Sensing of concealed ventricular extrasystoles by pacemakers. Fifty years later

Whether a pacemaker can sense concealed ventricular extrasystoles still remains debatable since its occurrence was first proposed in 1972. It must remain a diagnosis of exclusion if it really exists. Isoelectric complexes and all the causes of oversensing especially discrete false signals generated by a defective pacemaker lead must be excluded before concealed ventricular extrasystoles can be postulated.     

Cryosurgery for ventricular bigeminy using a transaortic closed ventricular approach

Disabling monomorphic ventricular bigeminy has not been describedas an indication for surgery. Three young patients with thisarrhythmia sometimes deteriorating into ventricular tachyarrhythmiasand in whom drug therapy failed completely were accepted forsurgical ablation of the arrhythmogenic area. The earliest endocardialsite of origin was located preoperatively by catheter mappingof the spontaneously occuring ventricular bigeminy in the leftand right ventricles. For maximum preservation of myocardialmuscle and function, the peroperative mapping and surgical procedurewere preformed through the aortic root; mapping by transaorticmultipolar balloon was done during normothermic coronary perfusionand cryocoagulation was done during cardioplegic arrest. Cryocoagulationof the endocardial site was performed using the transaorticapproach and epicardial cryocoagulation at the opposite sitewas done afterwards. In the two patients in whom the peroperativemapping results were consistent with those of preoperative cathetermapping, the arrhythmia could be abolished, as documented duringlong-term follow-up. In the only patient in whom the mappingresults were not in agreement, the ventricular arrhythmia reoccurredand was the cause of death at five months after surgery. Postoperativewall-motion studies performed in the two surviving patientsshowed limited scars in the area of cryocogulation and minordamage to the coronary arteries in that area. The transaorticapproach can be considered as a new and important surgical optionfor endocardial mapping and cryocoagulation which prevents thedamaging effects of a left ventriculotomy.     

Prognostic significance of right ventricular extrasystoles

Extrasystoles (RVES) from the right ventricular outflow tract(RVOT) are a common arrhythmia in routine ECGs. METHODS: In this prospective study 56 consecutive patients with RVES(22 males, 34 females) were examined for morphological and/orfunctional right ventricular (RV) abnormalities by 12-lead,Holter, exercise ECGs, transthoracic echocardiography and signalaveraging. The follow-up time was 3.1–15.8 years (arithmeticmeanSD=7.21.6 years; median, 6.9 years). Patients with hyperthyroidism,structural cardiovascular and/or lung diseases were excluded. RESULTS: A total of 57.1% of the patients with RVES presented with echomorphologicabnormalities of the right ventricle (RV). In 26.8% the echomorphologicright ventricular abnormalities progressed in 33.3% of patientswith normal RVs at baseline (group I) and in 21.9% of thosewith abnormal RVs at baseline (group II). No significant differences were found between the 2 patientgroups in terms of age at onset, family history, ECG changes,late potentials and malignant right ventricular outflow tractarrhythmias on 24-h and exercise ECGs. While females predominatedin group I, males were numerous in group II (p=0.006). Sustainedventricular tachycardia, syncope or sudden death were absentthroughout the follow-up. CONCLUSION: Patients with RVES carry a good prognosis in terms of morbidityand mortality no matter whether echomorphologic abnormalitiesare present or not.     

Unifocal origin of multiform extrasystoles in concealed bigeminy

A case of concealed bigeminy is presented in which two forms of extrasystolic complexes were evident on the ECG. One form (type B) appeared after a single conducted sinus beat, in a pattern of manifest bigeminy. The other form (type A) occurred after a sequence of more than one conducted sinus beat. The two configurations have previously been explained on the basis of different foci and mechanisms. Certain features of the ECG from our patient suggested that the two forms originated from a common site. An experimental model was developed in which the right ventricle of a dog was stimulated at sub- or suprathreshold voltages on alternate sinus beats to simulate concealed bigeminy. The ECG obtained during stimulation of a single site was remarkably similar to that recorded from the patient. We have proposed that the extrasystoles that occur after a compensatory pause may spread in a manner different from those that follow a basic cardiac cycle length. The different pattern of propagation is probably ascribable to the lengthening of the refractory period of the cardiac tissues by the compensatory pause.     

