The effect of sinus rhythum on the periodicity and coupling interval of ventricular parasystolic rhythm

Ventricular parasystole was studied in three patients. Longperiods of the ECG were analysed allowing features of the ectopicmechanism to be deduced.The ECGs were recorded on magnetic tapeand analysed with the aid of special purpose and digital computers.Sinusrhythm was found to alter the periodicity of the ectopic rhythmand to adjust its phase relation–ship relative to sinusrhythm. These effects were more marked when the ectopic periodwas similar to the sinus period or its multiple. In one patientphase adjustment resulted in periods of bigeminy with fixedcoupling.The adjustment of periodicity and phase probably resultsfrom subthreshold stimuli due to sinus rhythm modifying thefunction of spontaneous depolarization of the ectopic pacemaker.     

Bradycardia-dependent bundle branch block Relation to supernormal conduction and phase 4 depolarization

An electrocardiogram is presented in which spontaneous conversion of 2:1 block with first degree block and incomplete left bundle branch block resulted in 3:2 block with normal conduction of the QRS complex after the short R-R interval. Alternation of rate and block with every second beat is a variation of previously described bradycardia-dependent bundle branch block.

Phase 4 depolarization and supernormal conduction are inseparable concepts, and both may play a causal role in bradycardia-dependent bundle branch block. Criteria for recognition of this type of block should not disqualify cases in which supernormal conduction may be present, particularly since proximity of the QRS interval to the preceding T wave may not be an adequate test for supernormal conduction in clinical situations.

A knowledge of phase 3 and phase 4 events allows one to relate different types of clinical aberrance, from premature aberrance through early beat “normalization,” as in bradycardia-dependent bundle branch block, to normal rate aberrance as in typical bundle branch block and, finally, to escape beat aberrance.     

"Supernormal" Conduction and Excitability

"Supernormal" Conduction and Excitability. Electrocardiograph manifestation of "supernormal" conduction is defined as conduction that is more rapid than expected or presence of conduction when block is anticipated. It is not supernormal in the sense of being more rapid than normal. Therefore, the term relative supernormality or "supernormality" is more appropriate. The mechanism of "supernormal" conduction is conduction during a period of supernormal excitability and conduction associated with altered membrane potential. Some of the more common phenomena that are not dependent on conduction during the supernormal period but manifest better than expected conduction, thus simulating "supernormal" conduction, include dual AV nodal conduction, the "gap" phenomenon, "peeling back" of the refractory period, summation of subthreshold responses, diastolic phase 4 depolarization, and phasic autonomic influences.     

Effects of supernormal capture on directly measured nonmodulated parasystolic cycles

Pacemaker capture during the supernormal period was seen in a case of modulated parasystole where ectopic cycles occurred without any interposed nonparasystolic beat. This contrasts with previous clinical reports, since, in the latter, the parasystolic cycle length could not be measured directly. As in experimental studies, supernormal modulation resulted in a triphasic phase response curve. Although less likely, similar electrocardiographic changes could be produced by a conceptually different phenomenon, namely full parasystolic resetting due to loss of protection occurring exclusively early in the cycle, combined with modulation in the other (late) parts of the cycle.     

Second degree entrance block with supernormal conduction in intermittent ventricular parasystole

A patient with intermittent ventricular parasystole is reported in whom the presence of second degree entrance block with supernormal conduction was suggested for the first time. In this patient, ventricular extrasystoles with variable coupling frequently occurred. The QRS configuration of the extrasystoles was different from that of the parasystolic beats. When extrasystoles did not occur, the parasystolic beat was never seen because the conducted sinus impulse always reset the parasystolic rhythm. When an extrasystole occurred 0.52 sec or more after the preceding sinus beat, this extrasystolic impulse also reset the parasystolic rhythm. On the other hand, when an extrasystole occurred between 0.47 and 0.51 sec after the sinus beat, the parasystolic focus was protected from this extrasystolic impulse. When, however, an extrasystole occurred in a short terminal portion of the T wave of the preceding sinus beat, this extrasystolic impulse reset the parasystolic rhythm again, suggesting entrance block failure during the supernormal phase.     

