Electrophysiologic evidence for selective retrograde utilization of a specialized conducting system in atrioventricular nodal reentrant tachycardia.

In 12 patients with atrioventricular (A-V) nodal reentrant tachycardia, the existence and utilization of retrograde ventriculoatrial bypass tracts in the reentrant process were excluded, and the characteristics of the anterograde and retrograde limbs of the reentrant circuits were studied using His bundle electrograms, incremental atrial and ventricular pacing and atrial and ventricular extrastimulus techniques before and after the administration of 0.01 mg/kg of intravenous ouabain. Similar studies were also performed in five control patients without tachycardia. Paroxysmal supraventricular tachycardia could be induced in all 12 patients during atrial pacing-induced A-V nodal Wenckebach periods or premature atrial stimulation, or both. On the basis of conduction time in the retrograde limb during tachycardia and during retrograde studies, two groups were identified. Group I (seven patients) had (1) short (39 ± 10 msec) and constant conduction time in the retrogarde limb measured from the anterograde His bundle deflection to the retrograde atrial echo response (H-Ae interval), (2) no change in ventriculoatrial conduction time up to maximal ventricular pacing rates, (3) H₂-A₂ intervals during retrograde refractory period studies that were identical to the H-Ae intervals and that did not increase with decreasing V₁-V₂ intervals, and (4) increased conduction time of the anterograde limb (Ae-H intervals) after the administration of ouabain without any effect on retrograde limb conduction (H-Ae and H₂-A₂ intervals) and refractoriness. Group II (five patients) had (1) long and variable H-Ae intervals (60 to 180 msec), (2) a progressive increase in ventriculoatrial intervals during incremental ventricular pacing, (3) an increase in H₂-A₂ intervals in response to decreasing V₁-V₂ intervals, and (4) increased anterograde (Ae-H interval) and retrograde limb (H-Ae and H₂-A₂ intervals) conduction and refractoriness after the administration of ouabain. Changes in the H₂-A₂ interval corresponded to the changes in four of the five control patients. These findings suggest that (1) in group I the anterograde limb was the A-V node, whereas the retrograde limb was an A-V nodal bypass tract or an insulated intranodal tract physiologically unlike the A-V node; and (2) in group II the A-V node comprised both the anterograde and retrograde limbs of the reentrant circuit.     

A demonstration of differential refractoriness within a single fascicle of the human ventricular specialized conduction system

In 15 patients with left bundle branch block (LBBB), atrial (A), His bundle (H), and ventricular (V) electrograms were recorded. Successively more premature atrial depolarizations were introduced via a catheter in the right atrium. In eight patients, the ventricular specialized conducting system (VSCS) was the most refractory portion of the entire atrioventricular conducting system (AVCS) and A-V conduction, which had been occurring via the right bundle branch (RBB), failed below the His bundle as the effective refractory period (ERP) of the VSCS was reached. In two of these eight patients, after the ERP of the VSCS was exceeded, further shortening of the H₁-H₂ interval (by 40 to 50 msec.) resulted in an unexpected resumption of A-V conduction, but with markedly prolonged H-V intervals (160 to 230 msec.). This demonstrates that differential refractoriness exists within the RBB of these patients. A zone of maximal refractoriness was initially encountered within the RBB when the premature impulse first blocked below the His bundle. In relative terms, this zone was distal to a more proximal area of the RBB where, with further shortening of the H₁-H₂ interval, sufficient conduction delay occurred to permit recovery of excitability distally and the resumption of A-V conduction.     

