Concealed Conduction Research Articles

Syncope in the setting of trifascicular block and retrograde concealed conduction: A case report

Syncope in the setting of trifascicular block and retrograde concealed conduction: A case report

Aberrant Ventricular Conduction: Revisiting an Old Concept.

The well-defined concept of aberrant ventricular conduction was introduced over 100 years ago and, despite advances in cardiac physiology and electrophysiologic testing, it is still widely misunderstood. Aberrant ventricular conduction is due to physiologic refractoriness of the His-Purkinje system and in most cases does not reflect underlying conduction system disease. Electrophysiologically, aberrant ventricular conduction can manifest with premature atrial ectopics, the Ashman phenomenon with atrial tachyarrhythmias, concealed conduction, echo beats and with the sinus mechanism including rate dependent bundle branch block, bradycardia dependent bundle branch block and early sinus beats. It is important to recognise aberrant ventricular conduction in the context of a broad complex tachycardia, as the differentiation between supraventricular tachyarrhythmias with aberrant ventricular conduction and ventricular tachyarrhythmias carry different therapeutic and prognostic implications. This review will define the ECG footprints of aberrant ventricular conduction to allow accurate ECG interpretation.

Characteristics of the Dynamic Electrocardiogram in the Elderly with Nonvalvular Atrial Fibrillation Combined with Long R-R Intervals.

Objective To investigate the characteristics of dynamic electrocardiogram and their clinical implications in elderly patients with nonvalvular atrial fibrillation combined with long R-R intervals. Methods Elderly patients diagnosed with nonvalvular atrial fibrillation who were admitted as an inpatient or attended the outpatient department from January 2015 to January 2020 were selected. Patients were divided into two groups based on the presence of a long R-R interval. The characteristics and therapeutic significance of dynamic electrocardiogram between the two groups were compared. Results A total of 532 patients were included in our analyses. Of these, 399 patients were in the long R-R interval group and 133 in the nonlong R-R interval group. In 399 patients, there were 48,840 long R-R intervals manifested within 24 hours. The average, slowest, and fastest ventricular rates during sleep time were higher than those in nonsleep time, while the number of long R-R intervals in sleep time was significantly smaller than that in nonsleep time (P < 0.05). Clinical parameters including dizziness/syncope, cerebral infarction, ST-segment changes, platelet count, average hematocrit, prothrombin time (PT), left ventricular systolic function, end-diastolic diameter, pulmonary artery pressure, and left ventricular ejection fraction were comparable between the groups (P > 0.05). When compared with the nonlong R-R interval group, the level of C-reactive protein was slightly lower in the long R-R interval group (P < 0.05). In addition, the long R-R interval group had a higher incidence of atrial premature beats but a lower incidence of ventricular premature beats. Furthermore, the probability of long R-R interval combined with paroxysmal atrial tachycardia, transient ventricular arrest, second-degree atrioventricular block, and complete or incomplete right bundle branch block was higher than that of nonlong R-R interval (P < 0.05). In patients with long R-R interval >3 s, the risk of having second-degree atrioventricular block and complete or incomplete right bundle branch block was significantly lower, while the risk of having transient ventricular arrest was higher when compared to patients with long R-R intervals of 2-3 s (P < 0.05P). Conclusions Long R-R interval is a common electrocardiographic phenomenon among the elderly with nonvalvular atrial fibrillation. The long R-R interval mostly occurs in nonsleeping time. The average ventricular rate, slowest ventricular rate, and fastest ventricular rate of sleep time are higher than nonsleeping time. Analysis of the characteristics of the dynamic electrocardiogram of these patients may shed light on the mechanisms for long R-R intervals, including the likelihood of concealed conduction and physiological interference in the atrioventricular node, overspeed inhibition, increased vagus nerve tension, or pathological atrioventricular block.

