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PubMed1983

Differentiation of the atrioventricular node, the atrioventricular bundle and the bundle branches in the bovine heart: an immunohistochemical and enzyme histochemical study.

The previous observations of differences between different cardiac regions (ventricular myocardium, atrial myocardium, Purkinje fibre system) with respect to the maturation of the M-line region and the establishment of mature metabolic characteristics, have been extended. It was found that M-line maturation proceeds differently also between different regions of the conduction system. The M-line proteins, myomesin and MM-creatine kinase, were detected earlier, by means of immunohistochemistry, in the AV bundle and bundle branch cells than in the AV node cells. Also, a difference was observed in large foetuses. Striations in the AV node were less evident than in the AV bundle and the bundle branches in sections incubated with antibodies against myomesin as well as against MM-creatine kinase. Using enzyme histochemistry it was observed that the differences in metabolic properties between the AV node, the AV bundle and the bundle branches on the one hand, and the ordinary myocardium on the other, of adult hearts, are not established at the early stages. No clear difference in activity of succinate dehydrogenase was seen between the conduction tissues and the ordinary myocardium in the foetal hearts, while the conduction tissues showed a lower activity in the adult hearts. Furthermore, the pattern of activity of mitochondrial glycerol-3-phosphate dehydrogenase between the conduction tissues and the atrial and ventricular myocardium was quite different in early foetal stages compared with the adult stage.

Animals↗
PubMed1995

Radiofrequency catheter ablation for atrioventricular node reentry tachycardia with multiple slow atrioventricular node pathways.

Catheter ablation was attempted in 2 patients with atrioventricular node reentry tachycardia which showed fast, intermediate and slow anterograde atrioventricular node pathways. Radiofrequency currents were applied within a restricted area of the tricuspid annulus between the His bundle and the ostium of the coronary sinus where presumed slow pathway potentials were identified. Elimination of both the intermediate and the slow pathways, with preservation of anterograde and retrograde fast pathway conduction, was achieved in both patients.

Aged↗
PubMed1992

Surgery for atrioventricular node reentry tachycardia. Results with surgical skeletonization of the atrioventricular node and discrete perinodal cryosurgery.

Surgical treatment options for interruption of atrioventricular node reentrant tachycardia include (1) skeletonization of the atrioventricular node by dissecting it from most of its atrial inputs and (2) discrete cryosurgery of the perinodal tissues by applying a series of sequential cryolesions to the atrial tissues immediately adjacent to the atrioventricular node. Both these techniques attempt to interrupt one of the dual atrioventricular node conduction pathways while preserving the other. This report describes 17 consecutive patients who underwent surgical treatment, 10 patients with skeletonization of the atrioventricular node and seven patients with discrete perinodal cryosurgery. There were 10 female and seven male patients and their ages ranged from 28 to 56 years (mean 38). Two of the 17 patients had Wolff-Parkinson-White syndrome and their accessory pathways were interrupted before the atrioventricular nodal reentrant tachycardia was ablated. All the procedures were performed in a normothermic beating heart while atrioventricular conduction was monitored closely. In the skeletonization technique, the right atrial septum was mobilized and the atrioventricular node exposed anterior to the tendon of the Todaro. The perinodal cryosurgical procedure was also performed through a right atriotomy and a series of sequential 3 mm cryolesions were placed around the borders of the triangle of Koch on the inferior right atrial septum. There were no operative deaths. Two patients who underwent the skeletonization operation had heart block necessitating pacemaker therapy. At postoperative electrophysiologic study, no echoes or atrioventricular nodal reentrant tachycardia were inducible in any of the 17 patients. All patients have remained free of arrhythmia recurrence and have required no antiarrhythmic therapy after a follow-up of 5 to 28 months (mean 14). In conclusion, both atrioventricular node skeletonization and perinodal cryosurgery successfully ablate atrioventricular nodal reentrant tachycardia; however, perinodal cryosurgery appears to be safer in avoiding heart block, is more easily performed, and is our procedure of choice for the management of medically refractory atrioventricular nodal reentrant tachycardia.