Cod liver oil does not reduce ventricular extrasystoles after myocardial infarction

Previous work has shown that in experimental animal models a lower incidence of arrhythmias and sudden death was observed if the animals were fed cod liver oil or fish oil. After a 48-h control period starting, on average, 8 days after the onset of symptoms, 18 men who were recovering from acute myocardial infarction were given 20 ml d-1 cod liver oil for 6 weeks, either immediately after the control period, weeks 0-6 (n = 10), or during weeks 6-12 (n = 8). Forty-eight-hour Holter monitoring was carried out before cod liver oil administration and at the end of weeks 6 and 12. The eicosapentaenoic acid content of plasma phospholipids was increased by 230% during cod liver oil administration. However, no significant change was observed in the 24-h prevalence of ventricular extrasystoles or other arrhythmias during the study period. The mean ln number of ventricular extrasystoles was 2.95 +/- 0.51 (+/- SEM) during cod liver oil ingestion and 2.63 +/- 0.30 when not taking cod liver oil.     

AV Nodal Function During Atrial Fibrillation:

AVN Function in Atrial Fibrillation. The irregular ventricular rhythm that accompanies atrial fibrillation (AF) has been explained in terms of concealed conduction within the AV node (AVN). However, the cellular basis of concealed conduction in AF remains poorly understood. Our hypothesis is that electrotonic modulation of AVN propagation by atrial impulses blocked repetitively within the AVN is responsible for changes in function that lead to irregular ventricular rhythms in patients with AF. We have tested this idea using two different simplified computer ionic models of the AVN. The first (“black-box”) model consisted of three cells: one representing the atrium, another one representing the AVN, and a third one representing the ventricle. The black-box model was used to establish the rules of behavior and predictions to be tested in a second, more elaborate model of the AVN. The latter (“nine-cell” model) incorporated a linear array of nine cells separated into three different regions. The first region of two cells represented the atrium; the second region of five cells represented the AV node; and the third region of two cells represented the ventricle. Cells were connected by appropriate coupling resistances. During regular atrial pacing, both models reproduced very closely the frequency dependence of AV conduction and refractoriness seen in patients and experimental animals. In addition, atrial impulses blocked within the AV node led to electrotonic inhibition or facilitation of propagaticm of immediately succeeding impulses. During simulated AF, using the nine-cell model, random variations in the atrial (A-A) interval yielded variations in the ventricular (V-V) interval but there was no scaling, i.e., the V-V intervals were not multiples of the A-A intervals. As such, the model simulated the statistical behavior of the ventricles in patients with AF, including: (1) the ventricular rhythm was random; and (2) the coefficient of variation (standard deviation/mean) of the ventricular rhythm was relatively constant at any given mean V-V interval. Analysis of cell responses revealed that repetitive atrial input at random A-A intervals resulted in complex patterns of concealment within the AVN cells. Consequently, the effects of electrotonic modulation were also random, which resulted in a smearing of the AV conduction curve over A-A intervals that were larger than those predicted for 1:1 AV conduction. Hence, during AF, electrotonic modulation acts in concert with the frequency dependence of AVN conduction to result in complex patterns of ventricular activation. Finally, similarly to what was shown in patients, VVI pacing of the ventricle in the nine-cell model at the appropriate frequency led to blockade of nearly all anterograde (i.e., A-V) impulses. The essential feature here was that the retrograde impulse invading the AVN cells was followed by refractoriness with slow recovery of excitability, setting the stage for electrotonic inhibition of anterograde impulses. Overall, the results provide insight into the cellular mechanisms underlying AVN function and irregular ventricular response during AF.     

Bigeminal and trigeminal distribution of ventricular extrasystoles as an expression of "atypical" concealed bigeminy

This report reflects a case of bigeminal and trigeminal ventricular extrasystoles where bigeminal extrasystoles are associated with short coupling intervals, while trigeminal extrasystoles manifest long coupling intervals. The arrhythmia is interpreted as an "atypical" form of concealed bigeminy.     

Decremental conduction properties in overt and concealed atrioventricular accessory pathways.

