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.     

Effect of verapamil on retrograde conduction in atrioventricular nodal reentrant tachycardia

Using His bundle electrograms, incremental ventricular pacing and the ventricular extrastimulus (V2) technique, the effects of intravenous verapamil, 0.2 mg/kg, on retrograde atrioventricular (AV) nodal conduction during ventricular pacing, premature ventricular stimulation (H2A2 interval) and paroxysmal supraventricular tachycardia (SVT) (H-Ae interval) were evaluated in 11 patients with AV nodal reentrant tachycardia. During the control study, SVT could be induced in all 11 patients. After verapamil administration, SVT or atrial echo beats could be induced in 5 patients. Verapamil produced ventriculoatrial (VA) block at a longer cycle length than that during the control study in 10 of 11 patients (295 +/- 27 vs 352 +/- 40 ms, p less than 0.01), but prolonged H2A2 interval in only 5 of 11 patients (37 +/- 6 vs 60 +/- 31 ms, p less than 0.05). In all 5 patients with persistence of inducible SVT or atrial echo beats after verapamil treatment, the H-Ae interval remained unchanged even though in 4 of these 5 patients VA conduction time or H2A2 interval was prolonged. Correlation between the paced cycle length which induced VA block, the shortest V1H2 interval achieved during premature ventricular stimulation and the cycle length of SVT revealed that in all instances in which verapamil induced VA block at a longer cycle length than in controls but did not prolong H2A2 or H-Ae interval, the shortest V1H2 interval and the cycle length of SVT (H-H interval) were significantly longer than the ventricular paced cycle length which produced VA block.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ventricular Echo Beats and Retrograde Atrioventricular Nodal Exits in the Dog Heart: Multiplicity in Their Electrophysiologic and Anatomic Characteristics

INTRODUCTION: A single ventricular echo beat frequently is induced in the dog heart by ventricular pacing, but it has not been investigated using a concomitant ablative technique. We studied the effects of ablating the anterior atrial input to the AV node on ventricular echo beats induced in the dog heart to evaluate their electrophysiologic characteristics, the anatomic reentrant circuit, and the retrograde AV nodal exits. METHODS AND RESULTS: In 20 dogs, an epicardial radiofrequency current was applied to the right anterior septum in an attempt to ablate the anterior input to the AV node. Ventricular programmed stimulation was performed to evaluate the ventricular echo beat and the retrograde AV nodal exit before and after ablation. The AV junction was examined with light microscopy. Seventeen dogs in which the PR interval was prolonged significantly from 108+/-17 msec to 153+/-19 msec (P < 0.001) were selected for ventricular echo evaluation; 3 dogs in which persistent second- or third-degree AV block was induced by ablation were excluded. Ventricular echo beats, which were induced in 13 of 17 dogs, were classified into the anterior type (n = 6) or posterior type (n = 7) according to the earliest atrial activation site during the echo beat. The retrograde AV nodal exit site showed anterior-exit only (n = 10), posterior-exit only (n = 2), and dual-exit (n = 5) patterns. After ablation, the anterior-type ventricular echo beat was noninducible in all 6 dogs, whereas the posterior-type ventricular echo beat was noninducible in only 3 of 7 dogs. In 17 dogs, VA conduction was not demonstrated after ablation in 3 dogs, all of which showed the anterior-exit only pattern. CONCLUSION: The effect of ablation on the ventricular echo beats and retrograde AV nodal exit site suggests multiplicity in their electrophysiologic and anatomic characteristics in the dog heart.     

