Slow Pathway Effective Refractory Period Research Articles

Electrophysiological changes in the conducting properties of fast pathway following modification of the slow pathway of the atrio ventricular node for atrio ventricular nodal re-entrant tachycardia.

Objectives:To determine the possible changes in the conducting properties of the fast pathway after modification of the atrioventricular slow pathway for AVNRT which leads to the failure of the induction of tachycardia.Methods:This study was conducted in the Cardiac electrophysiology Laboratory of Hayatabad Medical Complex, Peshawar, Pakistan from March 2017 to March 2018. All the patients underwent radiofrequency modification of the slow pathway for AVNRT. Patients in whom typical AVNRT was inducible with demonstration of dual AV nodal physiology were included in the study.Results:A total of 171 cases were included in the study, 42 (25%) were males, mean age recorded was 47 ± 15 years. There were no significant changes pre and post ablation in the base line parameters like VV interval, atrioventricular nodal (AV nodal) Wenckebach cycle length, slow pathway effective refractory period (SPERP) or fast and slow pathways maximal Atrio His interval. However significant change was observed in the effective refractory period of the fast pathway 350±49 Vs 290±32 (p value 0.0001). The difference between slow and Fast pathway ERP was also decreased significantly 82±36 Vs 56± 24 (p value 0.004).Conclusion:Our study showed that ablation of AV nodal slow pathway for atrioventricular nodal reentrant tachycardia leads to changes in the effective refractory period of the fast pathway.

The prevalence and characteristics of coexisted atrioventricular nodal reentrant tachycardia and idiopathic left fascicular ventricular tachycardia.

Coexistence of idiopathic left fascicular ventricular tachycardia (ILFVT) and atrioventricular nodal reentrant tachycardia (AVNRT) has been rarely reported. The study aimed at elucidating the prevalence of coexisted AVNRT in patients with ILFVT during longitudinal follow-up. The electrophysiological properties and clinical predictors of coexisted ILFVT and AVNRT were investigated. From 1999 to 2017, a total of 108 patients (age: 33.7 ± 14.3, 84 male) with ILFVT from one tertiary center were consecutively enrolled. The prevalence of coexisted arrhythmias was explored during a longitudinal follow-up and the electrophysiological parameters from the index procedure were compared. During a mean follow-up period of 106.8 ± 69.5 months, 21 of 108 patients (19.4%) had coexisted AVNRT. The electrophysiological study demonstrated patients with coexisted ILFVT and AVNRT were characterized by more antegrade dual AV node conduction (52.4%vs. 19.5%, P=0.002; 9.5%), shorter antegrade slow pathway effective refractory period (285.1 ± 34.1ms vs. 329.2 ± 69.2ms, P=0.034), longer retrograde fast pathway effective refractory period (368.9 ± 56.7ms vs. 312.5 ± 95.2, P=0.036), and less VA dissociation (19.0%vs. 60.9%, P=0.001) than those without a coexisted AVNRT. Multivariate logistic analysis showed that presence of antegrade dual AV nodal physiology and retrograde VA conduction could predict a coexisted AVNRT in patients with ILFVT (P=0.005, OR: 4.80, 95% CI: 1.65-14.37 and P=0.002, OR: 0.14, 95% CI: 0.04-0.49, respectively). There was a high prevalence of coexisted AVNRT in patients with ILFVT during longitudinal follow-up. The presence of antegrade dual AV nodal physiology and retrograde VA conduction can predict the coexisted AVNRT in patients with ILFVT.

Electrophysiology of anterograde right-atrial and left-atrial inputs to the atrioventricular node in patients with atrioventricular nodal re-entrant tachycardia

To study anterograde atrioventricular (A-V) nodal electrophysiological properties through the right-atrial (Ri) and left-atrial inputs (Li) under the pharmacological autonomic blockade (AUB) in patients with slow-fast A-V nodal re-entrant tachycardia (AVNRT) and in controls. Twenty-nine patients with slow-fast AVNRT and 15 control subjects were included. Programmed stimulation with single extrastimulus was performed from the right atrial appendage to test the Ri, and from the posterolateral coronary sinus to test the Li. The AUB was induced with intravenous atropine (0.04 mg/kg) and metoprolol (0.15 mg/kg). The A-V nodal conduction times, refractoriness, discontinuous conduction (≥ 40 ms atrial-His interval 'jump'), and inducibility of AVNRT or reciprocating beats were compared. The A-V nodal conduction times were longer: (i) through the Ri than Li, (ii) in patients than controls, and (iii) in baseline than after AUB--at slow rates in both groups and at fast rates in patients through the right input only (P < 0.05-0.001). A significantly longer slow pathway effective refractory period was demonstrated through the Li than the Ri in patients in baseline (P < 0.05). The discontinuous conduction was demonstrated 94 times in 25 of 29 (83%) patients and 15 times in 6 of 15 (40%) controls (P < 0.01), and was most frequently encountered with the Ri testing. Likewise, inducibility was manifested most frequently with the Ri testing (P = 0.08), and decreased after AUB during this testing only (P = 0.05). The inherent magnitude of discordance of A-V nodal conduction velocity, refractoriness, and parasympathetic modulation between the Ri and Li to the A-V node may play a role in the aetiology of AVNRT.