AIM: Most atrioventricular accessory pathways (AV-APs) exhibit Kent bundle physiology characterized by fast and non-decremental conduction properties. In contrast, atriofascicular APs, which are only capable of reaching slow levels of long antegrade decremental conduction, are uncommon. The aim of this study was to describe antegrade and/or retrograde AV-APs with unusual decremental properties. METHODS AND RESULTS: Five patients with unusual decremental AV-APs underwent electrophysiological evaluation and radiofrequency catheter ablation for symptomatic tachycardias. Three were found to have structural heart disease, and three latent decremental AV-APs in the anterograde and/or retrograde direction that could not be demonstrated by routine electrophysiological testing. In Case 1, a right posteroseptal AV-AP with bidirectionally latent decremental conduction was associated with clinical antidromic circus movement tachycardia (CMT) mimicking ventricular tachycardia and orthodromic CMT, the latter inducible only with isoprenaline. In Case 2, incessant orthodromic CMT was due to a latent retrograde left posterolateral AV-AP. In both cases, double atrial responses to a single paced ventricular beat, initiating orthodromic CMT, were observed. In Case 3 with latent preexcitation unmasked by adenosine and atrial pacing, retrograde latent decremental conduction over a right posteroseptal AV-AP could be shown only with isoprenaline. This patient and the remaining two with overt preexcitation demonstrated anterograde decremental AP conduction that was discontinuous over a right posteroseptal AV-AP in Cases 3 and 4 and was continuous over a midseptal AV-AP in Case 5. In the latter case, the site of decremental conduction could be localized at the proximal AP origin. All five AV-APs were successfully ablated at the annulus level. CONCLUSION: AV-APs with unusual decremental properties that are either latent, demonstrable only during CMT or overt, exhibiting functional longitudinal dissociation are described. These APs could be identified and successfully ablated after detailed electrophysiological analysis.     

Mechanism of bradycardia-dependent appearance of manifest extrasystoles in concealed bigeminy. A theoretical model derived from the concepts of longitudinal dissociation and multilevel block in the reentrant pathway of extrasystoles.

A case of bradycardia-dependent appearance of manifest extrasystoles in concealed bigeminy is presented. To explain the mechanism of such bradycardia-dependent appearance, a theoretical model is derived from the concepts of "longitudinal dissociation" and "multilevel block" in the reentrant pathway of extrasystoles. In the theoretical model, functional longitudinal dissociation divides the reentrant pathway into dual pathways F and S. When manifest extrasystoles are not found for a long time, alternate sinus impulses pass through both pathways F and S, but become concealed extrasystoles because of insufficient conduction delay in the pathways. The other alternate sinus impulses are blocked in the pathways; in pathway F, the impulses are blocked at the entrance, while in pathway S, the impulses are blocked at a more distal level. When sinus cycles gradually lengthen, one of such alternate sinus impulses passes through the entrance of pathway F and, traveling very slowly, is blocked at a more distal level. The next sinus impulse is blocked at the entrance of pathway F; namely, 3:2 Wenckebach block occurs at the entrance of pathway F. Thus this sinus impulse enters only pathway S and passes through pathway S with enough conduction delay to become a manifest reentrant extrasystole.     

Double ventricular response in dual AV nodal pathways mimicking supraventricular as well as ventricular tachycardia

Supraventricular tachycardias confined to the AV junction areusually thought to be due to reentry using a slow and a fastconducting pathway. In the case presented, a marked differenceof conduction velocity in dual AV nodal pathways and retrogradeblock in the slow conducting pathway caused a ventricular doubleresponse to a single atrial depolarization. At a critical heartrate this phenomenon occurred in a bigeminal fashion, mimickingsupraventricular as well as ventricular tachycardia.     

Alternate Patterns of Ventricular Activation during Supraventricular Bigeminy

Several investigators have previously noted that in the presence of bigeminal atrial extrasystoles, the premature beats may exhibit an alternate pattern of ventricular excitation either in the form of alternating left and right bundlebranch block, or alternating right bundle-branch block and normal intraventricular conduction. However, the association of alternating intraventricular conduction with other types of supraventricular bigeminy has rarely been documented. In this report we present five diverse forms of supraventricular bigeminy exhibiting the phenomenon of alternating ventricular excitation on the early beats. Our findings suggest that the exact mechanism of supraventricular bigeminy is irrelevant in terms of subsequent ventricular events. Practically any type of supraventricular bigeminy may result in an alternate pattern of ventricular activation.     