Adolescent↗
PubMed1996

Multiple anterograde atrioventricular node pathways in patients with atrioventricular node reentrant tachycardia.

OBJECTIVES: This study sought to investigate electrophysiologic characteristics and possible anatomic sites of multiple anterograde slow atrioventricular (AV) node pathways and to compare these findings with those in dual anterograde AV node pathways. BACKGROUND: Although multiple anterograde AV node pathways have been demonstrated by the presence of multiple discontinuities in the AV node conduction curve, the role of these pathways in the initiation and maintenance of AV node reentrant tachycardia (AVNRT) is still unclear, and possible anatomic sites of these pathways have not been reported. METHODS: This study included 500 consecutive patients with AVNRT who underwent electrophysiologic study and radiofrequency ablation. Twenty-six patients (5.2%) with triple or more anterograde AV node pathways were designated as Group I (16 female, 10 male, mean age 48 +/- 14 years), and the other 474 patients (including 451 with and 23 without dual anterograde AV node pathways) were designated as Group II (257 female, 217 male; mean age 52 +/- 16 years). RESULTS: Of the 21 patients with triple anterograde AV node pathways, AVNRT was initiated through the first slow pathway only in 3, through the second slow pathway only in 8 and through the two slow pathways in 9. Of the five patients with quadruple anterograde AV node pathways, AVNRT was initiated through all three anterograde slow pathways in three and through the two slower pathways (the second and third slow pathways) in two. After radiofrequency catheter ablation, no patient had inducible AVNRT. Eleven patients (42.3%) in Group I had multiple anterograde slow pathways eliminated simultaneously at a single ablation site. Eight patients (30.7%) had these slow pathways eliminated at different ablation sites; the slow pathways with a longer conduction time were ablated more posteriorly in the Koch's triangle than those with a shorter conduction time. The remaining seven patients (27%) had a residual slow pathway after delivery of radiofrequency energy at a single or different ablation sites. The patients in Group I had a longer tachycardia cycle length, poorer retrograde conduction properties and a higher incidence of multiple types of AVNRT than those in Group II. CONCLUSIONS: Multiple anterograde AV node pathways are not rare in patients with AVNRT. However, not all of the anterograde slow pathways were involved in the initiation and maintenance of tachycardia. Radiofrequency catheter ablation was safe and effective in eliminating critical slow pathways to cure AVNRT.

Adult↗
PubMed1998

Comparison of adenosine effects on atrioventricular node reentry and atrioventricular reciprocating tachycardias.

BACKGROUND: Adenosine is an established first line therapy for the treatment of narrow complex tachycardias. The two most common etiologies of paroxysmal supraventricular tachycardia (SVT) are atrioventricular node reentry tachycardia (AVNRT) and atrioventricular reciprocating tachycardia (AVRT). HYPOTHESIS: We postulated that adenosine might have different effects on the termination of AVNRT vs. AVRT, and that these differences might assist in the noninvasive differentiation between these diagnoses. METHODS: Fifty-nine patients referred for the diagnosis and treatment of SVT were included in the study. All patients had SVT induced during electrophysiology testing, and each patient received adenosine during SVT. The adenosine dose, time to tachycardia termination, and site of tachycardia termination were recorded. Seventeen patients required isoproterenol administration to initiate SVT. This subset of patients was compared with those not requiring isoproterenol. RESULTS: There was no statistically significant difference in the adenosine dose or time to tachycardia termination when comparing patients with AVNRT with those with AVRT. All patients with AVNRT had termination of tachycardia in the antegrade direction with final activation in the atria. Patients requiring isoproterenol for tachycardia initiation experienced tachycardia termination significantly faster than those not requiring isoproterenol, although there was no difference in the dose of adenosine required for termination. CONCLUSION: These data demonstrate that patients with dual AV node physiology and AVNRT do not have altered sensitivity to adenosine compared with patients with AVRT and normal AV nodes. Further investigation will be required to determine the clinical utility of the significantly shorter time to tachycardia termination for patients receiving isoproterenol.