Alternative mechanisms of apparent supernormal atrioventricular conduction

Alternative mechanisms were found to explain several different electrocardiographic examples of apparent supernormal atrioventricular (A-V) conduction in man using programmed premature atrial and ventricular stimulation and His bundle recordings. Sudden shortening of the P-R interval during A-V nodal Wenckebach phenomenon was due to manifest or concealed reentry within the A-V node. Gap phenomena in which late atrial premature depolarizations blocked while earlier atrial premature depolarizations conducted were shown to result from delay of earlier atrial premature depolarizations in the A-V node (type I gap) or in the His-Purkinje system (type II gap). Mechanisms analogous to the latter were found in cases of apparent supernormality of intraventricular conduction: Late atrial premature depolarizations resulted in aberration whereas earlier atrial premature depolarizations conducted normally because of delay within the A-V node or His-Purkinje system. Unexpected normalization of a bundle branch block pattern also resulted from Wenckebach phenomenon in the bundle branches. Atypical Wenckebach phenomenon with the first beat of the period demonstrated that aberration was due to phase 4 depolarization. Preexcitation of the ventricle before the delivery of a previously blocked atrial premature depolarization allowed conduction through the area of block (A-V node) because of earlier depolarization of the latter with earlier recovery. In the His-Purkinje system, 2:1 A-V block was converted to 1:1 conduction when a premature ventricular depolarization shortened the refractoriness of the His-Purkinje system.     

Effect of mexiletine on conduction of premature ventricular beats in man: a study using monophasic action potential recordings from the right ventricle.

Ventricular conduction intervals between a stimulating pacemaker electrode at the right ventricular apex and an impulse detecting monophasic action potential electrode at the right ventricular septum were measured in nine subjects. The right ventricle was paced at a constant rate and programmed premature ventricular stimuli were introduced after every eighth paced beat beginning at the refractory period. The ventricular conduction intervals were measured from the pacemaker artefact to the onset of depolarisation of the MAP recording. In the control recordings a short period of prolonged (subnormal) conduction lasting for 5 to 26 ms after the refractory period was present in six of the nine subjects. In eight subjects a period of 'supernormal' conduction lasting from 50 to 180 ms was present. The effect of mexiletine was to increase the subnormal conduction and to abolish the supernormal conduction. It is concluded that a small degree of supernormal conduction occurs in the normal human ventricle possibly as a result of phase 4 depolarisation of cells of the specialised conducting system.     

阈下电刺激对心律及异位节律点影响的实验研究

采用持续（２～８ｓ）阈下电刺激的方法，对９只家兔进行了研究，以探讨其安全性和对室性异位节律点传播的抑制效果。结果提示：（１）用不同频率，以起搏阈值的７０％为阈下刺激持续刺激心房或心室，对心律无影响。未发现心房颤动、心室颤动等心律失常。Ｐ─Ｅ、ＱＲＳ、Ｑ─Ｔ间期无变化（Ｐ＞０．０５）．（２）这种阈下刺激可有效地阻滞模拟室性心动过速的传播（８／９），其作用有空间限制性。作者认为简化的阈下电刺激方法更便于临床应用。     

The safety factor for electroventilation measured by production of cardiac ectopy in the anesthetized dog

The safety factor of electroventilation (ie, the ratio of the current required to produce an ectopic beat to the current required to produce an inspired volume of 225 ml, which is approximately twice tidal volume) was determined in 12 pentobarbital-anesthetized dogs using transthoracic electrodes positioned at the optimal electroventilation site. The optimal stimulation site for electroventilation was first determined using hand-held, stimulating electrodes. Then electrodes, 4.1 cm in diameter, were sutured bilaterally to the optimal stimulation site. The relationship between inspired volume and stimulus intensity was determined using a 0.8-s burst of stimuli (60/s) with a pulse duration of 0.1 ms. Using the same electrodes, the threshold current for producing ectopic beats was determined for single pulses ranging from 0.1 to 10 ms duration. In all dogs, the current required to produce an ectopic beat increased greatly as the pulse duration decreased. At 0.1 ms, the safety factor for electroventilation was calculated to be 25.8.     

Clinical significance of ventricular ectopic beats in the early posthospital phase of myocardial infarction.

