Analysis of Luciani-Wenckebach periodism in A-V node. I. Typical features (author's transl)

Electrocardiograms of 20 patients developing Wenckebach A-V block duting atrial pacing and 20 with spontaneous Wenckebach block were reviewed to determine the frequency of typical features of classical Wenckebach periodicity. Few cases only met all six typical criteria. Cases with long cycles with conduction ratios of 5/4, with Wenchkebach point less than 130 min, and with first greater than A-H 110 msec were the most likely to show typical features. The implications of these observations are discussed on the basis of modern hypothesis of electrophysiological mechanisms of Wenckebach periodism.     

Extra AV nodal Wenckebach periodicity

Extra AV nodal Wenckebach periodicity was diagnosed in seven patients. The most frequent form of this conduction abnormality was an exit block. The underlying block was localized in the sinoatrial junction and in the atria in two patients; the AV junction and the ventricle were the site of the Wenckebach periodicity in one case each. In extra AV nodal exit block, the actual conduction delay is not seen on the ECG and the diagnosis is based on the progressive shortening of the P-P or R-R intervals followed by a pause which is less than twice the shortest P-P (R-R) interval depending on the level of the block. A Wenckebach periodicity in the bundle branches or within the reentry pathway each occurred in one patient. In these forms of Wenckebach periodicity, the diagnosis is established more readily because the conduction delay can be demonstrated on the surface ECG. The clinical significance of extra AV nodal Wenckebach periodicity is discussed.     

A new method for evaluating the effect of antiarrhythmic drugs on atrioventricular nodal conduction

Electrophysiological variables were studied in 19 patients before and after one of three commonly used antiarrhythmic agents. The pacing rate at which alternating Wenckebach periods appeared in eight patients was significantly reduced by intravenous digoxin (0.01 mg/kg body weight). The atrioventricular nodal conduction time (A-H interval) and Wenckebach point were not significantly altered by digoxin. Intravenous propranolol (0.1 mg/kg body weight) in four patients did not affect the A-H interval, but it reduced the pacing rates at which the Wenckebach point and alternating Wenckebach periods occurred. Intravenous disopyramide (2 mg/kg body weight) significantly increased the pacing rate required to produce alternating Wenckebach periods but did not significantly alter the other indicators of atrioventricular conduction in seven patients. It is concluded that the pacing rate required to produce alternating Wenckebach periodicity may be a useful and sensitive variable in the evaluation of the effect of antiarrhythmic agents on atrioventricular nodal conduction.     

A new method for evaluating the effect of antiarrhythmic drugs on atrioventricular nodal conduction.

Electrophysiological variables were studied in 19 patients before and after one of three commonly used antiarrhythmic agents. The pacing rate at which alternating Wenckebach periods appeared in eight patients was significantly reduced by intravenous digoxin (0.01 mg/kg body weight). The atrioventricular nodal conduction time (A-H interval) and Wenckebach point were not significantly altered by digoxin. Intravenous propranolol (0.1 mg/kg body weight) in four patients did not affect the A-H interval, but it reduced the pacing rates at which the Wenckebach point and alternating Wenckebach periods occurred. Intravenous disopyramide (2 mg/kg body weight) significantly increased the pacing rate required to produce alternating Wenckebach periods but did not significantly alter the other indicators of atrioventricular conduction in seven patients. It is concluded that the pacing rate required to produce alternating Wenckebach periodicity may be a useful and sensitive variable in the evaluation of the effect of antiarrhythmic agents on atrioventricular nodal conduction.     

Atrial pacing-induced alternating Wenckebach periodicity and multilevel conduction block in children

Multilevel block within the atrioventricular (AV) node has not been previously described in children. Six children with atrial pacing-induced repetitive block are presented. The conduction patterns satisfy the requisites for alternating Wenckebach periodicity or multilevel AV block. In 2 patients the block is documented in the AV node and infra-His region. In 4 patients multilevel block within the AV node is postulated by deductive reasoning. In this study, 2 patterns of alternating Wenckebach periodicity are reported for the first time: sequences of 3:1 block with progressive prolongation of the conducted impulses terminating in 4:1 block; and sequences of 2:1 block with progressive prolongation of the conducted impulses terminating in 2 series of 3:1 block, in which the first conducted impulse following the first 2 blocked beats is not the shortest one, whereas that following the second 2 blocked beats is the shortest.     