Adenosine↗
PubMed1993

[Block of the slow pathway of the double atrioventricular node: a new technique for treatment of atrioventricular node reentry tachycardia].

The aim of this work is to summarize the first experience in Chile modifying the slow pathway in patients with tachycardias due to atrio-ventricular node reentry. Until now, the only available treatment was the use of antiarrhythmic drugs. The radiofrequency fulguration or cauterization of part of the atrioventricular node has been reported as a treatment for these arrhythmias. The initial technique fulgurated the rapid pathway with a significant risk of atrioventricular block. The modification of the slow pathway has been recently described. We report two patients, 9 and 45 years old, with a history of recurrent tachycardias, refractory to pharmacological treatment. An electrophysiological study demonstrated that the mechanism of their arrhythmias was a nodal reentry. In the same session one of the mapping catheters was changed by a fulguration one and radiofrequency was applied, using a variation of the technique described by Jackman. In both, the slow pathway was modified or blocked with definitive interruption of the nodal reentry circuit and preservation of atrioventricular conduction.

Catheter Ablation↗
PubMed1979

Effect of hypoxia on the sinoatrial node, atrium, and atrioventricular node in the rabbit heart.

We used intracellular microelectrodes to study the effects of hypoxia on the isolated, superfused sinoatrial (SA) node, atrium, and atrioventricular (AV) node of the rabbit heart. Hypoxia decreased the rate of spontaneous impulse initiation in SA nodal fibers by decreasing the slope of diastolic depolarization. With gradually decreasing Po2, the sinus rate was reduced; concomitantly, the corrected sinus node recovery time after rapid atrial stimulation was much less affected demonstrating marked prolongation only under severe anoxic conditions. Hypoxia decreased the amplitude of action potentials of the SA node and of the AV node but not of the atrium. SA and AV nodal conduction were slowed by hypoxia; intraatrial conduction was not significantly affected. AV nodal conduction block occurred at lower atrial rates, and the effective refractory period of the AV node was prolonged. Inhomogeneity of SA and AV nodal impulse propagation often was observed in the presence of hypoxia. This was associated with concealed reentry within both nodal areas. The extracellular K+ concentration of the atrial tissue was measured with ion-sensitive microelectrodes. [K+]o remained unchanged even after prolonged periods of severe hypoxia. These results are consistent with the hypothesis that acute hypoxia predominantly inhibits slow response activity but has only little effect on the fast inward sodium current.

Action Potentials↗
PubMed1989

Role of intravenous isoproterenol in the electrophysiologic induction of atrioventricular node reentrant tachycardia in patients with dual atrioventricular node pathways.

To assess the role of intravenous isoproterenol for the facilitation of electrophysiologic induction of atrioventricular (AV) node reentrant tachycardia, 20 patients with dual AV node pathways who lacked inducible AV node reentrant tachycardia at control study had a constant isoproterenol infusion administered and underwent repeat study. Six (30%) of 20 patients (group I) had inducible AV node reentrant tachycardia during isoproterenol infusion whereas the other 14 (70%) patients (group II) did not. Paroxysmal supraventricular tachycardia was clinically documented in all 6 group I patients compared to 3 (21%) of 14 group II patients (p = 0.002). The sensitivity and specificity of isoproterenol-facilitated induction of AV node reentrant tachycardia were 67 and 100%, respectively. The isoproterenol-facilitated induction of sustained AV node reentry was mediated by resolution of the weak link in anterograde slow pathway in 2 (33%) patients, in retrograde fast pathway in 3 (50%) and in both anterograde slow and retrograde fast pathways in 1 (17%) patient. Four group I patients were given intravenous propranolol, 0.2 mg/kg body weight, and had complete suppression of isoproterenol-facilitated induction of AV node reentry. Thus, intravenous isoproterenol is a rather sensitive and highly specific adjunct to electrophysiologic induction of AV node reentrant tachycardia in patients with dual AV node pathways but without inducible sustained AV node reentry.