The clinical significance of ventricular ectopic beats in the posthospital phase of myocardial infarction was studied in 272 patients aged 65 years or less who were followed up for 1 year after the infarction. Ventricular ectopic beats, identified in 6 hour electrocardiographic tape recordings, obtained before hospital discharge (study 1) and 5 months after discharge (study 2) increased in frequency and complexity in the 5 month interval. Ventricular ectopic beats at a rate of 20 or more per hour recorded before discharge were associated with complex ventricular ectopic patterns in the same 6 hour recording and with frequent (20 or more per hour), early cycle and bigeminal patterns in recordings mad 5 months later. Analysis with log-linear modeling indicated that the occurrence of complex ventricular ectopic beats at follow-up examination was associated with the concomitant use of antiarrhythmic agents,but not with use of digitalis, propranolol or tranquilizers. A ventricular ectopic beat frequency of 20 or more per hour at discharge was associated with increased (P less than 0.05) cardiac mortality in the initial 0 to 4 months after discharge but not in the subsequent 8 months; ectopic beats recorded in the 5 month follow-up study were not associated with increased cardiac mortality in the subsequent 5 to 12 months. The prognostic significance of ventricular ectopic beats is discussed in the light of these findings.     

Mechanisms of intermittent ventricular parasystole due to type II second degree entrance block

Three patients with intermittent ventricular parasystole are reported in whom the presence of second degree entrance block of type II or a type similar to that was shown. In all the patients, when a sinus beat occurred within a certain (the first) critical period after the preceding ectopic beat, the parasystolic focus was protected from this sinus impulse. When, on the other hand, a sinus beat occurred beyond another (the second) critical period after the ectopic beat, this sinus impulse reached and discharged the focus without an appreciable conduction delay. In one patient the second critical period was equal to the first one, while, in the other two, the second one was longer than the first one. In these two patients, when a sinus beat occurred between the two critical periods after the ectopic beat, this sinus impulse reached and discharged the focus after marked delay, and thereafter became a manifest or concealed re-entrant ventricular extrasystole. On the basis of these observations, an attempt was made to clarify the difference in mechanism between type I and type II second degree entrance block.     

Inhibition of premature ventricular extrastimuli by subthreshold conditioning stimuli

The purpose of this study was to determine whether trains of subthreshold high frequency conditioning stimuli (333 Hz, 1 ms duration, 2 ms interval) delivered to the canine ventricle inhibited the response to a premature stimulus (S2) more effectively than did a single subthreshold conditioning stimulus. It was found that trains of conditioning stimuli (mean 1.21 mA) inhibited the response to S2 152 ms beyond expiration of the ventricular effective refractory period, whereas a single conditioning stimulus inhibited S2 only 20 ms or less beyond the ventricular effective refractory period. In late diastole, trains of conditioning stimuli failed to inhibit S2 when the train of stimuli caused ventricular depolarization or the latter occurred in response to the next sinus impulse. Trains of conditioning stimuli did not induce ventricular arrhythmias. Lidocaine or autonomic blockade did not alter the response to trains of conditioning stimuli. Trains of conditioning stimuli or a single conditioning stimulus inhibited the response to S2 only when they were delivered at the same electrode site. By lengthening the ventricular effective refractory period, trains of conditioning stimuli could prevent or terminate tachycardias, but this possibility is constrained, at present, by the spatial limitations of the technique.     

Accelerated cardiac escape rhythms caused by ouabain intoxication

In anesthetized dogs treated with ouabain, the ventricular escape intervals were measured after (1) vagally induced atrioventricular block, (2) ventricular premature stimulation, or (3) cessation of a period of regular pacing at various cycle lengths. The escape intervals were a direct function of the basic cycle length and were significantly influenced by the last cycle length, whether premature or postmature. Postpacing acceleration of atrial ectopic responses was also demonstrated. When compared with results obtained in isolated Purkinje tissue, ectopic activity associated with early ouabain toxicity appears to be caused by frequency-related transient depolarizations rather than “true” phase 4 depolarization.     

Subthreshold atrial pacing in patients with a left-sided accessory pathway: an effective new method for terminating reciprocating tachycardia