B-PO04-222 ELECTRIC CARDIOVERSION DURING SINUS RHYTHM TO ASSESS PULMONARY VEIN ISOLATION

Pulmonary vein (PV) isolation for the treatment of atrial fibrillation (AF) is a safe and effective intervention. Most recurrences post ablation are due to reconnection of a PV, highlighting the importance of a robust assessment of PV isolation. To describe a situation where an electrical cardioversion was performed in a patient in sinus rhythm while one PV was still in AF, revealing residual exit and entrance conduction despite apparent exit block. N/A We present the case of a 58 year old gentleman who was referred for AF ablation. During ablation around the left superior PV (LSPV), the rhythm changed to typical atrial flutter, while the LSPV persisted in AF. Cavo-tricuspid isthmus ablation was performed after completing the wide antral circumferential ablation, leaving the circumferential mapping catheter in the LSPV. When sinus rhythm was restored, the PV remained in AF, with exit block. Electrical cardioversion using 100 Joules was performed, terminating PV fibrillation, and revealing residual entrance and exit conduction. Exit conduction was intermittent while pacing at 600 ms. Subsequently, further ablation was delivered until entrance and exit block were demonstrated. This case highlights the importance of performing electrical cardioversion when a PV is in AF, despite the patient being in sinus rhythm, to truly confirm the existence of PV isolation. We believe that the bombarding impulses of the fibrillating PV can provoke an inhibition of the exit conduction due to concealed conduction that makes the slow conducting tissue refractory, preventing propagation to the left atrium. This may then lead to the misdiagnose of exit block.

Abstract 14912: Sotalol-induced Wide Complex Rhythm: What is the Mechanism?

Introduction: Delta waves associated with atrioventricular accessory pathways (APs) may manifest with autonomic tone, heart rate, and rhythm changes. Rarely, drugs like sotalol can block AV nodal conduction, revealing latent WPW, one treatable cause of sudden death. Case report: A 38-year-old man was admitted for sotalol loading due to frequent typical atrial flutter and SVT and a desire to avoid catheter ablation. He had a history of cardiac arrest with adenosine and tachycardia-induced cardiomyopathy. After recovery, cardiac MRI showed a normal heart without scar. Admission 12-lead ECG ( Figure A ) revealed normal sinus rhythm without other abnormality. With administration of sotalol, the patient developed a wide complex rhythm ( Figure B ). Interpretation of the rhythm indicated presence of a latent AP and a repeat ECG ( Figure C ) confirmed manifest preexcitation. After consenting to electrophysiology study, the patient developed a short RP tachycardia ( Figure D ) which terminated with Valsalva. The patient underwent successful catheter ablation of the pathway located at the anterior floor of the coronary sinus body and the cavotricuspid isthmus. Discussion: The differential diagnosis for a wide complex rhythm in this setting includes rate-related aberrancy, idioventricular rhythm, phase 4 aberrancy, and preexcitation from an AP. Shortened and consistent PR intervals in the tracing lead to preexcitation as the only possible mechanism. APs that are capable of anterograde conduction but are not manifest in sinus rhythm are termed latent APs. Conditions that may cause this phenomenon include opposite autonomic effects on the AP and the AV node, increased atrial conduction time, or concealed retrograde conduction into the AP. Sotalol typically increases the retrograde effective refractory period of the AP but has variable anterograde effect. Sotalol has not previously been reported to reveal a latent AP but may have acted through one of the stated mechanisms.

Role of concealed conduction and allied phenomena in the genesis, maintenance, and termination of cardiac arrhythmias

Concealed conduction is a common electrocardiographic phenomenon whereby a series of events may occur as a result of incomplete propagation of an impulse. The occurrence, maintenance, and resolution (termination) of several events such as functional block and cardiac arrhythmias are linked to concealed conduction. This phenomenon should be suspected on the surface electrocardiogram whenever an arrhythmic event occurs unexpectedly. Several electrophysiological concepts such as transseptal conduction and linking phenomenon are close allies of concealed conduction. His-bundle electrocardiography and comprehensive electrophysiology may be needed to verify this phenomenon.

Concealed conduction in atrial tachyarrhythmia illustrated in a heartbeat

Concealed conduction is not seen directly on the surface electrocardiogram but is evident from its effect on subsequent impulses; it includes concealed incomplete penetration of the atrioventricular (AV) junction during atrial fibrillation (AF) and contributes mechanistically to so-called “slow AF.”1 Manifestations of concealed conduction are numerous. We present a case that demonstrates a common consequence: unexpected failure of propagation of an impulse from atrium to ventricle.2

Syncope, Junctional Premature Complexes, and Pseudo-Type II Atrioventricular Block

In a woman with syncope, junctional premature complexes and what appeared to be intermittent atrioventricular block suggested concealed conduction of His bundle extrasystoles.