Adrenergic beta-Antagonists↗
PubMed1989

Direct surgical treatment of atrioventricular node reentrant tachycardia.

Atrioventricular node reentry tachycardia is a common type of supraventricular tachycardia. Rarely is it incapacitating and refractory to drug therapy, but when it is, the only option in therapy until recently has been atrioventricular node ablation or antitachycardia pacemaker insertion. The purpose of this paper is to review the case histories of four patients in whom we have surgically abolished atrioventricular node reentrant tachycardia while intentionally preserving atrioventricular node conduction. All four patients had atrioventricular node reentrant tachycardia confirmed by electrophysiologic study as diagnosed by established criteria. One patient had a left posterior atrioventricular accessory pathway, in addition to atrioventricular node reentrant tachycardia. All patients underwent intraoperative epicardial and endocardial mapping. Direct surgical dissection of the atrioventricular node node was performed in all four patients during normothermic cardiopulmonary bypass. Early and late postoperative electrophysiologic studies were used to evaluate the success of the surgical dissection. None of the patients had any evidence of dual atrioventricular node pathways or spontaneous or inducible atrioventricular node reentrant tachycardia postoperatively. At last follow-up (15 weeks to 21 months postoperatively), all patients were free from arrhythmias and cardiac medications, all were in normal sinus rhythm, and all had a subjectively improved life-style. This technique of direct surgical dissection of the atrioventricular node during normothermic cardiopulmonary bypass has allowed for complete cure of atrioventricular node reentrant tachycardia, while maintaining normal atrioventricular node function in these four patients.

Adult↗
PubMed1993

Comparative atrioventricular node properties after radiofrequency ablation and operative therapy of atrioventricular node reentry.

The anatomical substrate for atrioventricular (AV) node reentry is unclear. To gain insights into the mechanism of cure of AV node reentry by nonpharmacological techniques, we compared AV node properties in 53 patients undergoing operative therapy (perinodal dissection) and 43 undergoing radiofrequency ablation (28 posterior approach, 15 anterior approach). Anterior radiofrequency ablation was associated with significant AH prolongation (62 +/- 18 msec vs 136 +/- 64 msec, P < 0.0001), loss of "fast" pathway physiology, and no change in the anterograde refractory period of the AV node (273 +/- 24 msec vs 268 +/- 28 msec, P = NS). Posterior radiofrequency ablation did not change the AH interval (67 +/- 17 msec vs 68 +/- 17 msec, P = NS), prolonged AV node effective refractory period (275 +/- 48 msec vs 320 +/- 55 msec, P < 0.0001), and was associated with loss of "slow pathway" physiology. Operative treatment prolonged the AH interval (66 +/- 18 msec vs 83 +/- 37 msec, P < 0.0001) and the AV node effective refractory period (264 +/- 52 msec vs 364 +/- 112 msec, P < 0.0001), and affected dual pathway physiology inconsistently. These data support the view that the "fast" and "slow" pathways are distinct perinodal entities that can be selectively ablated. The operative approach causes more diffuse and variable injury to the AV node region.

Adolescent↗
PubMed1984

Congenital endodermal heterotopia of the atrioventricular node: evidence for the endodermal origin of so-called mesotheliomas of the atrioventricular node.

A case of so-called mesothelioma of the atrioventricular node is presented. Controversy exists as to whether this lesion is of mesodermal or endodermal origin. The light and electron microscopic morphologic characteristics in this case were identical to those reported previously. The glandular component produced mucin that resisted digestion with both hyaluronidase and diastase; this staining pattern is characteristic of endodermal rather than of mesodermal tissue. Immunohistochemical methods demonstrated abundant carcinoembryonic antigen (CEA) in the cytoplasm of the cells composing the lesion. The presence of CEA strongly argues for an endodermal origin, since this antigen characterizes tissue derived from endoderm and is generally absent from mesoderm. The lesion probably represents endodermal foregut tissue that is displaced during embryogenesis. As such, it is not a true neoplasm. It is proposed that this lesion be designated "congenital endodermal heterotopia of the atrioventricular node."

