Centennial of the original description of Mobitz type II second-degree atrioventricular block.

The year 2024 marks the centenary of Mobitz's description of type II second-degree atrioventricular block. Its definition remains valid to this day with only minor modification for the diagnosis of infranodal conduction block. Mobitz a century ago indicated that his type II atrioventricular block was associated with Stock-Adams attacks and a prolonged duration of the QRS complex before the eventual description of bundle branch block.

Clinical use of CRT-D devices with left ventricular sensing: Impact of the desynchronization-detection algorithm.

The use of CRT-D devices with left ventricular (LV) sensing has created controversy about programming various parameters especially the left ventricular T wave protection (LVTP) designed to prevent the delivery of a pacing stimulus into the LV vulnerable period. Such devices are available from two manufacturers. This review focuses only on those provided by Biotronik. As the LVTP controls LV sensing, some investigators have advocated turning off the LVTP to prevent episodic desynchronization known a CRT pacing interrupt. However, LVTP off reduces but does not eliminate this type of desynchronization if triggering of an LV stimulus upon right ventricular sensing (RVs) is programmed on. Deactivation of the LVTP incurs loss of diagnostic data provided by CRT pacing interrupt itself. By choice, the occurrence of CRT pacing interrupt can be totally eliminated by appropriate programming of the LV upper rate interval, LVTP and triggering of an LV pacing event upon RVs. Various programmability options are available according to clinical circumstances. As a rule, clinical judgement must weigh the potential diagnostic benefit of preserving the LVTP capable of recording of episodic CRT pacing interrupt against the loss of diagnostic benefit when LVTP is programmed off (with or without triggering of an LV stimulus upon RVs).

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.

Unusual manifestation of atypical type I second degree atrioventricular block.

A 25 year-old woman exhibited atypical type I second degree atrioventricular block characterized by constant PR intervals except the PR interval of the beat after the block. This was attributed to vagally induced AV block with failure of the vagal effect to depress the sinus node.

Problematic definitions of Mobitz type II second degree AV block: Historical aspects.

Problems with the definition of type II second degree AV block are best understood by reviewing the historical aspects that include Mobitz's original description, the contributions of the Chicago Arrhythmia School and the growing importance of excluding slowing of the sinus rhythm.

Definitions and Pitfalls in the Diagnosis of Atrioventricular Block.

The widespread use of disparate definitions of atrioventricular block has created important diagnostic problems. Adherence to the correct definitions provides a logical and simple framework for clinical evaluation. This review focuses on the clinical importance of the definitions in the diagnosis of the various types of atrioventricular (AV) block and the associated diagnostic pitfalls.

Left ventricular inhibition during cardiac resynchronization caused by sensed left-sided ventricular premature complexes.

A recently published case documented left ventricular (LV) inhibition of a Boston Scientific device by a premature complex (VPC) that was undetected by the right ventricular channel. We have observed a similar response in two patients with a BIOTRONIK cardiac resynchronization device also designed with LV sensing. A spurious response simulating that of the two true cases was also observed in a third patient with a defective LV lead which created isolated false signals. The responses of the BIOTRONIK devices were identical to that of the previously reported findings with the Boston Scientific device. The observations provide insight into the timing function of cardiac resynchronization devices designed with LV sensing.

Diagnosis of slow ventricular tachycardia by cardiac resynchronization devices utilizing a desynchronization detection algorithm.

Some cardiac resynchronization therapy (CRT) devices equipped with left ventricular (LV) sensing can develop a specific desynchronization rhythm. Contemporary BIOTRONIK devices are designed with an algorithm called "CRT pacing interrupt" exclusively designed to record the occurrence of the specific form of desynchronization. We report six patients in whom the CRT pacing interrupt function permitted the diagnosis of slow ventricular tachycardia (VT). Slow VT was defined as slower than the programmed VT intervention rates. Although the CRT pacing interrupt function is not designed to detect slow VT, certain episodes of the CRT pacing interrupt function were falsely interpreted by the device as a desynchronization arrhythmia, and the recordings then provided data consistent with the presence of slow VT. The CRT pacing interrupt algorithm permitted a diagnosis of slow VT irrespective of the relationship of LV upper rate interval and cycle length of slow VT.

Apparent dual exit pathways during ventricular tachycardia recorded by an ICD.

