy: Electrocardiographic and Pathologic Correlation and Review of the World Literature

The clinical, features, serial electrocardiograms, and autopsy findings of a patient with symptomatic complete AV block, who had received mediastinal radiation therapy 81/2 years previously, are presented. The cardiac histopathology disclosed immense fibrosis of the conduction system and of the atria and ventricles. The enormous amount of fibrosis was similar in location and intensity to that observed in our previously reported patient (Cohen et al., Arch Intern Med 1981;141:676-679) who had undergone mediastinal radiation. We conclude that the severe fibrosis was primarily due to radiation, rather than secondary to atherosclerotic coronary artery disease, which also has been described as a consequence of mediastinal radiotherapy. This patientÆs serial electrocardiograms disclosed evidence of complete block both in the AV nodal area and infra His system, which correlated well with the histopathology. The characteristic clinical features of patients with symptomatic complete AV block post mediastinal radiation therapy are presented, along with a review of the world literature.     

Differential effects of defibrillation on systemic and cardiac sympathetic activity

OBJECTIVE: To assess the effect of defibrillation shocks on cardiac and circulating catecholamines. DESIGN: Prospective examination of myocardial catecholamine balance during dc shock by simultaneous determination of arterial and coronary sinus plasma concentrations. Internal countershocks (10-34 J) were applied in 30 patients after initiation of ventricular fibrillation for a routine implantable cardioverter defibrillator test. Another 10 patients were externally cardioverted (50-360 J) for atrial fibrillation. MAIN OUTCOME MEASURES: Transcardiac noradrenaline, adrenaline, and lactate gradients immediately after the shock. RESULTS: After internal shock, arterial noradrenaline increased from a mean (SD) of 263 (128) pg/ml at baseline to 370 (148) pg/ml (p = 0.001), while coronary sinus noradrenaline fell from 448 (292) to 363 (216) pg/ml (p = 0.01), reflecting a shift from cardiac net release to net uptake. After external shock delivery, there was a similar increase in arterial noradrenaline, from 260 (112) to 459 (200) pg/ml (p = 0.03), while coronary sinus noradrenaline remained unchanged. Systemic adrenaline increased 11-fold after external shock (p = 0.01), outlasting the threefold rise following internal shock (p = 0.001). In both groups, a negative transmyocardial adrenaline gradient at baseline decreased further, indicating enhanced myocardial uptake. Cardiac lactate production occurred after ventricular fibrillation and internal shock, but not after external cardioversion, so the neurohumoral changes resulted from the defibrillation process and not from alterations in oxidative metabolism. CONCLUSIONS: A dc shock induces marked systemic sympathoadrenal and sympathoneuronal activation, but attenuates cardiac sympathetic activity. This might promote the transient myocardial depression observed after electrical discharge to the heart.     

快速心室率心房纤颤的房室传导改良

对１３例药物难以控制的快室率心房纤颤（房颤）病人进行经射频消融房室传导改良，射频消融靶点选择右房内房间隔之后、中或前部。射频能量为２０～３０Ｗ，平均发放射频８±３次。结果：９例房室改良成功，３例失败，１例于术后３天发生Ⅲ°房室传导阻滞。９例术后２天及２个月休息时心率、活动时心率、最高心率及最低心率较术前有明显下降（Ｐ＜０．０５）．１例于术后１１个月复发，其机理与部分或全部损伤后结间束或部分损伤房室结有关。认为射频消融房室传导改良为治疗药物难以控制的快室率房颤的一种相对安全有效的方法。     

三磷酸腺苷对窦房结及房室传导的电生理作用

为探讨三磷酸腺苷对窦房结及房室传导的电生理作用,在20例阵发性室上性心动过速患者(隐匿性预激征8例、显性预激征及房室结双径路各6例)窦性心律时经右股静脉弹丸式注射三磷酸腺苷20mg.结果注射后窦性频率出现先减慢、继而窦性心动过速的双相反应;16例出现一过性房室传导阻滞,保护性心室起搏时8例1:1室房传导(均为隐匿性预激征),8例出现室房传导阻滞(其中6例为房室结双径路,2例为右侧显性预激综合征).提示三磷酸腺苷对窦房结、房室结传导及少数旁道有抑制作用.