Unintentional Resetting Phenomenon Caused by Catheter-induced Mechanical Stimulation of the Left Anterolateral Accessory Pathway during Orthodromic Atrioventricular Reciprocating Tachycardia

<span style=font-size:11.0pt;font-family: times= new= roman,serif;mso-fareast-font-family:times= roman=>1. Abstract An 80-year-old woman was admitted to our hospital for treatment of paroxysmal supraventricular tachycardia which had been increased sharply after the antiarrhythmic drug was decreased. Electrophysiological study demonstrated orthodromic atrioventricular reciprocating tachycardia via the left anterolateral accessory pathway with relatively slow concealed conduction, which we supposed to be a target for catheter ablation. Interestingly, only while the ablation catheter tip was being placed just on the accessory pathway, the tachycardia cycle length was occasionally altered with the atrial sequence advancing forward a little, and the culprit pathway was successfully ablated at this point. We concluded, based on some electrophysiological findings, that this phenomenon was caused by electrophysiological mechanism of resetting, certainly induced by direct mechanical stimulation onto the accessory pathway. <span style=font-size:11.0pt;font-family: times= new= roman,serif;mso-fareast-font-family:times= roman=>2. Keywords: <span style=font-size:10.0pt;font-family: times= new= roman,serif=> Accessory Pathway; Atrioventricular Reciprocating Tachycardia; Mechanical Stimulation; Resetting Phenomenon; Slow Concealed Conduction

0034: Preexcitation syndrome and atrioventricular nodal reentrant tachycardia: coincidence or not?

Reciprocating tachycardia which occurs in patients with a preexcitation syndrome (PS) generally is directly related to the presence of the accessory pathway (AP) and is called atrioventricular re-entrant tachycardia (AVRT). The purpose of the study was to evaluate the incidence of re-entrant tachycardia of other nature among patients with a PS. 785 patients with paroxysmal tachycardia were admitted AP ablation, 294 patients with a concealed AP (group I) and 491 patients with a Wolff-Parkinson-White syndrome (WPW) (group II). Programmed atrial stimulation was performed in the control state and if necessary after isoproterenol to induce the clinical tachycardia and determine its mechanism. AVRT was induced in 760 patients (97%), 282 of group I (96%)and 478 of group II (97%) (NS). Atrioventricular nodal re-entrant tachycardia (AVNRT) was induced in 13 group I patients (4.6%) and 12 group II patients(2.5%) (NS; 0.11). In 9 group I patients (3%) and in 4 group II patients (1%) (p<0.015), both AVRT and AVNRT were induced. In patients with only induced AVNRT, slow pathway ablation was performed and accessory pathway was respected because there was no inducible tachycardia using AP and the conduction over AP was poor. These patients remained free of symptoms after ablation of AV node slow pathway. Among this population 3 families were identified as having either AVRT or AVNRT. In patients with concealed or patent accessory pathway and complaining of paroxysmal tachycardia, a careful evaluation of the mechanism of tachycardia is required before ablation. Patients with concealed conduction over an AP have more frequently an association of AVRT and AVNRT than patients with a patent preexcitation syndrome. Rarely AVNRT can be the only mechanism of symptoms.

0038: Impact of accessory pathway ablation on the risk of atrial fibrillation in patients with overt conduction and patients with concealed conduction over accessory pathway

to evaluate the impact of accessory pathway (AP) ablation on the risk of subsequent atrial fibrillation (AF) of patients with a pre-excitation syndrome (PS) and patients with a normal ECG but with AV reentrant tachycardia (AVRT) over a concealed AP. 103 patients were studied: 93 patients, mean age 41±16 years, with a PS presented with a well or poorly-tolerated AF (group I). They were issued from a group of 905 patients (10%) with a PS (mean age 34±17 years). Ten patients, mean age 50±21, with a normal ECG in sinus rhythm and with AVRT were referred for AF (group II). They were issued from a group of 303 patients (3%) with AVRT and a normal ECG (mean age 42±18 years). Electrophysiological study was performed in control state and after isoproterenol. Patients were followed from 3 months up to 20 years. The incidence of AF at the admission was higher in PS than in patients with concealed AP (p<0.0001). In group I, a re-entrant tachycardia was induced in 59 patients (63%). AF was induced in 65 patients (70%). In group II AF was induced in 4 patients (40%)(0.06). AP ablation was performed in 75 group I patients (81%) and 7 group II patients (70%) (NS). After a mean follow-up of 3±2 years, 17 group I patients (18%) presented AF recurrence, despite AF ablation performed in 13 of them. In patients with a PS but without AF at admission, AF occurred only in 14 patients (2%)(p<0.0001). Three group II patients (30%)(p<0.005) in whom AP ablation was performed had AF recurrence. In patients with AVRT, normal ECG and no history of AF, AF only occurred in 3% (9/293). The differences were highly significant (p<0.0001). AF incidence at the admission was higher in patients with a PS than in patients with concealed AP (p<0.0001). After ablation, AF risk remained higher in patients with PS and AF than in patients with PS without AF at the admission (18 vs 2%). However the risk of recurrence of AF despite AP ablation was lower than in patients with a concealed AP. These last patients also remained at high risk to have AF after ablation compared to patients with a concealed AP and without AF.