Ventricular tachycardia (VT) with dual exit pathways has been demonstrated in many ways. In this respect we found suggestive evidence of dual exit behavior during VT in a patient with an implanted cardioverter-defibrillator. The evaluation was done with continuous recordings of the right ventricular (RV) and left ventricular (LV) electrograms. The recordings documented the varying duration of the LV to RV delay and no change in the RV rate during increases in the LV-RV delay. The unchanged rate ruled out RV participation in the VT circuit. This ruled out the presence of VT with dual exit pathways and provided proof of an unusual RV bystander that did not participate in the VT circuit.

Termination of desynchronization rhythm and restoration of cardiac resynchronization by left-sided ventricular premature complexes.

Cardiac resynchronization devices that sense left ventricular (LV) activity and can detect interruptions of resynchronization therapy are able to record all forms of desynchronization rhythms, which are triggered by misalignment of LV timing cycles. We report five cases of this desynchronization rhythm that were terminated by isolated left-sided ventricular premature complexes (LVPC) undetected by the right ventricular (RV) channel and unaccompanied by changes in the duration of the RV pacing cycles. In three cases, the devices did not even sense the LVPCs responsible for desynchronization termination. The restoration of resynchronization in our cases is in contrast to the traditional termination mode that is invariably associated with changes in the duration of the RV cycles.

Interruption of cardiac resynchronization therapy triggered by the automatic right-ventricular pacing threshold test.

We report on three patients with heart failure and left bundle branch block who received a BIOTRONIK implantable defibrillator with resynchronization therapy which manifested loss of resynchronization only at a specific time of the night. Desynchronization was sudden and repeatedly initiated by the daily automatic right ventricular pacing threshold test. Loss of resynchronization occurred after switching back from the temporary test mode to the permanent biventricular pacing mode due to the reactivation of the left ventricular (LV) control of the timing cycles. LV sensed events prevented the emission of an LV paced event by virtue of a realigned LV upper rate interval, thus inhibiting LV pacing.

Patients with right bundle branch block and concomitant delayed left ventricular activation respond to cardiac resynchronization therapy.

Aims: Right bundle branch block (RBBB) typically presents with only delayed right ventricular activation. However, some patients with RBBB develop concomitant delayed left ventricular (LV) activation. Such patients may show a specific electrocardiographic (ECG) pattern resembling RBBB in the precordial leads in association with an insignificant S-wave in lateral limb leads (atypical RBBB). We therefore postulated that the ECG pattern of atypical RBBB might be able to identify a subgroup of patients likely to respond to cardiac resynchronization therapy (CRT). The purpose of this study was to assess the impact of RBBB ECG morphology on CRT response in patients with heart failure (HF). Methods and results: We evaluated the echocardiographic clinical response of 66 patients with RBBB treated with CRT and followed up for almost 2 years. The patients were divided electrocardiographically into 2 groups: 31 with typical RBBB and 35 with atypical RBBB. Responders were classified in terms of reduction in LV end-systolic volume index (ESVi) ≥ 15% or reduction in the New York Heart Association (NYHA) Class ≥ 1 or Packer score variation (NYHA response with no HF-related hospitalization events or death). The atypical RBBB group presented a longer LV activation time compared with the typical RBBB group (111.9 ± 17.6 vs. 73.2 ± 15.4 ms; P < 0.001). In the atypical and typical RBBB groups, respectively, 71.4% and 19.4% of patients were ESVi responders (P = 0.001) 74.3% and 32.3% were NYHA responders (P = 0.002); similarly, 71.4% and 29.0% of patients exhibited a 2-year Packer score of 0 (P = 0.002). Conclusion: Patients with atypical RBBB, which is a pattern highly suggestive of concomitant delayed LV conduction, may show a satisfactory response to CRT.

Alternans during fascicular ventricular tachycardia due to digitalis toxicity.

This report describes a digitalis-induced regular fascicular ventricular tachycardia characterized by marked QRS alternans a manifestation not usually associated with this arrhythmia. The striking alternation of QRS configuration suggested alternating ventricular activation from either a single focus with two exits in distal branches of the left anterior fascicle or 2 different foci localized in the Purkinje-myocardial network of the left anterior fascicle.

Interruption of cardiac resynchronization therapy by atrial premature complexes.