Determinants of sustained slow pathway conduction and relation to reentrant tachycardia in patients with dual atrioventricular nodal transmission

In 24 patients with dual atrioventricular (AV) nodal pathways, multiple incremental atrial pacing studies were performed to obtain atrial (A) to His (H) basic driven (A₁ and H₁) and extrastimulus (A₂ and H₂) intervals. Discontinuous A₁-A₂ and H₁-H₂ intervals were analyzed for relations between initial coupling times and subsequent A-H responses, and to examine curves of sequential paced cycle lengths (A-A intervals) versus A-H intervals. Seventeen patients showed sustained slow pathway (SP) conduction with demonstration of discontinuous A-A and A-H curves. Sustained SP conduction occurred at critical atrial paced rates when the first paced beat was blocked in the fast pathway (FP) with conduction via the SP. Eleven of these 17 patients had inducible sustained supraventricular tachycardia (SVT). A-H interval during SVT in these 11 patients was closely related to SP A-H interval during atrial pacing at the paced rate comparable to SVT rate (r = +0.89, p < 0.001). The seven remaining patients showed continuous A-A and A-H curves. In three of these seven patients, sustained SVT was inducible, suggesting ability to sustain SP conduction. All of these three patients had continuous A₁-A₂ and H₁-H₂ curves during sinus rhythm so that the first atrial paced beat could not be blocked in the FP for subsequent SP conduction. In the other four of the remaining seven patients, despite block of the first atrial paced beat in the FP with SP conduction, the second paced beat was blocked in the SP so that all subsequent beats resumed FP conduction. In conclusion, sustalned SP conduction in patients with dual AV nodal pathways requires (1) an initiating beat being blocked in the FP, (2) a critical rate cycle length, and (3) the ability of SP for repetitive conduction at critical rates.     

Demonstration of multiple antegrade and retrograde atrioventricular pathways

A patient with paroxysmal supraventricular tachycardia had discontinuous antegrade (A₁-A₂, H₁-H₂) and retrograde (V₁-V₂, A₁-A₂) conduction curves suggesting dual A-V nodal pathways in both directions. Atrial echoes occurred with premature atrial pacing only at short A₁-A₂ coupling intervals after long antegrade (A₂-H₂) and retrograde (H₂-A_e) conduction intervals. Premature ventricular stimulation revealed ventricular echoes simultaneously with a sudden increase in the V₂-A₂ interval. The echo zone coincided with the slow pathway curve. Following atropine the echo zone was extended over the slow and fast pathway curves. Slow pathway conduction was observed at long and short V₁-V₂ coupling intervals, fast pathway conduction at intermediate V₁-V₂ coupling intervals. Following isoproterenol premature ventricular stimulation initiated two cycles of ventricular echoes with relatively long retrograde (V₂-A₂, V_e-A_e) and short antegrade (A₂-H_e, A_c-H_e) conduction times, the earliest atrial activation being observed in the low right atrium before the left atrium and the high right atrium. Antegrade fast and slow pathway as well as retrograde fast pathway conduction appeared to be confined to the A-V node. Retrograde slow pathway conduction may progress through a slow or fast A-V nodal pathway slowed by antegrade concealed conduction. However, an accessory pathway with long conduction times located near the septum cannot be ruled out entirely.     

Complete AV block developing in a patient with manifest ventricular preexcitation

This case report describes a 37-year-old man with manifest atriofascicular and fasciculoventricular connections who developed complete atrioventricular block. After resumption of 1:1 atrioventricular conduction, an electrophysiological study was conducted. During sinus rhythm, manifest ventricular preexcitation was observed and the AH and HV intervals were 80 msec and 50 msec, respectively. No change in AH interval during constant atrial pacing was observed by bolus injection of 20 mg of adenosine triphosphate. No changes in the morphology of the delta wave or HV interval were observed by changing the atrial pacing site. This patient developed HV block by atrial extrastimulus (S1S1: 600 msec, S1S2 相似文献   

Hemodynamic benefits of atrioventricular sequential pacing after cardiac surgery

The hemodynamic effects of atrioventricular (A-V) sequential pacing were assessed and compared with those of ventricular and of atrial pacing in 10 patients with and without heart block after cardiac surgery. Ventricular pacing alone was either hemodynamically detrimental or of no benefit in six of the eight patients who initially had sinus or accelerated junctional rhythms. Atrial pacing alone produced significant improvement in cardiac output in all patients who were not pacemaker-dependent. However, five of the eight patients with intact A-V conduction had further increases in cardiac output through A-V sequential pacing at shorter than intrinsic A-V intervals. Optimal A-V intervals for maximal cardiac output could be identified in all patients and varied widely. Significant changes in cardiac output occurred with relatively small deviations in the A-V interval. In selected patients after cardiac surgery, temporary A-V sequential pacing is a workable and valuable adjunctive form of hemodynamic support and is preferable to ventricular or atrial pacing.     