Mobitz Type II Second‐Degree Atrioventricular Block with Narrow QRS and Junctional Extrasystoles: What is the Mechanism?

A 74-year-old man underwent an electrophysiological study because of Mobitz type II second-degree atrioventricular (AV) block with narrow QRS and frequent junctional extrasystoles. During the study, there were very frequent single His bundle depolarizations with multiple coupling intervals that reproduce the ECG findings. In this case, some His bundle extrasystoles result in retrograde concealed conduction and prolonged local refractoriness in the AV node that manifest as block of the next atrial impulse.

Is atrioventricular nodal reentrant tachycardia possible in patients with first degree AV block?

Purpose of the study: Typical Atrioventricular (AV) Node Re-entrant Tachycardia (AVNRT) occurs in patients with dual AV nodal pathway, a rapid pathway used for retrograde conduction and a slow pathway used for the anterograde conduction. In sinus rhythm the patients have generally the signs of conduction through the rapid pathway with a normal or short PR interval. The purpose of the study was to evaluate the prevalence of patients with 1st degree AV block and with AVNRT and their clinical characteristics. Methods: 1040 patients, 366 males, 665 females were admitted for typical AVNRT. They were aged from 6 to 90 years (mean age 50±19). Initial ECG and clinical data were collected. Electrophysiological study was systematic. Results: Spontaneous 1st degree AV Block (AVB) was rare and noted in 8 patients. The prevalence of the association 1st degree AV Block and AVNRT was 0.8%. AVB was suprahisian in 7 of 8 and infrahisian in one of them. Five patients complained of AVNRT at exercise. Two patients had an ischemic heart disease. Patients with AVB were significantly older (71.5±16 years) than patients without AVB (50±19) (p<0.002). AVNRT was induced in control state in 5 patients. The rate of tachycardia was slow between 130 and 160 bpm. AVNRT was induced after isoproterenol in 3 patients and the rate was higher (180 to 200 bpm). Ablation of slow pathway was performed in 7 patients. Transitory 2nd degree AVB was noted in 1 patient. AVNRT was not inducible after ablation. PR interval remained unchanged. At atrial pacing, the rate of 2nd degree AVB occurrence decreased, due to the disappearance of the conduction through the slow pathway. Two patients developed transitory well-tolerated 2nd degree AVB one day after ablation. One patient presented apparent sinus bradycardia related to a concealed conduction through AV node. One year after ablation none of the patients required pacemaker implantation and patients were free of tachycardia. Conclusions: The occurrence of AVNRT in patients with 1st degree AV block is exceptional and concerns old patients. The prevalence was 0.8%. Ablation of slow pathway might be safely performed without a need of pacemaker implantation. Transitory 2nd degree AVB can be noted the day after ablation.