Biotronik devices used for cardiac resynchronization therapy (CRT) combined with defibrillation function (CRT-D) are capable of left ventricular (LV) sensing. Under certain circumstances, LV sensing may cause loss of CRT. The third generation of the Biotronik i-family CRT-Ds enables the recording of event-triggered tracings of the electrogram particularly those involving "CRT pacing interrupt" episodes. We report three cases of a sudden "CRT pacing interrupt" initiated by an atrial premature complex. This was caused by realignment of the LV timing cycles induced by the APCs whereupon LV pacing was inhibited and a self-perpetuating desynchronization process was initiated. In all cases it is the repeated occurrence of LV sensed events that prevents the emission of LV paced events because it displaces the LV upper rate interval from its normal position. Prevention of desynchronization requires programming an LV upper rate faster than the maximum sensor-driven rate or right ventricular upper rate.

Desynchronization in a cardiac resynchronization device induced by a pacemaker-mediated tachycardia algorithm.

This report describes the occurrence of desynchronization in a patient with a cardiac resynchronization device programmed with an active pacemaker-mediated tachycardia algorithm based on AV delay modification. Desynchronization was precipitated by sinus tachycardia and the abrupt return of the prevailing AV delay that followed the periodic prolongation of the AV delay mandated by activity of the algorithm. Prevention of desynchronization in this setting requires programming a right ventricular upper rate interval longer than the sum of the programmed ventriculoatrial interval and the AV delay.

The Analog Blanking Period of Implantable Cardiac Rhythm Devices.

BACKGROUND: Analog blanking periods (BPs) that hold down the display of electrograms (EGMs) in cardiac rhythm devices have received much less attention than the well-known digital BPs which do not influence the EGM display. In Biotronik devices (Biotronik GmbH, Berlin, Germany), when a paced event initiates an analog BP in one chamber (right atrium, right ventricle [RV], or left ventricle [LV]), an identical cross-chamber analog BP starts in the other two chambers. METHODS: All clinical observations were recorded from patients with Biotronik devices. The effect of the atrial cross-chamber analog BP initiated by a ventricular paced event on the atrial EGM was studied in the records of seven patients with frequent paroxysmal atrial flutter to determine the effect of critically timed RV paced event (RVp) or LV paced event (LVp) upon the atrial EGM. The effect of atrial pacing triggering cross-chamber analog BPs in the RV and LV channels on the RV and LV EGMs was also investigated in cases of conducted supraventricular beats and ventricular premature complexes. The effect of a triggered LVp initiating a cross-chamber analog BP in the RV channel on the EGM of a sensed RV sensed event was evaluated in 10 cases. Simulation studies were also performed to verify the clinical observations. RESULTS: Patients with atrial flutter showed intermittent truncation or deformity and even disappearance of the atrial signals due to an atrial cross-chamber analog BP initiated by RVp and/or LVp. Three patients demonstrated deformity of the signal shape of ventricular premature beats falling within a ventricular cross-chamber analog BP initiated by right atrial paced event (RAp). We found only one case of a supraventricular QRS complex trapped in a ventricular cross-chamber analog BP initiated by RAp. All the recordings of LVp triggering upon RVs revealed a variety of RV signal deformities occasionally with preservation of the terminal part of the RV signal. Simulation studies confirmed the effect of the analog BP on the atrial and the ventricular EGMs. CONCLUSION: The analog BP of Biotronik devices may cause truncation or deformity of atrial and ventricular signals and the occasional disappearance of an atrial signal during atrial flutter. These effects must not be interpreted as device malfunction. In the clinical evaluation of the EGM curves, the effects of the analog BPs have to be carefully considered in order to avoid possible misinterpretation.

Utilization of Permanent His-Bundle Pacing for Management of Proarrhythmia Related to Biventricular Pacing.

Biventricular pacing has occasionally been associated with ventricular proarrhythmia, which at times can be refractory to conventional antiarrhythmic drug therapy and ablative intervention. Recently, permanent His-bundle pacing has emerged as a reasonable alternative to right ventricular and biventricular pacing. In addition, by maintaining the physiologic pattern of ventricular electrical activation, it is less likely to be arrhythmogenic. We report the use of permanent His-bundle pacing to manage ventricular proarrhythmia that developed after initiation of biventricular pacing and was unresponsive to antiarrhythmic and ablative therapy.

Permanent His Bundle Pacing in Intra-Hisian Conduction Block: Mechanistic Insights.

We are reporting a patient with discrete intra-His conduction block and describe a refined technique of permanent His bundle pacing assuring reliable ventricular capture. Meticulous mapping of the site of block with lead placement distal to the site of block and non-selective His bundle pacing with local myocardial capture as an additional safety back up appears to be the technique of choice.