Transient entrainment and interruption of atrioventricular node tachycardia

The possibility of transiently entraining and interrupting the common type of atrioventricular (AV) node tachycardia (anterograde slow, retrograde fast AV node pathway) was studied using atrial and ventricular pacing in 18 patients with paroxysmal AV node tachycardia. Transient entrainment occurred in all patients. During atrial pacing, localized block in the AV node for one beat followed by anterograde conduction over the fast pathway was observed in three patients. During ventricular pacing, localized block for one beat followed by retrograde conduction over the slow pathway was not observed in any patient. Neither atrial nor ventricular fusion beats were observed during entrainment. These observations indicate in a way not previously shown that reentry involving two functionally dissociated pathways in the AV node is the underlying mechanism of paroxysmal AV node tachycardia. The inability to demonstrate atrial or ventricular fusion beats during entrainment suggests a true intranodal location of the reentrant circuit. Finally, the ability to transiently entrain intranodal tachycardia demonstrates that this electrophysiologic phenomenon is not exclusively limited to macroreentrant circuits.     

Triple antegrade nodal pathway in a patient with supraventricular paroxysmal tachycardia

A 69-year-old patient is described in whom programmed atrial extrastimulus testing revealed dual discontinuity of atrioventricular nodal conduction suggesting a triple antegrade nodal pathway. In this patient, programmed right ventricular pacing initiated two types of tachycardia due to intranodal reciprocating rhythms. In both cases, antegrade conduction occurred via the slow nodal pathway, and retrograde conduction by the fast and intermediate pathways, respectively. During ventricular extrastimulus testing, a single echo beat was elicited via a third circuit: the intermediate nodal pathway in a retrograde direction, and the fast pathway in an antegrade direction.     

Differential effects of sympathetic activity on AV junctional automaticity and AV conduction

Summary Rapid ventricular response during episodes of supraventricular tachycardia are often followed, on abrupt cessation of the tachycardia, by prolonged pauses terminated by a sluggish and sometimes erratic escape of a supraventricular pacemaker. Such chronotropic-dromotropic paradoxes are readily reproduced in the animal laboratory following elimination of the sinus node and bilateral decentralization of the stellate ganglia and vagi. This study examined whether left stellate stimulation (0.5, 1, 2, 4, 8 and 16 Hz) or lack thereof differentially affected AV junctional automaticity and AV conduction. In the absence of any sympathetic neural activity (maximal sympathetic deficit), the AV junctional rate averaged a mere 22±2 percent of its peak performance, whereas under the same conditions, anterograde AV conduction averaged 73±5 percent and retrograde VA conduction 56 ±13 percent of their respective peak performances. On comparing the response curve (normalized responses) for AV junctional automaticity with that obtained for anterograde AV conduction the differences were significant at all frequencies between 0 and 4 Hz. Retrograde VA conduction (as assessed by the fastest ventricular pacing rate still conducted 11 to the atria) was always significantly less than anterograde AV conduction (as assessed by the fastest atrial pacing still conducted 11 to the ventricles). These results indicate that AV junctional automaticity is considerably more affected by sympathetic deficit than are either anterograde or retrograde AV conduction. In other words, AV junctional automaticity is far more dependent upon sympathetic input than AV conduction. While sympathetic influence is critical to the escape and maintenance of AV junctional automaticity both anterograde and retrograde AV conduction are remarkably resilient even under conditions of severe sympathetic deficit.     

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.     

Procainamide and retrograde atrioventricular nodal conduction in man

Recent studies that show a depressant effect of procainamide (PA) on retrograde conduction in patients with atrioventricular (AV) nodal reentrant tachycardia (RT) have suggested possible incorporation of AV nodal bypass tracts. Electrophysiologic effects of i.v. PA, 10 mg/kg, on retrograde AV nodal conduction were examined in 13 patients without RT, demonstrable AV nodal refractory period curves, or accessory pathways. Ventriculoatrial (VA) conduction was recorded before and after PA using intracardiac electrograms, incremental ventricular pacing and extrastimulation. With incremental pacing during the control, VA block occurred at a mean cycle length (CL) of 364.6 +/- 87.9 msec. After PA, VA conduction was abolished in five of 13 patients due to onset of retrograde block in the AV node; in seven of 13, VA block occurred at a longer paced CL after PA (344.2 +/- 51.2 msec vs 477.1 +/- 93.2 msec). In one patient, PA did not affect VA conduction. PA invariably produced prolongation in the VA interval at comparable CL of pacing. With ventricular premature stimulation, the retrograde H2A2 intervals during the control period were short (less than 50 msec) in seven of 13, intermediate (60-100 msec) in three of 13 and long (greater than 100 msec) in three of 13 cases. PA either abolished H2A2 conduction (H2 but no A2) or prolonged the H2A2 intervals by 5-20 msec in most cases in this series. The data suggest that i.v. PA almost uniformly depresses retrograde AV nodal conduction in the intact human heart. This depressant response to PA is not indicative of presence of partial or complete AV nodal bypass tracts.     