Gender Differences in the Clinical Characteristics and Atrioventricular Nodal Conduction Properties in Patients With Atrioventricular Nodal Reentrant Tachycardia

The detailed electrophysiological characteristics of the gender differences associated with atrioventricular nodal reentrant tachycardia (AVNRT) have not been clarified. This study investigated the gender-related electrophysiological differences in a large series of patients undergoing radiofrequency catheter ablation. A total of 2,088 consecutive AVNRT patients (men/women 869/1,219) who underwent catheter ablation were enrolled in this study. We evaluated the gender differences in their electrophysiological characteristics. Women had a significantly younger age of onset, higher incidence of multiple jumps, shorter AH interval, atrial effective refractory period (ERP), anterograde fast pathway ERP, anterograde slow pathway ERP, and retrograde slow pathway ERP, and longer ventricular ERP than men. The incidence of baseline ventriculoatrial dissociation was lower in women than in men. Women needed less isoproterenol/atropine to induce AVNRT. No gender differences in the radiation exposure time, procedure time, complication rate, acute success rate, or second procedure rate were noted. Both typical and atypical AVNRT were more predominant in women. In the patients with atypical AVNRT, there was no significant gender difference in incidence of baseline ventriculoatrial dissociation; however, the retrograde slow pathway ERP was significantly shorter in women than in men. Women of premenopausal age (≤50 years old) had a significantly higher incidence of anterograde multiple jumps and a retrograde jump phenomenon, and a shorter anterograde slow pathway ERP and retrograde slow pathway ERP than those of women over 50 years old. Gender differences in the anterograde and retrograde AV nodal electrophysiology were noted in the patients with AVNRT.

Abnormal Atrioventricular Node Conduction and Atrioventricular Nodal Reentrant Tachycardia in Patients Older Versus Younger Than 65 Years of Age

We examined the possible role of atrioventricular node (AVN) conduction abnormalities as a cause of AVN reentrant tachycardia (RT) in patients >65 years of age. Slow pathway radiofrequency catheter ablation (RFCA) was performed in 104 patients. Patients in group 1 (n = 14) were >65 years of age and had AV conduction abnormalities associated with structural heart disease. Patients in group 2 (n = 90) were <65 years of age and had lone AVNRT. Patients in group 1 versus group 2 (66% vs. 46% men) had a first episode of tachycardia at an older age than in group 2 (68 +/- 16.8 vs 32.5 +/- 18.8 years, P = 0.007). The history of arrhythmia was shorter in group 1 (5.4 +/- 3.8 vs 17.5 +/- 14, P = 0.05) and was associated with a higher proportion of patients with underlying heart disease than in group 2 (79% vs 3%, P < 0.001). The electrophysiological measurements were significantly shorter in group 2: atrial-His interval (74 +/- 17 vs 144 +/- 44 ms, P = 0.005), His-ventricular (HV) interval (41 +/- 5 vs 57 +/- 7 ms, P = 0.001), Wenckebach cycle length (329 +/- 38 vs 436 +/- 90 ms, P = 0.001), slow pathway effective refractory period (268 +/- 7 vs 344 +/- 94 ms, P = 0.005), and tachycardia cycle length (332 +/- 53 vs 426 +/- 56 ms, P = 0.001). The ventriculoatrial block cycle length was similar in both groups. The immediate procedural success rate was 100% in both groups, and no complication was observed in either group. One patient in group 2 had recurrence of AVNRT. One patient with a 98-ms HV interval underwent permanent VVI pacemaker implantation before RFCA procedure. In patients undergoing RFCA for AVNRT at >65 years of age had a shorter history of tachycardia-related symptoms than patients with lone AVNRT. The longer AVN conduction intervals and refractory period might explain the late development of AVNRT in group 1.