Value of Electro‐Vectorcardiogram in Hypertrophic Cardiomyopathy

The electrocardiogram is an important tool for the initial diagnostic suspicion of hypertrophic cardiomyopathy in any of its forms, both in symptomatic and in asymptomatic patients because it is altered in more than 90 percent of the cases. Electrocardiographic anomalies are more common in patients carriers of manifest hypertrophic cardiomyopathy and the electrocardiogram alterations are earlier and more sensitive than the increase in left ventricular wall thickness detected by the echocardiogram. Nevertheless, despite being the leading cause of sudden death among young competitive athletes there is no consensus over the need to include the method in the pre-participation screening. In apical hypertrophic cardiomyopathy the electrocardiographic hallmarks are the giant negative T waves in anterior precordial leads. In the vectorcardiogram, the QRS loop is located predominantly in the left anterior quadrant and T loop in the opposite right posterior quadrant, which justifies the deeply negative T waves recorded. The method allows estimating the left ventricular mass because it relates to the maximal spatial vector voltage of the left ventricle in the QRS loop. The recording on electrocardiogram or Holter monitoring of nonsustained monomorphic ventricular tachycardia in patients with syncope, recurrent syncope in young patient, hypotension induced by strain, bradyarrhythmia, or concealed conduction are markers of poor prognosis. The presence of rare sustained ventricular tachycardia is observed in mid-septal obstructive HCM with apical aneurysm. The presence of complete right bundle branch block pattern is frequent after the percutaneous treatment and complete left bundle branch block is the rule after myectomy.

189: Clinical and electrophysiological data of patients with first degree AV block and AV node reentrant tachycardia

Typical atrioventricular (AV) node re-entrant tachycardia (AVNRT) occurs in patients with dual AV nodal pathway, a rapid pathway used for retrograde conduction and a slow pathway used for the anterograde conduction. In sinus rhythm, the patients have generally the signs of conduction through the rapid pathway with a normal or short PR interval. The purpose of the study was to evaluate the prevalence of patients with 1 st degree AV block and with AVNRT and their clinical characteristics. 973 patients, 348 males, 625 females, were admitted for typical AVNRT. They were aged from 6 to 90 years (mean age 50±19). Initial ECG and clinical data were collected. Electrophysiological study was systematic. Spontaneous 1 st degree AV block (AVB) was rare and noted in 7 patients. The prevalence of the association 1 st degree AV block and AVNRT was 0.7%. Five patients complained of AVNRT at exercise. Two patients had an ischemic heart disease. Patients with AVB were significantly older (71.5± 16 years) than patients without AVB (50±19)(p<0.002). AVNRT was induced in control state in 4 patients. The rate of tachycardia was slow between 130 and 150 bpm. AVNRT was induced after isoproterenol in 3 patients and the rate was higher (180 to 200 bpm). Ablation of slow pathway was performed in 6 patients. Transitory 2 nd degree AVB was noted in 1 patient. AVNRT was not inducible after ablation. PR interval remained unchanged. At atrial pacing, the rate of 2 nd degree AVB occurrence decreased, due to the disappearance of the conduction through the slow pathway. Two patients developed transitory well-tolerated 2 nd degree AVB one day after ablation. One patient presented apparent sinus bradycardia related to a concealed conduction through AV node. One year after ablation none of the patients required pacemaker implantation and patients were free of tachycardia. The occurrence of AVNRT in patients with 1 st degree AV block is exceptional and concerns old patients. Ablation of slow pathway might be safely performed without a need of pacemaker implantation. Transitory 2 nd degree AVB can be noted the day after ablation.

Letter by Obeyesekere Regarding Article, “Functional Pace-Mapping Responses for Identification of Targets for Catheter Ablation of Scar-Mediated Ventricular Tachycardia”

HomeCirculation: Arrhythmia and ElectrophysiologyVol. 5, No. 5Letter by Obeyesekere Regarding Article, “Functional Pace-Mapping Responses for Identification of Targets for Catheter Ablation of Scar-Mediated Ventricular Tachycardia” Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBLetter by Obeyesekere Regarding Article, “Functional Pace-Mapping Responses for Identification of Targets for Catheter Ablation of Scar-Mediated Ventricular Tachycardia” Manoj N. Obeyesekere, MBBS Manoj N. ObeyesekereManoj N. Obeyesekere Mildura Cardiology, Victoria, Australia Search for more papers by this author Originally published1 Oct 2012https://doi.org/10.1161/CIRCEP.112.974055Circulation: Arrhythmia and Electrophysiology. 2012;5:e100To the Editor:The elegant study by Tung et al1 presents additional sites for ablation of scar-based ventricular tachycardia (VT). Pace-mapped induction sites predicted successful sites of termination during ablation. This study raises a hypothesis that pace-mapped induction may be viewed as a surrogate for entrainment.At induction as with at the end of entrainment, when pacing from within the scar and the exit site after the last paced impulse at induction is the same as the induced/entrained VT, conduction follows the same route, and the return cycle to the site of pacing may also be similar. Thus, the postpacing interval after entrainment may be the same as the postpacing interval measured from the last pacing stimulus that initiates VT (postpacing intervalInitiation). Similarly, the stimulus-QRS interval that initiates VT or during pacing is because of the same distance as the stimulus-QRS interval during entrainment if the exit is the same. In fact, the authors report that 71% of critical isthmus sites had a stimulus-QRS during pacing minus electrogram-QRS interval of <30 ms. Thus, the cycle at induction may provide comparable information to that derived after entrainment.2 This assumption can be confounded by decrement and concealed conduction at initiation, and remote site pace mapping may match VT morphology in up to 29% of sites.3 Could the authors provide data on analysis of the postpacing intervalInitiation minus tachycardia cycle length at pace-mapped induction sites, both when the last paced beat matched the VT and when it did not? Data on analysis of entrainment mapping at the 21 pace-mapped induction sites would also be valuable.DisclosuresNone.Manoj N. Obeyesekere, MBBSMildura CardiologyVictoria, Australia