His bundle recordings in atypical A-V nodal Wenckebach block during cardiac pacing

The features of the classic atrioventricular (A-V) nodal Wenckebach phenomenon are attributed to a conduction delay in the A-V nodal region. Changes in the P-R intervals merely represent the variations of the H-H intervals. The characteristic abnormalities of the latter consist of: (1) a gradual increase in P-H intervals; (2) a progressive decrease of the P-H increments; (3) a progressive diminution of the H-H intervals; (4) the long H-H interval produced by the nonconducted P wave is equal to the sum of the increments subtracted from twice the P-P intervals; and (5) the H-H interval after the intermission is longer than the H-H interval preceding the pause.     

Electrocardiographic patterns during Holter monitoring in patients with first and second degree A-V block due to 'dual A-V nodal pathways'

The electrocardiographic patterns, observed during 24-h Holter monitoring, of 10 patients (mean age 35 +/- 22 years) with first and second degree A-V block due to dual A-V nodal pathways are reported. Recordings were selected according to the presence of: sudden and persistent prolongation of the PR interval: sudden normalization of the PR interval: 'atypical' Wenckebach sequences showing sudden and pronounced prolongation of any PR interval prior to the blocked P wave. Besides the already recognized pattern, new aspects were identified: (1) Wenckebach sequences in the slow and fast pathways characterized by a progressive increase in the PR interval until a blocked P wave occurred during long and short PR interval periods, respectively; (2) Wenckebach periods first in the slow and then in the fast pathway; (3) 2:1 A-V block with a normal PR interval in the conducted beat after a Wenckebach sequence in the slow pathway; (4) Wenckebach in the fast pathway and, subsequently, in the slow one characterized by a slight prolongation of the PR interval for some beats followed by a sudden and pronounced increase in the PR interval of one beat and a subsequent progressive slight PR prolongation until a blocked P wave occurred; (5) Wenckebach sequence in the fast pathway with subsequent conduction over the slow pathway without a blocked P wave; (6) blocked P waves during both long and short PR interval periods with slight prolongation of the preceding PR interval. The electrophysiological mechanisms involved in these electrocardiographic patterns together with the nature (anatomical or functional) of the intranodal pathways and the clinical significance of this type of block are discussed.     

Effect of cold isotonic glucose infusion on A-V nodal conduction.

His bundle electrograms were performed in eight patients with organic heart disease. Recordings were made at various rates utilizing right atrial pacing. A solution of 100 cc of iced cold 5% glucose and water was infused through a cardiac catheter placed at the level of the tricuspid valve. The P-A, A-H, H-Q and H-S intervals were determined before and immediately after the cold water infusion. A significant prolongation of 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 increased from the control value of 116 to 125 msec after the infusion (P less than 0.02); at the pacing rate of 140/min, the A-H interval increased from 147 to 158 msec (P less than 0.01). This represents an impairment in conduction through the atrioventricular node.     

Electrophysiologic studies on atrioventricular nodal Wenckebach cycles

Wenckebach cycles with a 4:3 ratio, produced by rapid atrial pacing, were studied in 27 anesthetized denervated dogs using programmed stimulation. A test stimulus (S') could be inserted after any preselected beat of the Wenckebach cycle. An on-line computer measured the atrial (A) to His bundle (H) intervals. In all dogs a progressive increase in atrioventricular (A-V) nodal refractoriness was seen in the effective refractory period for each beat and a rightward shift of the A'-H' relative to the A-A' refractory curves. Atypical Wenckebach cycles could be produced by small changes in the basic cycle length. No evidence for reentry was found from the refractory curves of Wenckebach cycles and by interruption of stimulation after the third stimulus of a 4:3 Wenckebach cycle. Analysis of the A'-H' relative to the H-A' refractory curves did not confirm a positive feedback mechanism. In order to mimic a Wenckebach cycle, a blocked premature beat was inserted during stressed 1:1 conduction. The changes in the refractory curves for successive beats after the premature beat were rate-dependent and similar to those in Wenckebach cycles but smaller in magnitude. In Wenckebach cycles there is a progressive increase in refractoriness, caused by cumulative effect similar to that seen after a blocked beat during stressed 1:1 conduction, until block occurs and the cycle resets.     