Characteristics of Slow Pathway Conduction After Successful AVNRT Ablation

AV node slow pathway conduction can persist following successful ablation for AV node reentrant tachycardia (AVNRT). We hypothesized that careful examination of AV nodal conduction curves before and after effective AVNRT ablation in patients with persistent slow pathway conduction could shed light on this apparent paradox. Thirty patients (age 40.9 +/- 14.3; 8 male) were included. AV node function curves were created based on pre- and postablation atrial extrastimulus testing. Analysis of slow pathway function curves demonstrated significant decrease in AH for any given coupling interval after ablation (mean difference -68.1 [-94.5, -41.7] P < 0.001), graphically indicated by downward displacement of the curve. In addition, mean slow pathway effective refractory period (ERP) increased from 247.9 +/- 36.1 msec to 288.6 +/- 56.0 msec (P < 0.001); mean maximum AH interval decreased from 361.3 +/- 114.2 msec to 306.9 +/- 65.2 msec (P = 0.013); mean difference in minimum and maximum AH interval during slow pathway conduction decreased (from 94.5 +/- 75.8 msec to 59.6 +/- 46.2 msec (P = 0.016). Finally, mean difference between the fast and slow pathway effective refractory periods, the span of coupling intervals over which slow pathway conduction occurred, decreased (from 113.9 +/- 61.4 msec to 63.2 +/- 41.5 msec, P = 0.001). Ablation, which successfully eliminates inducible and spontaneous AVNRT in the presence of persistent slow pathway conduction, is associated with significantly altered slow pathway conduction characteristics, indicating the presence of a damaged or different slow pathway after ablation, incapable of sustaining tachycardia.

Gender-Related Differences in Patients With Atrioventricular Nodal Reentry Tachycardia

The present study sought to assess the extent of gender differences in electrophysiologic parameters in patients with atrioventricular nodal reentrant tachycardia (AVNRT). The study population consisted of 203 patients (women/men ratio 2:1) who underwent slow pathway ablation. Patients with associated heart disease experienced the first episode of tachycardia at a significantly older age than patients with lone AVNRT (women 50 +/- 18 vs 29 +/- 15 years, p < 0.0001; men 45 +/- 20 vs 31 +/- 17 years, p = 0.01). Sinus cycle length (797 +/- 142 vs 870 +/- 161 ms, p = 0.0001), HV interval (41 +/- 7 vs 45 +/- 8 ms, p = 0.0001), atrioventricular (AV) block cycle length (348 +/- 53 vs 371 +/- 75 ms, p = 0.01), slow pathway effective refractory period (ERP) (258 +/- 46 vs 287 +/- 62 ms, p = 0.006), and tachycardia cycle length (354 +/- 58 vs 383 +/- 60 ms, p = 0.001) were shorter in women. No gender differences were noted in fast pathway ERP and ventriculoatrial (VA) block cycle length. In women, an AV block cycle length <350 ms along with a VA block cycle length <400 ms predicted tachycardia induction without the need for autonomic intervention, with a positive predictive value of 93% (sensitivity 71%, specificity 82%). No such cut-off values could be found in men. The acute success rate (100% vs 98%) and the recurrence rate (3% vs 6%) were similar for the 2 genders. In conclusion, in patients with lone AVNRT, the onset of symptoms occurred at a younger age than in patients with concomitant heart disease. Women had shorter slow pathway refractory periods, AV block cycle lengths, and tachycardia cycle lengths. No gender differences were noted in the fast pathway ERP. Therefore, women have a wider "tachycardia window" (i.e., the difference between the fast and slow pathway refractory periods), a finding that may explain their greater incidence of AVNRT.

Effects of a blocked atrial beat on the atrioventricular nodal recovery property in patients with dual nodal pathways.

Dual AVN physiology can be demonstrated by a variety of maneuvers. To determine whether AVN recovery times following a blocked extrastimulus facilitate or obscure detection of dual AVN physiology, 11 patients (9-17 years) were studied with dual AVN pathways by using single and double atrial extrastimuli. With a single atrial extrastimuli, the premature atrial stimulus (A2) was coupled to basic atrial beats (A1). The fast and slow AVN recovery curves were constructed with plots of the nodal conduction time against the recovery time (A1A2,A2H2). With double atrial extrastimuli, a fixed blocked A2 beat (A2B) was followed by a scanning atrial beat (A3). The nodal recovery property post-A2B was studied by plots of A2BA3,A3H3. In all patients the recovery curve of the fast pathway post-A2B had a leftward shift when compared to that of the pre-A2B curve (i.e., the AH was shortened at the same recovery time). The window of slow pathway conduction post-A2B disappeared totally in five patients and decreased significantly in six patients (post-A2B: 26 +/- 42 ms; pre-A2B: 80 +/- 65 ms, P < 0.05). In the six patients that still had slow pathway conduction post-A2B, the slow pathway effective refractory period post-A2B was significantly less than that of pre-A2B (215 +/- 38 vs 268 +/- 16 ms, P < 0.05). The fast pathway effective refractory period post-A2B was also diminished significantly (235 +/- 62 vs 357 +/- 76 ms, P < 0.0001). The authors conclude that blocked atrial beats decrease the visibility of the slow pathway conduction.