Atrioventricular nodal gap conduction as a manifestation of dual nodal pathways

Electrophysiologic studies were performed in a 76 year old patient for evaluation of sinus bradycardia. Atrial extrastimuli were induced during sinus rhythm at progressively decreasing coupling (A1-A2) intervals. At an A1-A2 interval of 420 msec, right bundle branch block developed, and at 370 msec conduction failed below the His bundle. When the interval was reduced to 320 msec, conduction resumed with a normal QRS pattern with an abrupt increase in A-H intervals from 165 to 305 msec. These findings are interpreted as type I or atrioventricular (A-V) nodal gap conduction physiologically related to conversion from a rapid to a slow A-V nodal conduction mode.     

Effect of glucagon on cardiac conduction in man

His bundle electrograms were obtained in 26 patients before and after intravenous administration of glucagon (50 μg/kg). The group consisted of 4 patients with normal conduction and 22 patients with conduction disease. The P-A interval, measured in all patients, was 35 ± 1.4 msec (mean ± standard error of the mean) before and 30 ± 1.5 msec after infusion of glucagon (P < 0.001). The mean A-H interval during sinus rhythm in all patients and during pacing at 100/min in 21 patients was, respectively, 97 ± 6.0 msec and 114 ± 6.4 msec before, and 96 ± 6.0 msec and 114 ± 6.6 msec after infusion of glucagon (not significant). The mean H-V interval in 25 patients was 48 ± 2.6 msec before and 49 ± 2.0 msec after infusion of glucagon (not significant). The mean sinus rate and sinus recovery times were, respectively, 73 ± 3.0 beats/min and 1,025 ± 42.0 msec before and 81 ± 3.0 beats/min and 919 ± 27.0 msec after infusion of glucagon (P < 0.001 and < 0.01). Functional and effective refractory periods were measured (In milliseconds) with use of the atrial extrastimulus technique. The mean atrial functional and effective refractory periods (21 patients) were, respectively, 273 ± 11.6 and 252 ± 12.0 before and 256 ± 10.0 and 238 ± 9.6 after infusion of glucagon (P < 0.001 and < 0.01). Mean atrloventricular (A-V) nodal functional refractory period (22 patients) and effective refractory period (15 patients) were 465 ± 22.0 and 404 ± 33.0 before and 457 ± 23.0 and 395 ± 32.0 after the infusion (not significant). The mean effective refractory period of the His-Purkinje system (2 patients) was 440 ± 45.0 before and 425 ± 55.0 after infusion of glucagon (not significant).In summary, glucagon increased sinus nodal automaticity, as manifested by an increase in sinus rate and decrease of sinus nodal recovery time, and improved intraatrial conduction as manifested by a reduction of the P-A interval and atrial functional and effective refractory periods. Glucagon had no effect on A-V nodal or intraventricular conduction.     

A new mechanism for atrioventricular nodal gap-vagal modulation of conduction

The well-known paradoxic behavior of atrioventricular conduction, the so-called gap phenomenon, that occurs when impulses within a certain range of coupling intervals are blocked while impulses with shorter coupling intervals are conducted is attributed to differences in properties of refractoriness in neighboring regions of the conduction system. In contrast, in the present study a model was developed showing a similar phenomenon, dependent on different electrophysiologic mechanisms and localized within the atrioventricular node in an isolated rabbit heart tissue preparation (n = 11). The hearts were paced at cycle length of 400-500 msec, and atrioventricular nodal conduction times (A2H2) were measured versus atrial extrastimulus (A1A2) coupling intervals by standard extrastimulus techniques. Postganglionic vagal stimulation was applied in the atrioventricular node as short bursts of subthreshold (for myocardium) stimuli with duration of 50-150 msec, amplitude of 20-800 microA, and absolute phase (delay after A1) of 0-500 msec. Vagal bursts with appropriate parameters consistently produced bimodal conduction curves. Initially, gradual shortening of the A1A2 coupling interval was associated with an increasing A2H2, with an accentuated increase (or even atrioventricular block) within an intermediate A1A2 range. However, further shortening of the A1A2 coupling interval produced a decrease in A2H2, which subsequently was followed by a block at the effective refractory period. Microelectrode recordings indicated that this characteristic bimodal pattern of conduction curves, demonstrating a gap, reflected transient vagally induced hyperpolarization in the N region of the node. In those instances where conduction block occurred and gap was manifest, the most marked hyperpolarization coincided with the time of arrival of midcycle premature extrastimuli, whereas the conduction of extrastimuli with either more or less prematurity was under less-marked vagal influence. Thus, this study demonstrates a new electrophysiologic mechanism producing anomalous conduction curves and the gap phenomenon within the atrioventricular node based on vagal-induced nonuniform recovery of diastolic excitability.     