导管消融具有双向传导特性的Mahaim结室纤维

目的介绍具有双向传导特性Mahaim结室纤维的电生理机制及导管消融方法。方法患者女性,34岁,反复发作性心动过速病史7年。外院心电图示“阵发性室上性心动过速”。心动过速可被维拉帕米及普罗帕酮终止。入院各项检查排除器质性心脏病后行电生理检查及导管消融术。结果电牛理检查示窦性心律时AH=73ms、HV=42ms,QRS时限100ms。心动过速时QRS波形态与窦性心律时相似,伴有轻度电交替。心动过速在多数情况下室房呈分离状态,HV问期为42ms,与窦性节律时相同,有时室房呈1：1传导,最早心房激动位于希氏束记录处。右心室心尖部以400ms周长刺激时室房呈分离状态。心房增频刺激时QRS波逐渐增宽,直至充分预激。在QRS波增宽过程中,HV逐渐缩短直至H波融合于QRS波之中,刺激信号至QRS波的间期逐渐延长,反映了递减传导的过程。继续缩短心房刺激周长后突然旁路传导受阻,经房室结下传并出现传导跳跃现象,继传导跳跃后心动过速被诱发。心动过速可被三磷酸腺苷（ATP）终止,终止后房室经旁路前传,其QRS波形态与充分预激时相似。在心房刺激保持充分预激的前提下,沿三尖瓣环标测,于左前斜位45。三尖瓣环4点钟处标测到最早V波,此处较体表心电图QRS波提前25ms,单极记录呈Qs型,HA波与V波之间未见高频电位。于该点消融放电（60W×60℃）,2S后旁路传导消失。放电过程中未出现交界性心律。消融结束后心房程序电刺激仍有房室传导跳跃现象。随访18个月,未再有心动过速发作。结论本病例心动过速系Mahaim结室纤维所介导,该纤维具有双向传导功能,其上插入端位于房室结慢径区域,下插入端位于邻近房室沟的局部心室肌。心动过速时房室结-希氏-浦肯野系统为前传支,结室纤维作为逆传支。     

Isolated atrial segment pacing: an alternative to His bundle pacing after atrioventricular junctional ablation.

OBJECTIVES: This study was designed to investigate a practical alternative to His bundle pacing after atrioventricular (AV) junctional ablation by pacing a small area of isolated atrial tissue surrounding the AV node. BACKGROUND: His bundle pacing is preferred after AV junctional ablation in patients with refractory atrial fibrillation. However, it is technically difficult and not clinically useful at the present time. METHODS: This study was conducted in an isolated working swine heart model (n = 5), with real-time imaging capabilities. A small area of atrial tissue surrounding the AV node and the His bundle was isolated using sequential radiofrequency ablation lesions. RESULTS: Complete AV block created by segmental atrial isolation was achieved in 5 of 5 experiments. The isolated atrial segment was bordered by the ablation lines, the tricuspid annulus, and the AV node-His bundle. The AV conduction was characterized using a pacing electrode implanted into the isolated atrial segment. Pacing from the atria, the ventricles, and the isolated atrial segment at different rates confirmed complete bidirectional block between the atria and isolated area, whereas antegrade and retrograde AV nodal conduction between the isolated atrial segment and the ventricles remained intact. Pacing from the isolated area produced minimal changes in systolic left ventricular pressure compared with baseline sinus rhythm (mean -2 mm Hg). CONCLUSIONS: Isolation of a small area of atrial tissue surrounding the AV node is feasible by transcatheter radiofrequency ablation. This procedure may be a useful alternative to conventional AV junctional ablation because it can create complete AV block, while in effect permitting the equivalent of His bundle pacing after AV junctional ablation.     