Nodal recovery, dual pathway physiology, and concealed conduction determine complex AV dynamics in human atrial tachyarrhythmias

The genesis of complex ventricular rhythms during atrial tachyarrhythmias in humans is not fully understood. To clarify the dynamics of atrioventricular (AV) conduction in response to a regular high-rate atrial activation, 29 episodes of spontaneous or pacing-induced atrial flutter (AFL), covering a wide range of atrial rates (cycle lengths from 145 to 270 ms), were analyzed in 10 patients. AV patterns were identified by applying firing sequence and surrogate data analysis to atrial and ventricular activation series, whereas modular simulation with a difference-equation AV node model was used to correlate the patterns with specific nodal properties. AV node response at high atrial rate was characterized by 1) AV patterns of decreasing conduction ratios at the shortening of atrial cycle length (from 236.3 ± 32.4 to 172.6 ± 17.8 ms) according to a Farey sequence ordering (conduction ratio from 0.34 ± 0.12 to 0.23 ± 0.06; P < 0.01); 2) the appearance of high-order alternating Wenckebach rhythms, such as 6:2, 10:2, and 12:2, associated with ventricular interval oscillations of large amplitude (407.7 ± 150.4 ms); and 3) the deterioration of pattern stability at advanced levels of block, with the percentage of stable patterns decreasing from 64.3 ± 35.2% to 28.3 ± 34.5% (P < 0.01). Simulations suggested these patterns to originate from the combined effect of nodal recovery, dual pathway physiology, and concealed conduction. These results indicate that intrinsic nodal properties may account for the wide spectrum of AV block patterns occurring during regular atrial tachyarrhythmias. The characterization of AV nodal function during different AFL forms constitutes an intermediate step toward the understanding of complex ventricular rhythms during atrial fibrillation.

Protective role of simvastatin on isolated rabbit atrioventricular node during experimental atrial fibrillation model: role in rate control of ventricular beats

The purpose of the present study was to determine (1) whether simvastatin (SV) modifies the rate-dependent conduction time and refractoriness of the atrioventricular (AV) node and (2) how it can change the protective mechanism of the AV node during atrial fibrillation (AF). Predefined stimulation protocols were applied to detect the electrophysiological parameters of the AV node, including atrial-His conduction time, effective refractory period (ERP), functional refractory period (FRP), concealed conduction, excitable index, and fatigue in two groups of isolated, perfused rabbit AV nodal preparations (N=16). The stimulation protocols (fatigue, recovery) were carried out during control and in the presence of SV (0.5, 0.8, 3, and 10 μM). Simulated AF was executed in a separate group (N=8), and specific indexes, including H-H mean, zone of concealment (ZOC), and concealed beats were recorded. SV, in a concentration-dependent manner, prolonged ERP, FRP, and Wenckebach cycle lengths. It (10 μM) significantly increased fatigue and the excitable index. In addition, SV elicited prolongation of ZOC and H-H mean at 3 and 10 μM. SV-evoked prolongation of nodal refractoriness and concealed conduction caused rate-dependent ventricular slowing effects during AF. The ability of simvastatin to decrease the excitable gap by its heterogeneous effects on nodal dual pathways proposes its protective role in AF.