The effect of nitroglycerin on atrioventricular conduction in man

His bundle electrograms were performed on 10 patients with organic heart disease. Six patients had had a recent myocardial infarction. Recordings were made at various rates utilizing right atrial pacing. Nitroglycerin, $\text{1}\text{150}$ gr, was administered to all 10 subjects, and the P-A, A-H, H-Q and H-S intervals were determined before, and immediately after the disappearance of the sublingually administered nitroglycerin. A significant decrease in the A-H interval occurred with negligible effects on the P-A, H-Q and H-S intervals. At the atrial pacing rate of 100/min, the average A-H interval fell from the control value of 152 msec to 129 msec after the administration of nitroglycerin (p < 0.02); at the pacing rate of 130/min, the A-H interval decreased from 194 to 133 msec (p < 0.05). Second degree heart block occurred at higher pacing rates in six patients after nitroglycerin administration as compared to the control value. The average postsuppression sinoatrial recovery time control value of 1,083 msec decreased to 906 msec after nitroglycerin administration (p < 0.01). These findings demonstrate that nitroglycerin can improve conduction through the A-V node.     

Pathologic correlations in a case of complete heart block with split his potentials resulting from a stab wound of the heart

A 23 year old previously healthy man was stabbed in the anterior chest. This resulted in a ventricular septal defect and complete atrioventricular (A-V) block. The electrocardiogram revealed complete A-V block with a QRS pattern of right bundle branch block. His bundle recordings 26 days later revealed A-V dissociation with split His potentials (P-H₁ interval of 100 msec and H₂-V interval of 40 msec). During the study the escape QRS shifted from right to left bundle branch block with H₂ potentials still preceding each QRS interval with H₂-V intervals of 40 msec. A permanent pacemaker was implanted because of persistent congestive heart failure and bradycardia due to A-V block. The patient subsequently became asymptomatic. He died suddenly 3 $\text{1}\text{2}$ years later.Pathologically there were sizable openings in both the tricuspid and mitral valve substance and a ventricular septal defect involving the pars membranacea and part of the adjacent muscular septum. Serial sections of the conduction system revealed total destruction and fibrous replacement of the bifurcation and beginning of the right and left bundle branches and subtotal fibrous replacement of the branching bundle. Thus, the bifurcation of the bundle of His was totally absent at autopsy despite apparent electrophysiologic evidence of its existence 26 days after the stab wound. A possible explanation for this discrepancy is the subsequent fibrosis of the bifurcation produced by hemodynamic changes at the lower margin of the ventricular septal defect.     

Electrophysiologic findings in patients with idiopathic hypertrophic subaortic stenosis

Thirteen patients with catheterization-proved idiopathic hypertrophic subaortic stenosis underwent intracardiac electrophysiologic study. There was a large incidence of arrhythmias and a strikingly large incidence of conduction system abnormalities among these patients. The P-A and A-H intervals were normal in all patients. Atrial pacing resulted in Mobitz type 1 block proximal to the His bundle at an abnormal rate (less than 140/min) in 2 of 12 patients (17 percent). H-V intervals were prolonged (greater than 50 msec) in 10 of 12 patients (83 percent) and were greater than 60 msec in 7 patients (58 percent). The atrial effective refractory period was prolonged in 3 of 12 patients and was markedly prolonged in 1 of them. Effective refractory period of the atrioventricular (A-V) node, determined in five patients, was prolonged in three. Dual responses of the A-V node to atrial extrastimuli were found in seven patients. Dual A-V nodal repsonses were evoked with propranolol in three patients and persisted in the other four patients with dual responses despite propranolol administration.     