Atrioventricular Node↗
PubMed1992

Comparison of the cost of radiofrequency catheter modification of the atrioventricular node and medical therapy for drug-refractory atrioventricular node reentrant tachycardia.

The purpose of this study was to determine the charges for radiofrequency catheter modification of the atrioventricular (AV) node in 15 patients with symptomatic AV node reentrant tachycardia despite pharmacologic therapy and to compare these charges with the estimated charges for health care utilization by the same patients before the catheter procedure was performed. There were seven men and eight women with a mean age of 50 +/- 17 years. The mean duration and frequency of symptoms were 16 +/- 9 years and 4.5 +/- 6 episodes/month, respectively. Fourteen of the 15 patients required only one procedure for diagnosis and cure of AV node reentrant tachycardia and 1 patient required two sessions. All patients underwent electrophysiologic study before discharge from the hospital to confirm the short-term efficacy of the procedure. The mean duration of the hospital stay was 3 +/- 1.5 days and the mean total charge/patient expressed in 1991 dollars was $15,893 +/- $3,338 for catheter modification. These total charges consisted of hospital charges of $8,105 +/- $2,466 and physician charges of $7,788 +/- $971. All patients had a successful outcome and required no additional antiarrhythmic therapy. The estimated cost of health care utilization for these 15 patients before cure of AV node reentrant tachycardia was $7,651/patient per year. These estimated costs included charges incurred for emergency room visits, office visits, hospitalizations and antiarrhythmic drug therapy. In conclusion, the results of this study indicate that the annual health care costs incurred by patients who have symptomatic, drug-refractory paroxysmal supraventricular tachycardia caused by AV node reentry are substantial.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1996

Posterior fast atrioventricular node pathways: implications for radiofrequency catheter ablation of atrioventricular node reentrant tachycardia.

OBJECTIVES: This study sought to present evidence that fast atrioventricular (AV) node pathways with posterior exit sites may participate in typical AV node reentry. BACKGROUND: Catheter ablation of the slow AV node pathway in the posteroseptal right atrium is the preferred therapeutic approach in patients with AV node reentrant tachycardia. Despite the success achieved with this approach, electrophysiologic changes consistent with fast pathway ablation are occasionally observed. One potential explanation is the presence of an aberrant posterior fast pathway. METHODS: The location of fast and slow AV node pathways was determined by atrial activation mapping along the tricuspid valve annulus during tachycardia and was further confirmed by the effect of radiofrequency catheter ablation. RESULTS: Seven patients with AV node reentrant tachycardia had evidence of a posterior fast pathway near the coronary sinus os. Abolition of anterograde and retrograde fast pathway conduction followed radiofrequency ablation in the posteroseptal region in six patients. Consistent with fast pathway ablation, the AH interval increased from 70 +/- 24 to 195 +/- 35 ms (mean +/- SD), and tachycardia was no longer inducible. Selective slow pathway ablation was performed in one other patient with a posterior fast pathway. CONCLUSIONS: Functionally fast AV node pathways may be located in the posteroseptal right atrium, where slow pathway modification is performed. These data delineate the limitation of an anatomically guided slow pathway ablative approach and emphasize the importance of detailed mapping and localization of the retrograde fast pathway exit site before ablation. Failure to recognize the presence of posterior fast AV node pathways may account for sporadic examples of AV block, complicating posteroseptal ablation in patients with AV node reentry.

Adult↗
PubMed1994

The hyperpolarisation-activated current, I(f), is not required for pacemaking in single cells from the rabbit atrioventricular node.