Impulse Formation and Conduction of Excitation in the Atrioventricular Node

AV Nodal Conduction. Meijler et al. have recently challenged the classical concept of AV nodal conduction (the conduction hypothesis) and suggest that the AV node might he controlling ventricular rhythmicity through its automaticity electrotonically modulated In atrial excitation (the modulated pacemaker hypothesis). This article critically evaluates the three major arguments of Meijler: (1) the absence of convincing evidence for conduction of excitation in the AV node; (2) the prevalence of disproportionately short AV intervals in larger animals; and (3) elimination of KR intervals shorter than the cycle length of ventricular pacing during atrial fibrillation, to judge which of these two hypotheses would more satisfactorily explain various experimental and clinical findings accumulated in the past. Previous observations including microelectrode mapping of the rabbit AV junction during regular sinus rhythm as well as second–degree AV block, clinical and experimental studies on concealed conduction, and studies on the ventricular response to atrial fibrillation appear to he compatible with the conduction hypothesis, whereas clearcut evidence for automatic impulse formation in the AV node has not been presented, except in a small number of hearts showing spontaneous AV junctional rhythms. In view of these observations and theoretical considerations based on comparative anatomy of the AV node–His–Purkinje system and on the latest experimental study on the equine AV node, the authors conclude that the conduction hypothesis appears to better explain all the available data, except perhaps in a few cases with second–degree intra–AV nodal block.     

Atrioventricular Nodal Conduction Rather than Automaticity Determines the Ventricular Rate During Atrial Fibrillation and Atrial Flutter

AV Nodal Conduction During Atrial Fibrillation and Flutter . Introduction: Recent clinical studies have advanced the hypothesis that the atrioventricular (AV) node does not conduct cardiac impulses, but functions as a pacemaker whose discharge rate and rhythm are modulated electrotonically by atrial impulses. Major support for the hypothesis comes from the observation that the short ventricular cycles during atrial fibrillation can be totally eliminated by ventricular pacing at relatively long ventricular cycle lengths. Methods and Results: The hypothesis was tested in ten anesthetized open chest mongrel dogs with sustained atrial fibrillation or atrial flutter (AF). Large differences (> 120 msec) between the ventricular pacing cycle length that achieved > 95% ventricular capture and the shortest spontaneous RR cycle during AF were considered to be consistent with the modulated AV nodal pacemaker hypothesis, while values ≤ 120 msec were not. The results showed that the ventricular pacing cycle length capturing > 95% of ventricular complexes during AF depended on the spontaneous ventricular rate during AF. Short spontaneous RR cycles during AF required short ventricular pacing cycle lengths to achieve > 95% capture, and the difference between the ventricular pacing cycle length and the shortest spontaneous RR cycle length was narrow, i.e., ≤ 120 msec. Slower ventricular rates could be captured at longer ventricular pacing cycle lengths, and the difference between the ventricular pacing cycle length capturing > 95% of the ventricular complexes and the shortest spontaneous RR interval during AF was large, i.e., > 120 msec. A continuum existed, and values ≤ 120 msec could be transformed to values > 120 msec by increasing vagal intensity to slow the ventricular response. We also found in five dogs that we could not achieve overdrive suppression of automaticity of the putative AV nodal pacemaker focus by ventricular pacing at various cycle lengths and durations during atrial fibrillation. Conclusion: In conclusion, data from this study fail to support the modulated AV nodal pacemaker hypothesis and are more consistent with conventional concepts of AV nodal conduction.     