Influence of pacemaker-induced tachycardia with A-V block on left ventricular blood velocity in man.

Phasic instantaneous left ventricular blood velocity was measured by radiotelemetry in 28 subjects with a Doppler ultrasonic flowmeter catheter during atrial pacing and induced A-V block Type I Wenckebach A-V block with conduction ratios of 9:8 or lower generally produced a stepwise reduction of peak left ventricular blood velocity in relation to shortened R-R intervals. Longer Wenckebach periods resulted in little or no blood velocity alteration during 1:1 A-V conduction. Those beats following a blocked atrial depolarization were associated with augmented blood velocities. In three subjects, bigeminal periods of 3:2 A-V block resulted in larger left ventricular blood velocities when compared with 2:1 A-V block, despite identical R-R intervals following the blocked P wave. This latter phenomenon was attributed to diastolic augmentation of left ventricular contraction following the second and hemodynamically ineffective beat during 3:2 A-V block. Three patients manifested true blood velocity alternation during second-degree A-V block and changing R-R intervals. The variations in peak left ventricular blood velocity observed during atrial pacing and A-V block are related to changing inotropic state and cycle length dependent alterations of left ventricular diastolic filling.     

Effects of bundle branch block on experimental A-V reentrant tachycardia

The effects of bundle branch block on experimental A-V reentrant tachycardia (PSVT) were studied in 17 dogs using an anomalous pathway simulatory (APS). The APS was a programmable digital electronic circuit with ability for ventricular sensing, retrograde conduction with programmable conduction time, and atrial stimulation. Close bipolar electrodes were positioned at seven contiguous atrial and ventricular sites (V_l) along the A-V ring, these being; anterior, lateral, and posterior right (AR, LR, PR), septal (S), and posterior, lateral and anterior left (PL, LL, AL). Right (R) (seven dogs) and left (L) (10 dogs) bundle branch block (BBB) were produced with transcardiac needle. After BBB, cycle length (CL) of A-V reentrant PSVT was significantly increased only with ipsilateral sites. Thus, with RBBB, CL of PSVT increased by 37 ± 3 msec., 27 ± 3 msec., and 23 ± 4 msec. (P < 0.001), at AR, LR, and PR sites respectively. With LBBB, CL of PSVT increased only with left-sided sites. Thus, CL increased by 34 ± 2.6 msec., 38 ± 4.6 msec., and 32 ± 3.3 msec., (P < 0.001) with PL, LL, and AL sites, respectively. PSVT CL and septal site did not change significantly after either R or LBBB. The increase in CL was explicable in terms of corresponding increases in intraventricular conduction time (H-V_l). There were slight compensatory decreases in A-H intervals for the increases in H-V_l. These studies confirm findings suggested by clinical electrophysiological observation.     

Initiation of two distinct forms of atrioventricular nodal reentrant tachycardia during programmed ventricular stimulation in man