This study investigated the possibility of terminating reciprocating atrioventricular (AV) tachycardia using subthreshold atrial pacing. Ten patients with a left-sided accessory pathway and sustained AV tachycardia underwent subthreshold atrial pacing from the coronary sinus site closest to insertion of the accessory pathway. In seven of these patients, the tachycardia could be reliably terminated with subthreshold atrial overdrive pacing. When pacing at a cycle length of 80 +/- 23% of the tachycardia cycle length, the minimal subthreshold current that was effective in tachycardia termination was 64 +/- 14% of threshold current and the maximal ineffective current was 49 +/- 17% of threshold (p less than 0.05). In all cases, the tachycardia was terminated by one or two instances of atrial capture that resulted in a premature atrial impulse (20 +/- 4% advancement of the atrial cycle) that blocked the AV node limb of the tachycardia. Anterograde conduction over the accessory pathway never occurred, either during the tachycardia or during subthreshold pacing after a return to normal sinus rhythm. No instances of atrial fibrillation were provoked by subthreshold pacing. Possible explanations for the intermittent atrial capture with critically placed subthreshold impulses include supernormal atrial conduction or summation of impulses at the atrial insertion site of the accessory pathway. It is concluded that subthreshold pacing is effective in selected patients with AV tachycardia due to an accessory pathway. Furthermore, because neither atrial fibrillation nor anterograde conduction over the accessory pathway is seen with subthreshold pacing, this modality may hold significant promise for permanent antitachycardia pacing in these patients.     

Junctional ectopic tachycardia in children: electrocardiography, electrophysiology and pharmacologic response.

Junctional tachycardia due to an automatic ectopic focus occurs in children in one of two clinical settings: (1) in the immediate postoperative period after surgery, near the atrioventricular (A-V) junction, and (2) spontaneously, causing chronic supraventricular tachycardia. In the surface electrocardiogram, Junctional ectopic tachycardia appears as a narrow QRS tachycardia with A-V dissociation. This study evaluated four children, including two sisters, with Junctional ectopic tachycardia; intracardiac electrophysiologic recordings were performed in three of them. In each child, ventricular depolarization was preceded by a His bundle potential and a normal H-V interval. Neither overdrive pacing nor programmed premature stimulation of the atria or the ventricles influenced the tachycardia. Digoxin failed to alter the tachycardia, but alleviated congestive heart failure in all four patients. Propranolol slowed the rate of tachycardia in two patients, as did reserpine and phenytoin in one patient each. Chlorpromazine resulted in sinus rhythm in one patient. Quinidine and lidocaine were ineffective. Two patients died, one from low cardiac output associated with uncontrolled tachycardia, the other suddenly and unexpectedly while receiving digoxin and propranolol. The third patient's tachycardia regressed after repair of a ventricular septal defect. She has had sinus rhythm for 9 months without medication. The tachycardia of the fourth patient is uncontrolled despite treatment with digoxin, propranolol and phenytoin. On the basis of this study, acute treatment of Junctional ectopic tachycardia is recommended in the immediate postoperative period with intravenous propranolol (with a ventricular pacemaker available to treat bradycardia) and long-term treatment with oral digoxin plus either propranolol, phenytoin or Chlorpromazine.     

右室流出道室性早搏的射频消融治疗

目的探讨射频消融治疗右室流出道室性早搏的方法和疗效。方法选择52例右室流出道室性早搏患者进行射频消融法治疗,男28例,女24例,年龄15~67岁,平均45.1岁;病史3~14年,平均6.8年均有明显症状,但无器质性心脏病的证据。多种抗心律药物治疗无效,心电图显示室性早搏均呈左束支阻滞图形,Ⅱ、Ⅲ、AVF导联为高大的R波。采用起搏标测。结果即刻成功率94%(49/52)。术前与术后1周24h动态心电图检查室性早搏为(11250~37460)次/24h和(0~1120)次/24h,两者间差异(P<0.01)。随访2~32个月,无复发。结论无器质性心脏病顽固性右室流出道室早的导管射频消融是一种安全可靠的方法。     

Ouabain-induced Wenckebach conduction block in canine Purkinje fibers: The role of cycle length and time dependent changes in membrane potential

The purpose of this study was to determine the mechanism for digitalis-induced Wenckebach conduction block. Canine Purkinje cells were exposed to ouabain (2.0 × 10^?7 M) and studied with conventional microelectrode techniques. When trains of stimuli were interrupted by a 5 second pause, restoration of stimuli resulted in successive action potentials showing an increasing slope of phase 4 depolarization which was expressed after the last beat as a delayed afterdepolarization. For any given state of ouabain toxicity, a beat-to-beat reduction in maximal diastolic potential could be induced by shortening the basic cycle length. If basic cycle length remained constant, continued exposure to ouabain would increase the net voltage reduction in membrane potential occurring during the train of ten beats. During the 5 second pause, an increase in membrane potential was observed and this hyperpolarization was of the same magnitude as the depolarization occurring during stimulation. With successive beats as membrane potential was reduced, action potential amplitude and $\text{dV}\text{dt}$ were concomitantly reduced and conduction slowed. Intracellular current threshold measurements showed that the reduction in membrane potential initially was associated with decreased current threshold requirements, but later in toxicity current threshold was markedly increased for beats occurring late in the train. These data suggest that (1) the beat-to-beat reduction in membrane potential is due to both an increase in the height of the delayed afterdepolarization and a reduction in maximal diastolic potential; (2) trains of beats are associated with progressive prolongation of activation time with concomitant reduction in $\text{dV}\text{dt}$ and membrane potential; and (3) failure of conduction is probably related to Purkinje segments showing decreased excitability.     