Extra-and intracellular recordings from the AV junction: discerning the mechanisms for irregular ventricular responses during supraventricular arrhythmias

Introduction There has been a long-standing controversy regarding the mechanism(s) to explain the irregular ventricular response during atrial tachycardia (AT) or atrial fi brillation (AF) and where the site of block, if any, resides in the atrioventricular (AV) junction.Methods We studied 12 Langendorff preparations perfused with modifi ed Tyrode’s solution containing 5-10 mM diacetyl monoxime which suppressed contractility but allowed the use of intracellular action potential (AP) recordings. Octapolar catheters (2-mm rings, 2-mm spacing) were secured along the tricuspid annulus from the apex to the base of the triangle of Koch and along the anterior limbus of the fossa ovalis to record extracellular, slow pathway, fast pathway, His bundle (Hb) and AV nodal (AVN) extracellular potentials as well as intracellular action potentials.Results AT or AF induced by rapid atrial pacing showed a variety of irregular responses due to: (1) Wenckebach conduction showing decrement within the AVN and progressive diminution of extracellular AVN potentials (n = 5); (2) repetitive concealed conduction proximal to the AVN (n = 3); (3) ectopic beats arising within the AVN (n = 2); (4) ectopic beats arising at the Hb (n = 2).Conclusions In this experimental preparation, extracellular and intracellular recordings provided presumptive evidence for the mechanisms causing the irregularities of the ventricular response such as repetitive concealed conduction, enhanced automaticity or electrotonically triggered activity. Also more defi nitive determinations of the site of block in the AV junction were also obtained.

Higher rates to reduce irregularity: the use of overdrive pacing in atrial fibrillation

For a long time, it was a matter of debate whether fast rate or ventricular irregularity during atrial fibrillation (AF) was primarily responsible for the perception of palpitations, development of cardiomyopathy, and system emboli from the fibrillating atria. Recent studies have shown that ventricular irregularity associated with AF and manifested by random QRS intervals that constitute the diagnostic clue in scalar electrocardiography, can elicit symptoms and cardiomyopathy regardless of the rate. 1,2 Reduction of ventricular irregularity in AF patients in addition to control of fast ventricular rates, therefore, appears sensible to reduce symptoms and minimize the risk of cardiomyopathy. The underlying mechanisms of ventricular irregularity are uncertain and include concealed conduction within the atrioventricular (AV) node secondary to decremental conduction or electrical modulation of AV nodal propagation or pacemaker activity in the AV node. 1 If rate control is preferred to rhythm control, suppression of AV conduction with pharmacologic treatment and ablation of the AV junction are nowadays the established methods according to guidelines. However, the side effects and non-compliance associated with drug treatment or pacemaker dependency after ablation with potentially unfavourable effects of long-term right ventricular apical pacing often undermine the effectiveness of these therapies. These disadvantages urge the search for other therapeutic modalities for a safe and easy reduction of ventricular irregularity in AF. In 1983, Wittkampf and De Jongste 3 showed that continuous pacing in the right ventricle reduced the irregularity of QRS intervals during AF; faster pacing rates produced even more regularity by elimination of a large proportion of longer QRS intervals observed during slower ventricular rates. This phenomenon of rate stabilization is attributed to suppression or delay in AV nodal conduction by retrograde penetration of ventricular stimuli. This concept was incorporated in rate smoothing pacing algorithms that indeed significantly reduced variability of successive QRS intervals in AF patients. Unfortunately, the application of this algorithm was associated with a concomitant increase in mean heart rate by 21‐29%. 3 This drawback limited the widespread use of rate smoothing algorithms in paced patients with paroxysmal or permanent AF. In 1997, we tested a new rate smoothing programme delivered by the former Vitatron company, that uses a dynamic average of successive sensed or paced heart rates as a reference point. 4 The pacing rate followed the average heart rate and started pacing when the average ventricular rate dropped by 2.5 bpm. In addition, the algorithm prevented the occurrence of sudden brady- or tachyarrhythmia by pacing at a decelerating or accelerating rate at 2 bpm. In the acute pacing study, we observed that variability of the RR intervals could be reduced by 73% while the heart rate during pacing did not increase significantly (2%) compared with the preceding period without pacing. 5 In the unpublished randomized, single-blinded cross-over trial of patients with permanent (n ¼ 91) and paroxysmal AF (n ¼ 93), we observed a significant reduction in the variance of RR intervals in both patients categories. 6 However, quality of life, measured