The atrioventricular node (AVN) is vital for cardiac function. One of its properties is that it can act as a pacemaker for the ventricles if the sinoatrial node fails. This study investigates the role of the hyperpolarisation-activated inward current (I(f)) in generating pacemaker activity in morphologically normal single cells isolated from the rabbit AVN. Whole-cell patch-clamp recordings show that 80%-90% of AVN myocytes do not possess I(f), but nevertheless generate spontaneous action potentials with normal pacemaker depolarisations before each action potential upstroke. We have termed this type of cell "type 1". A small proportion (10%-20%) of spontaneously active AVN cells (type 2) do exhibit I(f). A 100 nM solution of isoprenaline increased the action potential rate of type 1 cells by 31%. In these cells isoprenaline did not activate any I(f) whereas in type 2 cells it clearly increased the amplitude of I(f). Manganese at 2 mM also increased the amplitude of I(f) in type 2 cells, but did not reveal I(f) in type 1 cells. We conclude that, whilst I(f) may play a role in modulating pacemaker activity in type 2 cells, in the majority of AVN cells (type 1) pacemaker depolarisation normally occurs in the complete absence of I(f). Furthermore, the inability of both isoprenaline and Mn to reveal I(f) in type 1 cells suggests that I(f) channels may be absent in these cells.

Animals↗
PubMed1994

L-type calcium current in rod- and spindle-shaped myocytes isolated from rabbit atrioventricular node.

The atrioventricular node (AVN) is vital to normal cardiac function. The present report describes the properties of L-type calcium current (ICa) in rod- and spindle-shaped myocytes isolated from the rabbit AVN. With depolarizing voltage clamps from a holding potential of -40 mV, a rapidly activating ICa was observed, which peaked at +10 mV in most cells and exhibited a "bell-shaped" current-voltage relation. ICa was abolished by nifedipine (2-20 microM) and cadmium (100-200 microM) and was greatly reduced by manganese (1 mM). At +10 mV, time to peak ICa was 3.3 +/- 0.15 (SE) ms (n = 12) and ICa current density was 9.3 +/- 1.2 pA/pF (n = 9). Steady-state activation and inactivation curves for ICa showed half-maximal activation at -3.6 mV [slope factor (k) = 6.6 mV] and half-maximal inactivation at -25.8 mV (k = 6.5 mV). The time course of decay of ICa during a depolarizing pulse was voltage dependent and biexponential. The time course of recovery of ICa from inactivation was also biexponential (with two time constants tau 1 = 194.7 and tau 2 = 907.4 ms). Under current clamp, spontaneous action potentials from AVN cells were blocked by nifedipine as well as by cadmium, suggesting that L-type ICa was largely responsible for the action potential upstroke.

Animals↗
PubMed1985

Examination of an exponential model of conduction through the human atrioventricular node.

The atrioventricular node (AVN) has been modeled by relating output (A2H2 or H1H2) to input (A1A2) where A and H are atrial and His bundle electrograms during fixed rate atrial pacing (A1A1) or with an extrastimulus (A2). (Formula: see text) This study examined this model in 61 nonselected patients, specifically for AVN (in)stability and the possibility of multiple pathways. After programmed atrial stimulation at two basic cycle lengths of 600 ms and 462 ms, A1H1, A2H2 and H1H2 were digitized and plotted as a function of A1A2. Seven of 104 trials were rejected as SD. A1H1 was greater than 15 ms, suggesting AVN instability. Another 26 and 34 plots, respectively, of A2H2 and H1H2 were rejected because of inadequate data. In the remainder, goodness of fit of the single exponentials was tested statistically in three ways: R2, the runs test, and the Kendall rank coefficient test. Results were compared with an electrophysiologist who examined plots for one or more pathways (either discontinuous curves or slope change in a continuous curve). Single exponentials were successfully fitted (by runs test) in 44/71 and 34/63 of A2H2 and H1H2 plots, respectively, usually in accordance with the cardiologist. Discordance between computations and the cardiologist could be attributed to data scatter and lack of a sufficiently rigid stimulation protocol. The identification of bifurcation points in the presence of multiple pathways, particularly when manifest as a change in slope (approximately 6% of trials) rather than discontinuity of plots (approximately 20% of trials) remains an outstanding problem.