Mechanisms of concealed ventricular bigeminy: the concept of concealed conduction in the reentrant pathway

To clarify the presence of concealed conduction in the reentrant pathway of extrasystoles, 20 patients with ventricular extrasystoles were studied in whom two forms of interectopic periods were found in the same recording. One form is the XS1S2X period, in which two sinus QRS complexes (S1 and S2) intervene between an interpolated extrasystole (the first X) and the next extrasystole (the second X). The other is the XS2X or XS1X period, in which one sinus QRS complex intervenes between two extrasystoles. In all patients except one, the XX interval in the XS1S2X period was longer than that in the XS2X or XS1X period though shorter than twice the latter XX interval. This strongly suggests the presence of two-level block in the reentrant pathway of the extrasystoles. It appears that the sinus impulse S1 in the XS1S2X period invaded a large portion of the reentrant pathway and then was blocked at a distal site of the pathway; namely, that concealed conduction of the impulse S1 occurred in the pathway. It is suggested that such concealed conduction prolonged the conduction time of the following sinus impulse, S2, in the reentrant pathway, resulting in lengthening of the XX interval. The presence of three- or four-level block is also suggested. By the use of such multilevel block, mechanisms of concealed ventricular bigeminy are explained.     

Rate stabilization by right ventricular apex or His bundle pacing in patients with atrial fibrillation.

AIMS: In patients with atrial fibrillation right ventricular pacing can block antegrade conduction at pacing intervals longer than the shortest spontaneous R-R interval, causing the stabilization of ventricular rhythm. In this study the effects of pacing at two sites were compared in order to evaluate the role of conduction times in determining the stabilization of ventricular rhythm. METHODS: In eight patients with permanent atrial fibrillation, the ventricular rate was recorded before and during pacing at the right ventricular apex and the His bundle with different cycle lengths. RESULTS: In all patients, we obtained a reduction in spontaneous QRS complexes with respect to those anticipated at pacing rates slightly above the spontaneous mean rate, and the ventricular rhythm stabilized at pacing intervals longer than the spontaneous shortest R-R intervals. Between pacing sites we did not observe any difference in the reduction in spontaneous beats and the cycle stabilizing the rhythm. Moreover, simulation of the interaction between antegrade and retrograde impulses in a computer model confirmed that results obtained by pacing at the His bundle cannot be readily explained as a consequence of conduction delays. CONCLUSION: This study suggests that the lag introduced by the His-Purkinje conduction cannot explain, as proposed, the stabilization of ventricular rhythm observed in patients with atrial fibrillation and right ventricular pacing.     

Premature ventricular contraction‐induced concealed retrograde penetration: Electrocardiographic manifestations on anterograde ventricular preexcitation

In patients with manifest anterograde ventricular preexcitation, the electrocardiographic manifestation of the anomalous conduction through the simultaneous conduction over the atrioventricular (AV) node and the accessory pathway (“delta wave”); depends on several factors, the most representative being the conduction velocity over one or another connection. Occasionally, ventricular ectopic beats may present with retrograde penetration over one or both conduction pathways (AV node and/or accessory pathway), impacting on the morphology of the next immediate anterogradely conducted QRS. We present a case of a young patient with WPW syndrome and ectopic ventricular beats with different manifestations on the postectopic QRS due to concealed penetration of different conduction pathways.     

Manifest and concealed AV nodal reentry in wenckebach type of AV conduction with AV junctional escape rhythm

An electrocardiogram was obtained that was characterized by sinus rhythm with progressive prolongation of the PR interval not followed by a blocked sinus impulse. After a critically long PR interval, the QRS complex was followed by a premature P′ wave, representing an echo beat, a manifest reentry in the atrioventricular (AV) node. The pause, occasioned by the premature P′ wave, was at times interrupted by an AV junctional escape beat, occurring with an escape interval of 1.21–1.24 seconds. On other occasions, however, the escape beat did not manifest on schedule, even though the pause was markedly longer than the escape cycle. This suggested that the manifest reentry was followed by a further concealed reentry, resulting in inapparent discharge of the AV junctional escape pacemaker, whose firing was postponed, thereby allowing the sinus impulse to capture the ventricles.     