Atrioventricular node reentry: Intravenous verapamil as a method of defining multiple electrophysiologic types

Fourteen patients with recurrent supraventricular tachycardia (SVT) underwent electrophysiological evaluation. Each patient was shown to have reentry confined to the region of the atrioventricular (AV) node. Verapamil, 0.075 to 0.15 mg/kg was administered intravenously to each patient during a stable episode of SVT, resulting in termination in each instance. There was more than one mechanism for termination of SVT. Nine patients showed termination by anterograde AV node block preceded by an increase in conduction time in the anterograde limb of the tachycardia circuit (Ae-H intervals) with no change in the conduction time in the retrograde limb (H-Ae intervals). Three patients showed termination by block in the retrograde limb of the circuit preceded by increases in both Ae-H and H-Ae intervals. An additional example of termination by spontaneous ventricular premature complexes and usurpation by sinus rhythm were also seen. Common features were that verapamil had significant effects on anterograde and retrograde conduction and refractoriness in the AV node. It prolonged the refractory periods of both fast and slow pathways in patients with dual anterograde AV node pathways, and observable effects on retrograde conduction and refractoriness were seen even in patients with constant ventriculoatrial conduction times during incremental ventricular pacing in a control study. However, three distinct groups of patients were identified on the basis of their response to ventricular pacing in a control study and upon verapamil effects recorded during their SVT. An explanation for these latter findings may be that there is a normal variation in the retrograde response of parts of the AV node to ventricular pacing, and a variability in some of the patients' responses to verapamil.     

Effect of atrioventricular sequential pacing in patients with no ventriculoatrial conduction

Candidates for the dual chamber "universal" (DDD) pacemaker are frequently tested for the presence of intact ventriculoatrial (VA) conduction to identify those at risk for developing endless loop tachycardia. However, recent reports have cited instances where clinical endless loop tachycardia has occurred even when no VA conduction could be demonstrated during ventricular pacing. A pacing protocol was designed to assess the effect of atrioventricular (AV) sequential pacing on VA conduction in 13 patients who showed no evidence of VA conduction during routine electrophysiologic testing. The absence of VA conduction was inferred by pacing the ventricle at several cycle lengths without obtaining a retrograde atrial capture. With the AV sequential method, which consisted of an AV sequential drive with a programmed AV interval of 100 to 160 ms, the presence or absence of VA conduction was tested utilizing a premature ventricular stimulus (V2) over a wide range of coupling intervals. During the AV sequential method, the V2 effectively propagated to the atria in 5 of 13 patients with V2A2 intervals ranging from 200 to 460 ms (mean 304 +/- 97). It is concluded that in patients showing absent VA conduction during routine testing, the ability of a paced ventricular impulse to propagate retrogradely can be demonstrated in a significant number of cases with AV sequential pacing. Although the exact mechanism could not be determined, it is postulated that as compared with ventricular pacing alone, a longer input into the AV node (first anterogradely during the AV sequential drive and then retrogradely with V2) may be partly responsible for the facilitative effect of the AV sequential method.     

Supraventricular tachycardia in patients without overt preexcitation

In this article, the authors discuss the features and differential diagnosis of supraventricular tachycardia with a regular ventricular rate that occurs in patients without overt preexcitation during sinus rhythm. In the authors' experience, the two most common mechanisms of these tachycardias are reentry within the atrioventricular node (AV nodal reentry) and atrioventricular reentry using a concealed accessory pathway for retrograde conduction and the AV node/His-Purkinje system for antegrade conduction (AV reentry). Sinus nodal reentry, intra-atrial reentry, automatic atrial tachycardia, and nonparoxysmal junctional tachycardia account for the remaining episodes of regular supraventricular tachycardia. Therapy for AV and AV nodal reentry is also discussed.     