Effect of glucose-insulin-potassium infusion on the human conduction system

His bundle electrograms were performed in 21 patients with organic heart disease. Recordings were made at various rates utilizing right atrial pacing. A mixture containing 50 g of glucose, 10 mEq of potassium and 20 units of insulin was given intravenously over 10 minutes to 10 subjects. The P-A, A-H, H-Q and H-S intervals were determined before and immediately after the glucose-insulin-potassium infusion. A significant prolongation 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 increased from the control value of 140 msec to 151 msec after the infusion (P < 0.05); at the pacing rate of 140/min, the A-H interval increased from 145 to 165 msec (P < 0.05). The identical study was performed in three additional patients who received an infusion of 50 g of glucose and 20 units of insulin. No significant change was observed in the conduction system. In eight patients a solution of 2.6 mEq of potassium in 65 cc of 5 percent glucose and water was infused over an 8 minute period. A significant prolongation of the A-H interval was observed. At the atrial pacing rate of 100/min, the average A-H interval increased from the control value of 122 to 133 msec after the glucose and potassium infusion (P < 0.05), whereas at the pacing rate of 140/min, the A-H interval increased from 165 to 188 msec (P < 0.05). These findings demonstrate that the potassium in a glucose-potassium-insulin infusion may cause impaired conduction through the atrioventricular node.     

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.     

Electrophysiologic studies in the syndrome of short P-R interval, normal QRS complex

Eighteen subjects with a short P-R interval (<0.12 second) and normal QRS complex were studied by means of His bundle recordings and programmed atrial premature depolarizations. Eight subjects had a history of supraventricular tachycardia. During sinus rhythm, the A-H interval was less than or at the lower limits of normal values (45 to 80 msec), and the H-V interval was normal (30 to 50 msec). Atrial pacing at rates of up to 160/min produced 3 types of responses. Thirteen subjects showed a progressive increase in A-H interval similar to that of normal subjects but to a lesser degree. Three subjects showed an initial increase at low pacing rates, followed by a plateau response and further increase at higher rates. Two subjects showed no significant increase in the A-H interval. In 6 of 8 subjects with supraventricular tachycardia, atrial premature depolarizations produced atrial echo beats and sustained supraventricular tachycardia in 4, indicating atrioventricular (A-V) nodal reentry as the mechanism for the supraventricular tachycardia. In 10 subjects, refractory periods of the various components of the A-V conducting system were found to be similar to those of subjects with a normal P-R interval. The data suggest the following possible explanations for the short P-R interval: (1) total or partial bypass of the A-V node; (2) an anatomically small A-V node; (3) a short or rapidly conducting intranodal pathway; or (4) isorhythmic A-V dissociation.     

Effects of the pacing site on A-H conduction and refractoriness in patients with short P-R intervals.

His bundle recordings were studied in four patients with short P-R and A-H intervals, and narrow QRS complexes, who had experienced several episodes of supraventricular tachyarrhythmias. The heart was paced from the high right atrium (HRA) and the coronary sinus (CS). In three patients the A-H Wenckebach phenomenon occurred at higher rates (greater than 200 pacing beats/min) when the CS was paced than when pacing was performed from the HRA. Moreover, CS stimulation produced smaller increments in the A-H interval than did pacing from HRA. The extrastimulus method of testing was done. In cases 1 and 2 the functional refractory period of the A-H tissues was 15 to 25 msec shorter during CS pacing than when pacing from the HRA. In case 3, the low right atrium (LRA) as well as the other two sites were paced. A type 1 gap was seen from HRA, a type 2 gap from CS, and both types appeared when the LRA was paced. Case 4, in which the mid-right atrium (MRA) was also stimulated, had a double pathway from HRA and CS with conduction through the accessory pathway late in the cycle and through the A-V node earlier in the cycle. However, the A-V node could not be penetrated during MRA stimulation. It appeared that the pacing site influenced the A-H conduction pattern and refractoriness, possibly by changing the site and/or mode of entry of the stimulus into the pathways that are responsible for this syndrome.     