Initiation patterns of monomorphic ventricular tachycardia in acute myocardial infarction: analysis of rhythm strips

OBJECTIVE: Monomorphic ventricular tachycardias (MVT) frequently occur in the acute phase of myocardial infarction (MI). In the past, some studies aimed to investigate the initiation pattern of ventricular tachycardias, although not in acute MI patients. The aim of the present study was to analyse the initiation pattern of MVT in acute MI using rhythm strips. METHODS: This study utilized data on 255 rhythm strips defined as MVT, from 173 patients with acute ST-segment elevation MI. Monomorphic ventricular tachycardias that were not preceded by ventricular ectopic beats were defined as sudden onset MVT. Monomorphic ventricular tachycardias which were preceded by a single or multiple ectopic beats, including a short-long-short sequence, were defined as non-sudden onset MVT. RESULTS: Non-sudden onset episodes were more common than sudden onset episodes (172 episodes, 67.4% versus 83 episodes, 32.5%). The morphology of the ventricular ectopic beat initiating tachycardia was similar to the first beat of MVT in 127 episodes (73.8%), but not in the remaining 45 episodes (26.1%). In the non-sudden onset group, 117 episodes (68%) initiated with a single ectopic beat, while 55 episodes (32%) initiated with multiple complexes. The left ventricular ejection fraction of the patients with non-sudden onset MVT was lower (50 +/- 6 versus 56 +/- 5, P < 0.05). Monomorphic ventricular tachycardias with no sudden onset also had shorter coupling intervals (CI) (P < 0.001) and shorter prematurity index (PI) (P < 0.001) than MVT with sudden onset. Similarly, the ventricular tachycardia cycle length was shorter in the group of MVT subjects with non-sudden onset as compared with sudden onset (P < 0.05). In contrast, tachycardias with sudden onset were associated with a shorter preceding RR interval (P < 0.01). CONCLUSIONS: Analysis of rhythm strips demonstrated that MVT is most often preceded by ventricular ectopic beats in the acute phase of MI.     

Intermittent parasystole with concealed extrasystolic bigeminy during myocardial infarction.

A 72-year-old man demonstrated persistent intermittent ventricular parasystole for 6 days during an acute inferior wall myocardial infarction. Entrance block failure occurred at a critical interval of 1.24 sec. after parasystolic beats with resetting of the parasystolic cycle length. The first ectopic beat in each parasystolic series showed coupling to its second preceding conducted beat, and successive cycle lengths in each series usually showed gradual shortening. Concealed extrasystolic bigeminy was also demonstrated between parasystolic series with the number of intervening conducted beats conforming to the formula 2n + 2. After interpolated parasystolic beats, this formula became 2n + 3.     

Changes in sinus RR interval patterns preceding ventricular ectopic beats: assessment with rate enhancement and dynamic heart rate trends.

Changes in heart rate preceding ventricular ectopic beats may be used to identify clinical subsets of patients. We evaluated RR interval patterns preceding ventricular ectopic beats with a rate enhancement method which estimates ventricular ectopic beat dependence on the sinus RR interval preceding the ventricular ectopic beat and the dynamic heart rate trend, which is based on the slope of the five RR intervals preceding the ventricular ectopic beat. Using these two methodologies in 176 patients with frequent ventricular ectopic beats we identified several unique subsets of patients: (1) bradycardia-enhanced patients were younger with a high proportion of males and longer, more variable coupling intervals; (2) tachycardia-enhanced patients exhibited sleep suppression of ventricular ectopic beats and had shorter, less variable coupling intervals; (3) patients with predominantly no change in RR preceding the ventricular ectopic beat were significantly older, with greater prevalence of cardiovascular disease and reduced sinus RR variability, indicating decreased autonomic nervous system activity. These two methods may serve as a basis for further investigations regarding the treatment and prognosis of ventricular ectopic beats.