The effect of variable retrograde penetration on dual AV nodal pathways: observations before and after slow pathway ablation LDD.

Retrograde VA conduction is usually over the fast pathway and rarely over the slow pathway in patients with dual AV nodal pathways. It is unknown whether this apparent unidirectional conduction of the slow pathway is due to the lack of its retrograde conducting ability or the result of concealment. The effect of variable retrograde AV nodal penetration on antegrade AV nodal conduction was determined in patients with typical AV nodal reentrant tachycardia before and after the slow pathway ablation. Variable retrograde penetration was produced by delivering a ventricular extrastimulus simultaneously with (VE-0), 50 ms after (VE-50), or 100 ms after (VE-100) the last basic atrial stimulus, while atrial extrastimuli were used to determine changes of anterograde AV nodal effective refractory period (ERP) and A-H interval. The AV nodal functions measured without the ventricular extrastimuli served as the baseline. Although the mean slow pathway ERP was not significantly different among the different stimulation protocols, a significant shortening of the slow pathway conduction time (A-H from 348 +/- 60 to 324 +/- 119 ms, P < 0.05) was observed with upper level retrograde penetration of the AV node (VE-0). This facilitating effect became a prolonging effect when the retrograde penetration level moved to the lower level (VE-100, A-H from 324 +/- 119 to 366 +/- 122 ms, P < 0.05). The fast pathway ERP shortened with an upper level penetration (VE-0) but tended to prolong with a lower level retrograde-penetration (VE-100) both before and after the slow pathway ablation (preablation, from 348 +/- 143 of the baseline to 302 +/- 114 to 360 +/- 143 ms, P < 0.05; postablation, from 314 +/- 101 of the baseline to 274 +/- 118 to 361 +/- 143 ms, P < 0.05). The mean A2-H2 interval of the slow pathway was significantly shorter than the baseline (350 +/- 44 ms) with VE-0 (249 +/- 48 ms, P < 0.05) and VE-50 stimulation (285 +/- 82 ms, P < 0.05) but not with VE-100 stimulation (330 +/- 83 ms, P = NS). Before slow pathway ablation, the A2-H2 interval of the fast pathway at equal coupling intervals was shorter than the baseline (165 +/- 53 ms) with VE-0 (144 +/- 47 ms, P < 0.01) and VE-50 stimulation (152 +/- 43 ms, P < 0.05) but tended to be longer with VE-100 stimulation (175 +/- 47 ms, P = NS). After slow pathway ablation, the mean A2-H2 interval at the same coupling interval was shorter than the baseline (173 +/- 39 ms) with VE-0 (139 +/- 35 ms, P < 0.05), VE-50 (153 +/- 32 ms, P = 0.05) but tended to be longer with VE-100 stimulation (178 +/- 49 ms, P = NS). We conclude that: (1) concealed retrograde conduction can be demonstrated in both the slow and the fast AV nodal pathways; and (2) concealed retrograde conduction may either shorten or prolong anterograde refractoriness and conduction time, depending on the level of retrograde penetration.

Similar Time-Dependent Recovery Property of Fast and Slow Atrioventricular Nodal Pathways

The purpose of this study was to determine whether fast and slow atrioventricular (AV) nodal pathways have the same recovery property. AV nodal recovery property is studied by delivering atrial extrastimuli coupled to atrial beats and plotting nodal coupling intervals against nodal conduction time. In patients with dual pathways the resultant curves will include a fast to fast (F-F) and a fast to slow (F-S) pathway coupled curves. Although fast pathway recovery property can be represented by the former, slow pathway recovery property requires further assessment by studying slow to slow (S-S) pathways coupled curve. In 9 patients with dual pathways F-F, F-S, S-F, and S-S curves were obtained by pacing protocols. In 8 patients (control) without dual pathways, F-F curve and atrial extrastimuli coupled to a preceding slowly conducted fast pathway beat (also designated as S-F curve) were obtained. (1) The S-S curve had a similar time constant as the F-F curve. (2) Although the S-S curve was markedly shifted upward and leftward from the F-F curve, the degree of leftward and upward shifts of the S-S curve from the F-F curve were both close to the difference of the basic fast and slow pathway conduction time (a constant). (3) Although the effective refractory period of the fast pathway in dual pathway patients was longer than that of the control patients, the slow pathway effective refractory period when corrected was close to that of fast pathway in control patients. These results suggest that the fast and slow AV nodal pathways have a similar time-dependent recovery property.Dual atrioventricular nodal pathway recovery properties were studied by delivering progressively shorter atrial extrastimuli coupled to atrial beats in which the last or last few beats were conducting either via fast (F) or slow (S) pathways, and F-F, F-S, S-F, and S-S coupled recovery curves were constructed. Our results suggest that the fast and slow atrioventricular nodal pathways have similar time-dependent recovery property.