Of 42 patients with supraventricular tachycardia related to dual atrioventricular (A-V) nodal pathway conduction, 8 had sustained tachycardia induced during programmed ventricular stimulation. The characteristics of the tachycardia in three patients suggested that the A-V nodal reentrant tachycardia used a slow pathway for anterograde conduction and a fast pathway for retrograde conduction (slow-fast form). In these patients, the retrograde effective refractory period was longer in the slow than in the fast pathway. Ventriculoatrial (V-A) conduction curves (V₁-V₂, A₁-A₂) were smooth. Ventricular premature beats, being conducted retrograde over the fast pathway, could activate the slow pathway in an anterograde direction, initiating the slow-fast form of A-V nodal reentrant tachycardia. In the remaining five patients, the tachycardia used a fast pathway for anterograde conduction and a slow pathway for retrograde conduction (fast-slow form). In these patients, the retrograde effective refractory period was longer in the fast than in the slow pathway. V-A conduction curves (V₁-V₂, A₁-A₂) could be either smooth or discontinuous if there was a sudden increase in V-A conduction time. Ventricular premature beats, conducted retrograde over the slow pathway, could activate the fast pathway in an anterograde direction, establishing a tachycardia circuit in reverse of the slow-fast form. In both groups of patients, the ventricular pacing cycle length appeared to be a crucial factor in the ability to expose functional discordance between the two A-V nodal pathways during retrograde conduction.The fast-slow form of A-V nodal reentrant tachycardia, similar to the slow-fast form, could also be induced during atrial premature stimulation in two patients. In this situation, the slow pathway having an anterograde effective refractory period longer, than that of the fast pathway was a requisite condition; anterograde A-V nodal conduction curves (A₁-A₂, H₁-H₂) were smooth. Atrial premature beats, conducted anterograde over the fast pathway, could activate the slow pathway in a retrograde direction resulting In an atrial echo or sustained fast-slow form of A-V nodal reentrant tachycardia.     

Evidence suggesting dual A-V nodal pathways in patients without supraventricular tachycardias.

Electrophysiologic evidence for dual pathways of conduction through the A-V node is presented in three patients without history of supraventricular tachycardia. In case 1, abrupt spontaneous changes in the PR interval from 0.17 to 0.42 second were seen. His bundle electrographic studies showed two sets of A-H intervals during sinus rhythm and at several atrial pacing rates, although at rates over 100 per minute only the slow pathway conducted. Using the extrastimulus method, different refractory periods for the fast and slow pathways were documented. Cases 2 and 3 underwent His bundle electrography studies to evaluate intraventricular conduction defects. During atrial pacing studies abrupt changes in the A-H interval, from 220 to 470 msec and from 220 to 370 msec, were observed on increasing the pacing rate from 90 to 95 per minute in case 2 and from 120 to 130 per minute in case 3. In these two patients, dual A-V nodal pathways were suggested by the sudden changes in the A-H -interval at critical pacing rates. These findings indicate that evidence suggesting dual pathways of conduction through the A-V node may not be an uncommon finding and may be present without the manifestation of recurrent supraventricular tachycardias.     

Wenckebach periods with repetitive block: evaluation with His bundle recording

Two patients are reported in whom repetitive block of two consecutive P waves occurred during Wenckebach beating induced by atrial pacing. His bundle recordings revealed block proximal to H in the first case, suggesting inhomogeneous conduction in the A-V node. In the second case, long cycle lengths were produced in the His-Purkinje system due to A-V nodal Wenckebach periods. The long cycles prolonged refractory periods in the His Purkinje system so that subsequent beats (short cycles) were blocked distal to H.The repetitive block of consecutive multiple atrial impulses could result in unexpected degrees of ventricular asystole during usually benign Type I second-degree A-V block.     

Analysis of anterograde and retrograde fast pathway properties in patients with dual atrioventricular nodal pathways: Observations regarding the pathophysiology of the Lown-Ganong-Levine syndrome

Anterograde and retrograde fast pathway properties were analyzed in 160 patients with anterograde dual atrioventricular (A-V) nodal pathways, with or without A-V nodal reentrant tachycardia. A-H intervals (reflecting anterograde fast pathway conduction) ranged from 46 to 234 ms (mean ± standard deviation 91 ± 30). The longest atrial paced cycle lengths at which block occurred in the anterograde fast pathway ranged from 231 to 857 ms (435 ± 112). Regression analysis of these cycle lengths versus A-H intervals revealed a correlation coefficient (r) value of 0.41 (p < 0.01). Retrograde fast pathway conduction was present (at a ventricular paced cycle length slightly shorter than sinus rhythm) in 84 of 125 patients: 15 of 16 with an A-H interval of less than 60 ms, 44 of 58 with an interval of 60 to 90 ms, 20 of 41 with an interval of 91 to 130 ms and 5 of 10 with an A-H Interval of more than 130 ms (p < 0.01). Retrograde fast pathway conduction was intact at a cycle length of 375 ms in 41 of 124 patients: 11 of 16 with an A-H interval of less than 60 ms, 22 of 57 with an interval of 60 to 90 ms, 7 of 41 with an interval of 91 to 130 ms and 1 of 10 with an A-H interval of more than 130 ms (p <0.01). Sustained A-V nodal reentrant tachycardia could be induced in 51 of 160 patients, being induced in 7 of 17 with an A-H interval of less than 60 ms, 27 of 72 with an interval of 60 to 90 ms, 15 of 59 with an interval of 91 to 130 and 2 of 10 with an interval greater than 130 ms (p < 0.05).In conclusion, in patients with dual A-V nodal pathways, there are relations between the A-H interval and the ability of the fast pathway to sustain sequential anterograde conduction, and between the A-H interval and the ability of the fast pathway to sustain sequential retrograde conduction. Among patients with dual pathways, patients with a shorter A-H interval are more likely to have A-V nodal reentrant tachycardia, because these patients are more likely to have excellent retrograde fast pathway sequential conduction (a requirement for the occurrence of reentrant tachycardia).     