The incidence of typical and atypical A-V Wenckebach periodicity

The classic pattern of the typical WP's consists of (1) progressive lengthening of the P-R intervals with the largest increment occurring in the second conducted beat, (2) progressive decrease in P-R increment which accounts for the progressive shortening of successive R-R intervals, and (3) the pause produced by the nonconducted P-wave is less than two P-P intervals. In 45 patients with atrial pacing-induced Wenckebach periods of A-V conduction, the structure of these was studied with His bundle recordings. Of the 128 periods analyzed exceeding 3:2 A-V conduction ratios, 66 per cent were atypical. In 24 patients with spontaneous WP's of A-V coduction, the electrocardiographic records were studied. Of the 98 periods analyzed exceeding 3:2 A-V conduction ratios, 86 per cent were atypical. WP's with A-V conduction ratios greater than 6:5 were all atypical. Five categories of atypical WP's are described.     

Wenckebach atrioventricular block (Mobitz type I) in children and adolescents

Mobitz type I atrioventricular block in children, adolescents and young adults without overt heart disease or drug intoxication has been considered less significant than Mobitz type II block. In highly trained athletes and some nonathletes it has been presumed to be a benign manifestation of heightened vagal tone. Experience with 16 young patients, 6 female and 10 male, tends to alter the concept of benignity. Known onset of Wenckebach and varying first degree block was between 6 months and 17 years of age. Of eight patients followed up for 5 to 18 years, five have fixed complete heart block and three first degree block. Of eight followed up for 1 to 4 years, two have fixed complete heart block and the others varying first, second and third degree block. Two have required a pacemaker implant. On intracardiac electrography performed in seven patients, four manifested during sinus rhythm a Wenckebach response to atrial pacing at abnormally slow rates; in addition, the His bundle electrograms showed A-H delay in one patient, H-V delay in two patients and delay in both intervals in one patient. Of three patients studied during complete heart block all manifested A-H block and one also H-V prolongation. The occurrence of Wenckebach block in 7 of 16 children and adolescents before the development of fixed complete heart block suggests that such block is probably more common than heretofore recognized and may be a phase in the natural history of the development of idiopathic heart block. It often represents significant disease of the cardiac conduction system, which may be progressive, and it has a guarded prognosis.     

Unique electrophysiologic characteristics of atrioventricular nodal reentrant tachycardia with different ventriculoatrial block patterns: Effects of slow pathway ablation and insights into the location of the reentrant circuit

BACKGROUND: The electrophysiologic mechanisms of different ventriculoatrial (VA) block patterns during atrioventricular nodal reentrant tachycardia (AVNRT) are poorly understood. OBJECTIVES: The purpose of this study was to characterize AVNRTs with different VA block patterns and to assess the effects of slow pathway ablation. METHODS: Electrophysiologic data from six AVNRT patients with different VA block patterns were reviewed. RESULTS: All AVNRTs were induced after a sudden AH "jump-up" with the earliest retrograde atrial activation at the right superoparaseptum. Different VA block patterns comprised Wenckebach His-atrial (HA) block (n = 4), 2:1 HA block (n = 1), and variable HA conduction times during fixed AVNRT cycle length (CL) (n = 1). Wenckebach HA block during AVNRT was preceded by gradual HA interval prolongation with fixed His-His (HH) interval and unchanged atrial activation sequence. AVNRT with 2:1 HA block was induced after slow pathway ablation for slow-slow AVNRT with 1:1 HA conduction, and earliest atrial activation shifted from right inferoparaseptum to superoparaseptum without change in AVNRT CL. The presence of a lower common pathway was suggested by a longer HA interval during ventricular pacing at AVNRT CL than during AVNRT (n = 5) or Wenckebach HA block during ventricular pacing at AVNRT CL (n = 1). In four patients, HA interval during ventricular pacing at AVNRT CL was unusually long (188 +/- 30 ms). Ablations at the right inferoparaseptum rendered AVNRT noninducible in 5 (83%) of 6 patients. CONCLUSION: Most AVNRTs with different VA block patterns were amenable to classic slow pathway ablation. The reentrant circuit could be contained within a functionally protected region around the AV node and posterior nodal extensions, and different VA block patterns resulted from variable conduction at tissues extrinsic to the reentrant circuit.     