Mechanism of ventricular tachycardia in a patient with double-outlet left ventricle

We report the case of ventricular tachycardia (VT) ablation procedure in a patient with history of surgically repaired double-outlet left ventricle. The electrophysiology procedure revealed a re-entry pattern between the right-ventricle to main-pulmonary-artery conduit and the tricuspid annulus. The re-entrant mechanism was most likely promoted by a fibrous remodeling of this area, related to the surgical repair. This case is the first to describe a re-entry mechanism between fixed anatomical barriers in a repaired right ventricle of a double-outlet left ventricle. A pace mapping technique was used to highlight the VT isthmus.     

Electrophysiologic characteristics at initiation of ventricular tachycardia and ventricular fibrillation in a canine infarct model

Local ventricular activation time and the conduction time during sinus rhythm at the induction of ventricular tachycardia (VT) and ventricular fibrillation (VF) were investigated using a canine model of chronic myocardial infarction. Of 26 dogs studied, 15 had inducible VT, 10 had inducible VF, and 1 had no inducible arrhythmias. Bipolar local ventricular electrograms were recorded during sinus rhythm from 136 sites in 10 dogs with VT and 164 sites in 11 dogs with VF. Mean activation time in dogs with inducible VT was significantly longer than in dogs with inducible VF. Furthermore, simultaneous local ventricular electrograms were recorded during the induction of VT (74 episodes) or VF (38 episodes) from the infarct border zone at the endocardium (B-EN), the epicardium (B-EP), and normal sites (N-EN, N-EP). During VT induction, the activation time at N-EN and N-EP was significantly longer than during VF induction (N-EN: 94 ± 21, 70 ± 19 ms; N-EP: 83 ± 21, 64 ± 10 ms; p < 0.05). Conduction time was measured at the initiation of VT or VF induced by orthodromic or antidromic pacing. The conduction times of the last paced beat between N-EN and B-EP (35 ± 11, 62 ± 24 ms), N-EN and N-EP (35 ± 12, 14 ± 13 ms), B-EN and B-EP (16 ± 10, 38 ± 25 ms), and B-EP and N-EP (77 ± 27, 44 ± 12 ms) were significantly different in dogs with inducible VT (p < 0.05), but not in dogs with VF. Dispersion of effective refractory period was also observed in dogs with VT. Percent infarct in inducible VT was larger than in inducible VF (VT: 16 ± 5%; VF: 10 ± 2%; p < 0.001). These studies suggest that dogs with inducible VT have prolonged ventricular activation time and significantly different bidirectional conduction time during VT induction. This may serve as a substrate for reentry.     

Prevalence of a shared isthmus in postinfarction patients with pleiomorphic, hemodynamically tolerated ventricular tachycardias

INTRODUCTION: Multiple forms of ventricular tachycardia (VT) after myocardial infarction may result from multiple reentrant circuits that share an isthmus or from separate reentrant circuits. The prevalence of a shared isthmus in patients with multiple hemodynamically tolerated VTs has not been determined. METHODS AND RESULTS: Criteria for a shared isthmus consisted of (1) concealed entrainment of >1 VT at a single pacing site; (2) concealed entrainment during VT and a perfect pace map of another VT at the same pacing site; or (3) concealed entrainment of VT of a given morphology that had at least two cycle lengths that varied by at least 100 msec. In a series of 19 patients (16 men and 3 women; age 65+/-14 years, ejection fraction 0.25+/-0.09) with 54 VTs (mean cycle length 494+/-98 msec), there was evidence of a shared isthmus in 23 VTs (43%) at 11 sites in 9 patients. Concealed entrainment of two different VTs was observed at 4 of 11 sites. At 5 of 11 sites there was concealed entrainment of one VT and a perfect pace map of another VT. At the remaining 2 of 11 sites, there was concealed entrainment of a VT that had two different cycle lengths. Nineteen of the 23 VTs were ablated successfully with radiofrequency energy applications at 11 sites. CONCLUSION: In postinfarction patients with pleiomorphic, hemodynamically stable VT, a shared isthmus may be present in approximately 40% of VTs.