Right atrial versus left atrial echo zones: A proposed new criterion for determining the atrial site of retrograde preexcitation

In a patient whose electrocardiogram (ECG) initially (1966) showed a Type A Wolff-Parkinson-White pattern, recurrent supraventricular tachycardia (SVT) developed but never subsequently showed antegrade bypass conduction. Intracardiac pacing studies (1975) revealed that premature high right atrial (induced 250–450 msec after atrial depolarization) or coronary sinus depolarization (250–550 msec) resulted in SVT. Late coronary sinus depolarization resulted in SVT without A-H prolongation. During SVT, P wave morphology changed and the coronary sinus atrial electrogram preceded that from the low right atrium; retrograde ventriculoatrial conduction time was 240 msec. Neither pacing the high right atrium or coronary sinus up to rates of 200 beats/min nor progressive atrial premature depolarizations from the high right atrium or coronary sinus resulted in antegrade bypass conduction. Failure of antegrade bypass conduction does not preclude SVT due to retrograde pre-excitation and must be distinguished from atrioventricular (A-V) nodal reentry. Atrial effective refractory period (200 msec) was shorter than the minimal time required for an atrial impulse to return to the atrium (380 msec), suggesting concealed antegrade bypass conduction. Stimulation of the atrium linked to the A-V bypass results in earlier bypass activation and recovery and explains the differing high right atrial vs coronary sinus echo zones.     

Inducibility of atrial fibrillation during atrioventricular pacing with varying intervals: role of atrial electrophysiology and the autonomic nervous system

INTRODUCTION: Patients receiving VVI pacemakers have a higher incidence of paroxysmal atrial fibrillation (AF) than those receiving DDD pacemakers. However, the mechanism behind the difference is not clear. The purpose of this study was to investigate whether atrial electrophysiology and the autonomic nervous system play a role in the occurrence of AF during AV pacing. METHODS AND RESULTS: The study population consisted of 28 patients who had (group I, n = 15) or did not have (group II, n = 13) AF induced by a single extrastimulus during pacing with different AV intervals. Atrial pressure, atrial size, atrial effective refractory periods, and atrial dispersion were evaluated during pacing with different AV intervals. Twenty-four-hour heart rate variability and baroreflex sensitivity also were examined. Atrial pressure, atrial size, effective refractory periods in the right posterolateral atrium and distal coronary sinus, and atrial dispersion increased as the AV interval shortened from 160 to 0 msec. During AV pacing, group I patients had greater minimal (52+/-17 vs 25+/-7 msec; P < 0.005) and maximal (76+/-16 vs 36+/-9 msec; P < 0.005) atrial dispersion than group II patients. The differences in atrial size and atrial dispersion among different AV intervals were greater in patients with AF than in those without AF. Baroreflex sensitivity (6.6+/-1.7 vs 3.9+/-1.0; P < 0.00005), but not heart rate variability, was higher in patients with AF than in those without AF. CONCLUSION: Abnormal atrial electrophysiology and higher vagal reflex activity can play important roles in the genesis of AF in patients receiving pacemakers.