Effects of partial and complete ablation of the slow pathway on fast pathway properties in patients with atrioventricular nodal reentrant tachycardia.

The purpose of this study was to prospectively compare the effects of complete and partial ablation of slow pathway function on the fast pathway effective refractory period (ERP). The subjects were 20 patients (mean age 43 +/- 13 years) with atrioventricular nodal reentrant tachycardia (AVNRT), no structural heart disease, and easily inducible AVNRT. Autonomic blockade was achieved with propranolol (0.2 mg/kg) and atropine (0.04 mg/kg). After elimination of AVNRT and during autonomic blockade, the presence of residual slow pathway function was determined by the presence of a single AV nodal echo and/or dual AV nodal physiology. After autonomic blockade and before ablation, the mean fast pathway ERP was 319 +/- 44 msec and the mean slow pathway ERP was 251 +/- 31 msec. After slow pathway ablation and during autonomic blockade, 7 patients had residual slow pathway function and 13 did not. Complete loss of slow pathway function was associated with a shortening of the fast pathway ERP from 334 +/- 35 msec to 300 +/- 62 msec (P < 0.01), while the fast pathway ERP did not change significantly in patients with residual slow pathway function (291 +/- 29 msec vs 303 +/- 38 msec, respectively; P = 0.08). A shortening of 30 msec or more in the fast pathway ERP was observed in 11 of 13 patients who did not have residual slow pathway function, compared to 0 of 7 patients with residual slow pathway function (P < 0.001). Shortening of the fast pathway ERP after successful ablation of AVNRT is dependent upon complete loss of slow pathway function. This observation is consistent with electrotonic inhibition of the fast pathway by the slow pathway.

Clinical, electrocardiographic, and electrophysiological observations of dual A-V nodal pathways.

In 45 (25%) of 182 patients with various cardiac arrhythmias, dual A-V nodal pathways (DPWs) were diagnosed with atrial extrastimulus technique at least at one or more basic cycle lengths and/or after intravenous administration of atropine (1 mg). The jump of discontinuous A1A2, H1H2 curve of these 45 ranged from 25 to 235 (92±56) msec and the jump of A1A2, A2H2 curve ranged from 40 to 260 (107±55) msec. The fast pathway FRP (functional refractory period), slow pathway FRP, fast pathway ERP (effective refractory period) and slow pathway ERP was 464±87 msec, 532±91 msec, 404±96 msec and 328±70 msec, respectively. DPWs were demonstrated in 10 (59%) of 17 patients with paroxysmal supraventricular tachycardia (PSVT), 3 (5%) of 55 with WPW syndrome, 2 (20%) of 10 with paroxysmal atrial fibrillation, 11 (29%) of 38 with sick sinus syndrome, 10 (38%) of 26 with first degree and/or second degree A-V (AH) block, none of 3 with second degree HV block, 3 (27%) of 11 with bundle branch block and 6 (27%) of 22 with the other cardiac arrhythmias. In 17 patients with PSVT, seven demonstrated A-V nodal reentrant tachycardia. Six of these 7 had evidence of DPWs. In the other 7 of the 17, concealed accessory pathway was demonstrated. Three of these 7 had DPWs, which did not constitute the reentrant circuit. Twenty-eight of 45 patients (62%) with DPWs had one or more electrophysiological abnormalities suggesting A-V nodal dysfunction: 1) prolonged AH interval (>130 msec) during sinus rhythm (10 patients), 2) atrial pacing rates of 130 or less inducing A-V nodal Wenckebach periods (24 patients), 3) prolonged A-V nodal ERP or slow pathway ERP (>400 msec) (8 patients), and 4) prolonged A-V nodal FRP or fast pathway FRP (>500 msec) ( 16 patients). However, in most patients, atropine improved A-V nodal dysfunction. We consider that DPWs are a common electrophysiological finding and have a strong association not only with PSVT but also with A-V nodal dysfunction.