心室电风暴的机制与起搏作用的实验观察

目的观察心室电风暴与室房逆传的关系和起搏的作用。方法以扎、松冠状动脉左前降支的方法制作25只犬缺血-再灌注室性心律失常模型,以针电极探查希氏-浦肯野系统(HPS)的电冲动。结果16只犬自发3次以上室性心动过速/心室颤动(简称室速/室颤),符合电风暴。电风暴时室房传导呈4种类型:Ⅰ~Ⅲ型HPS异位电冲动皆连续逆传,Ⅰ型间断夺获心房;Ⅱ型未夺获心房,但连续抑制前向房波下传,产生假性Ⅲ度房室阻滞;Ⅲ型连续夺获心房;IV型HPS逆向与前向传导交替。快速起搏心房可重建房室前传和稳定的血压。快速起搏心室作用有:①抑制异位电冲动形成,防止触发室颤,但不终止自律性异常室速;②拖带和终止折返性室速,显现室速的拖带变形现象和双向折返;③多不夺获快速室速/室颤,偶见HPS起搏和串刺激夺获心室,快速室速/室颤频率减慢后自发终止。结论HPS异位电冲动逆向传导,阻滞窦性心律下传,促使室速/室颤反复发作而呈现电风暴现象。起搏重建房室传导和抑制异位电冲动形成,有预防电风暴的作用。     

Effect of pharmacologic autonomic blockade on ventriculoatrial conduction

To determine the influence of autonomic tone on retrograde ventriculoatrial (VA) conduction, incremental atrial and ventricular pacing was performed before and after pharmacologic autonomic blockade in 28 patients. VA conduction during ventricular pacing was demonstrated, with highest frequency in patients capable of 1:1 atrioventricular (AV) conduction at atrial paced cycle lengths of 300 ms or less (7 of 7, 100%). In subjects with 1:1 AV conduction at minimum cycle lengths of 300 to 500 ms, 14 of 21 (67%) demonstrated VA conduction in the control state; however, only 12 of 21 (57%) did so after autonomic blockade. The lowest frequency was observed in those capable of 1:1 AV conduction at minimum cycle lengths of 505 ms or more before and after autonomic blockade (2 of 7, [29%], p less than or equal to 0.02 compared with values in the first group). No change in the mean minimum ventricular paced cycle length at which 1:1 VA conduction could be maintained was demonstrated after autonomic blockade. In individual subjects, incremental change in this cycle length after autonomic blockade correlated positively with the corresponding change in minimum atrial cycle length at which 1:1 AV conduction could be maintained (r = 0.62, p less than 0.005), and was concordant in direction in 18 of 21. In conclusion, the sympathetic and parasympathetic modulation of VA conduction is balanced and concordant in direction to the effect on AV nodal conduction.     

Patient with atrioventricular node reentrant tachycardia with eccentric retrograde left-sided activation: treatment with radiofrequency catheter ablation

We describe a patient with supraventricular tachycardia with triple atrioventricular (AV) node pathway physiology. A discontinuous curve was present in the antegrade AV nodal function curves. During right ventricular pacing, the earliest retrograde atrial activation was recorded at the left-sided coronary sinus electrode. The retrograde ventricular-atrial interval was long and had decremental conduction. We induced a slow-slow AV node reentrant tachycardia (AVNRT) with eccentric retrograde left-sided activation. After slow pathway ablation, dual AV nodal pathway physiology was present. AVNRT with eccentric retrograde left-sided activation is relatively rare, and our findings suggest that eccentric retrograde left-sided atrial inputs consist partially of a slow pathway and disappear with slow pathway ablation.     

Effects of verapamil on automaticity and conduction with particular reference to tachyphylaxis.

Verapamil delivered via the sinus node artery exerted a dose-related, exclusively negative chronotropic action at all concentrations studied. Perfusion through the AV node artery during AV junctional rhythm also caused a dose-related negative chronotropic response, but the concentrations required to depress this pacemaker were ten times higher than those required to depress sinus node automaticity. Verapamil administered into the AV node artery during sinus rhythm impaired AV conduction. His bundle electrograms demonstrated that depressed A-V conduction was exclusively located at the A-H level. In 5 out of 10 dogs verapamil (5 to 10 mg) delivered into the septal artery caused an abrupt onset of ventricular fibrillation without premonitory dysrhythmias. Verapamil (except at very high concentrations) did not alter the responsiveness of the sinus node and the AV junction to acetylcholine or norepinephrine, whether administered selectively into the sinus node artery or the AV node artery or released by neural stimulation. Serial injections of verapamil were associated with tachyphylaxis for the direct chronotropic and dromotropic properties of the drug.