Atrial fibrillation: minimal sampling interval to estimate average rate

The average heart rate and maximal heart rate (average R-R and shortest R-R intervals) in atrial fibrillation are frequently calculated to assess drug effect. The minimum recording sample to obtain accurate estimates of "instantaneous" average and maximum heart rate has not been established. We analyzed the R-R intervals after a 4 minute ECG recording in 40 supine patients with chronic atrial fibrillation. A "life table" analysis revealed that the average heart rate derived from a 20 second sample of atrial fibrillation approximates (+/- 5%) the true value in an estimated 92.5% of patients. On the other hand, a two minute sample is required to approximate the shortest R-R interval within 5% of the true value in 90% of patients. Studies utilizing average R-R interval and shortest R-R interval as an index of drug response should use electrocardiographic sampling intervals of at least 30 seconds and two minutes respectively.     

Simultaneous anterograde fast-slow atrioventricular nodal pathway conduction after procainamide

Three patients with paroxysmal supraventricular tachycardia underwent electrophysiologic studies that included His bundle recordings, incremental atrial and ventricular pacing and extrastimulation before and after intravenous infusion of 500 mg of procainamide. In all three patients the tachycardia was induced during atrial pacing or premature atrial stimulation, or both. Two of the three patients had discontinuous atrioventricular (A-V) nodal curves with induction of a slow-fast tachycardia during failure in anterograde fast pathway conduction and one patient had a smooth A-V nodal curve with induction of a slow-fast tachycardia at critical A-H interval delays. After procainamide: (1) in all three patients atrial pacing induced A-V nodal Wenckebach periodicity (cycle length 300 to 400 ms) resulting in simultaneous anterograde fast and slow pathway conduction (one atrial beat resulting in two QRS complexes) and retrograde fast pathway conduction initiating an echo response or a slow-fast tachycardia, or both; (2) in all three patients there was enhanced conduction and shortening of refractoriness of the anterograde fast pathway and depressed conduction and lengthening of refractoriness of the retrograde fast pathway; and (3) in two patients there was inability to sustain tachycardia because of selective block within the retrograde fast pathway. In conclusion: (1) procainamide altered conduction and refractoriness of the anterograde fast and slow pathways so that simultaneous conduction could occur during atrial pacing, resulting in a double ventricular response and a slow-fast echo or tachycardia, or both; and (2) the differential effects of procainamide on anterograde fast and retrograde fast pathways suggests two functional A-V nodal fast pathways, one for anterograde and the other for retrograde conduction.     

Baroreceptor control of atrioventricular conduction in man.

Although human baroreflexes are known to exert a powerful physiological control on heart rate, little information exists on the physiological control they exert on the atrioventricular conduction system. In 11 normotensive subjects with normal atrioventricular conduction, we altered baroreceptor activity by injection of pressor and depressor drugs (phenylephrine and trinitroglycerin) and recorded mean arterial pressure (MAP, catheter measurements), R-R interval, and pre-His and post-His intervals (A-H and H-V, His bundle recording). With the subjects in sinus rhythm, increasing MAP by 21+/- 1 mm Hg caused a marked lengthening (250 +/- 28 msec), and decreasing MAP by 17 +/- 2 mm Hg a marked shortening (142 +/- 16 msec) of the R-R interval. There was little change in the A-H interval and no change at all in the H-V interval. However, when the R-R interval was kept constant in these subjects by atrial pacing, a similar increase and decrease in MAP caused, respectively, a marked lengthening (49 +/- 6 msec) and shortening (19 +/- 3 msec) of the A-H interval, although the H-V interval remained unaffected. Thus physiological ranges of baroreceptor activation have a marked influence on the atrioventricular node but apparently not on the ventricular portion of the atrioventricular conduction system. This influence is unmasked when pacing prevents the baroreceptor influence on the sinoatrial node.     

Reverse alternating Wenckebach periodicity

An atrial pacing-induced reverse conduction pattern of the alternating Wenckebach periodicity was observed in 5 of 42 children (12%) during electrophysiologic study. This conduction pattern is a reverse of the usual alternating Wenckebach periodicity: During an underlying 2:1 atrioventricular conduction block there is progressive shortening of the conduction time of the conducted impulses with termination in a lower degree of block. This reverse alternating Wenckebach periodicity may be caused by a mechanism similar to that in other Wenckebach phenomena.