Adolescent↗
PubMed2000

Proximal atrioventricular bundle, atrioventricular node, and distal atrioventricular bundle are distinct anatomic structures with unique histological characteristics and innervation.

BACKGROUND: Direct 3D analysis (ie, stereotaxic analysis of 3 planes) has shown that the atrioventricular (AV) node (AVN) is continuous with only specialized myocardium of the proximal AV bundle (PAVB) and distal AV bundle (DAVB) or His bundle. The purpose of the present study was to determine whether the PAVB, AVN, and DAVB possess histological features distinct from each other and from the ordinary myocardium. METHODS AND RESULTS: A protocol that preserves the cytoplasmic and interstitial integrity of the tissue and permits serial sections of the AV junction region to be made in 3 orthogonal planes showed that the PAVB, AVN, and DAVB are characterized by myocardium aggregated into fascicles containing approximately 8 myofibers. Myofibers within the fascicles are coiled or spiraled about each other; and spiraling is most compact in the PAVB. Collagen encases individual fascicles and segregates primary fascicles into secondary fascicles. Fascicles, and not myofibers, are in parallel array in the PAVB, interwoven in the AVN, and parallel in the DAVB. Narrow junctions of parallel fascicles separate the AVN from the PAVB and DAVB. Myocytes, which are largest in DAVB, possess clear perinuclear regions; thin finger-like end processes, which are most numerous in the AVN; uniform, delicate cross-striations; and intercalated disks, which are broader in the PAVB and form short stacks in the AVN. Sheaves of nerve terminals are found, including boutons as in skeletal muscle [corrected]. CONCLUSIONS: The PAVB, AVN, and DAVB have distinct histological features. Collagen septation of primary and secondary fascicles presents natural barriers within the tissues and to surrounding myocardium and structures. These findings confirm that the AV junction region contains a specialized conduction system that is anatomically isolated from ordinary myocardium.

Animals↗
PubMed1995

Effect of dual atrioventricular node pathways on atrioventricular reentrant tachycardia.

BACKGROUND: Dual atrioventricular (AV) node pathway physiology is frequently observed in patients with AV accessory pathways. METHODS AND RESULTS: To examine the implications of this, we identified 36 patients (19 men and 17 women; mean +/- SD age, 30 +/- 13 years) with both phenomena. The 36 patients had 48 accessory pathways. Twenty-seven patients had bidirectional and 9 had unidirectional accessory pathways. Of the 34 patients with inducible atrioventricular reentry, 17 used the slow and 11 used the fast anterograde AV node pathway exclusively during AV reentrant tachycardia, whereas 6 patients used both the fast and the slow AV node pathways. AV node reentrant tachycardia was inducible in addition to AV reentry in 7 patients. Both the cycle length and AH intervals were significantly longer during slow pathway-dependent (cycle length, 411 +/- 58 milliseconds [ms]; AH, 229 +/- 42 ms) than during fast pathway-dependent (cycle length, 322 +/- 40 ms; AH, 121 +/- 25 ms; P < .05) reentrant tachycardias. Two patients had only AV node reentrant tachycardia inducible despite the presence of the accessory pathway. Four patients with technically difficult accessory pathways were managed by AV node modification with slow pathway (3) or fast pathway (1) ablation. Three of them remained free of symptoms 7, 14, and 25 months after the procedure whereas 1 patient had recurrence of arrhythmia. CONCLUSIONS: AV reentrance with dual AV node pathways frequently depends exclusively on either the slow or the fast AV node pathway for clinical tachycardia. This may provide additional options for ablation in technically difficult cases when the accessory pathway is not otherwise problematic.

Adolescent↗