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Barold S.S.,Florida Heart Rhythm Institute | Herweg B.,Florida Heart Rhythm Institute
Cardiology Journal | Year: 2011

Cardiac resynchronization therapy (CRT) has added a new dimension to the electrocardiographic evaluation of pacemaker function. During left ventricular (LV) pacing from the posterior or posterolateral coronary vein, a correctly positioned lead V1 registers a tall R wave and there is right axis deviation in the frontal plane with few exceptions. During simultaneous biventricular stimulation from the right ventricular (RV) apex and LV site in the coronary venous system, the QRS complex is often positive (dominant) in lead V1 and the frontal plane QRS axis usually points to the right superior quadrant and occasionally the left superior quadrant. The reported incidence of a dominant R wave in lead V1 during simultaneous biventricular pacing (RV apex) varies from 50% to almost 100% for reasons that are not clear. During simultaneous biventricular pacing from the posterior or posterolateral coronary vein with the RV lead in the outflow tract, the paced QRS in lead V1 is often negative and the frontal plane paced QRS axis is often directed to the right inferior quadrant (right axis deviation). A egative paced QRS complex in lead V1 during simultaneous biventricular pacing with the RV lead at the apex can be caused by incorrect placement of the lead V1 electrode (too high on the chest), lack of LV capture, LV lead displacement, pronounced latency (true exit block), conduction delay around the LV stimulation site, ventricular fusion with the intrinsic QRS complex, coronary venous LV pacing via the middle or anterior cardiac vein, unintended placement of two leads in the RV and severe conduction abnormalities within the LV myocardium. Most of these situations can cause a QS complex in lead V1 which should be interpreted (excluding fusion) as reflecting RV preponderance in the depolarization process. Barring the above causes, a negative complex in lead V1 is unusual and it probably reflects a different activation of a heterogeneous biventricular substrate (ischemia, scar, His-Purkinje participation). The latter is basically a diagnosis of exclusion. With a non-dominant R wave in lead V1, programming the V-V interval with LV preceding RV may bring out a diagnostic dominant R wave in lead V1 representing the contribution of LV stimulation to the overall depolarization process. In this situation the emergence of a dominant R wave confirms the diagnosis of prolonged LV latency (exit delay) or an LV intramyocardial conduction abnormality near the LV pacing site but it rules out the various causes of LV lead malfunction or misplacement. © 2011 Via Medica.


Barold S.S.,Florida Heart Rhythm Institute | Herweg B.,Florida Heart Rhythm Institute
Europace | Year: 2012

Recent reports suggest that first-degree atrioventricular block is not benign. However, there is no evidence that shortening of the PR interval can improve outcome except for symptomatic patients with a very long PR interval <0.3 s. Because these patients require continual forced pacing, biventricular pacing should be used according to accepted guidelines for third-degree AV block. Functional atrial undersensing may occur in patients with conventional dual-chamber pacing and first-degree AV block because the sinus P-wave tends to be displaced into the post-ventricular atrial refractory period (PVARP) an arrangement that may cause a pacemaker syndrome. Prevention requires programming a shorter AV and PVARP that is feasible because retrograde conduction is rare in first-degree AV block patients. A relatively new pacing mode to minimize right ventricular stimulation has been designed by eliminating the traditional AV interval but with dual-chamber backup. This pacing mode permits the establishment of very long AV intervals that may cause pacemaker syndrome. About 50 of patients undergoing cardiac resynchronization therapy (CRT) have a PR interval <200 ms. The CRT patients with first-degree AV block are prone to develop electrical desynchronization more easily than those with a normal PR interval. The duration of desynchronization after exceeding the upper rate on exercise is also more pronounced. AV junctional ablation is rarely necessary in patients with first-degree AV block but should be considered for symptomatic functional atrial undersensing or when the disturbances caused by first-degree AV block during CRT cannot be managed by programming. © The Author 2012.


Barold S.S.,Florida Heart Rhythm Institute | Herweg B.,Florida Heart Rhythm Institute
Herzschrittmachertherapie und Elektrophysiologie | Year: 2012

Type I second-degree atrioventricular (AV) block describes visible, differing, and generally decremental AV conduction. The literature contains numerous differing definitions of second-degree AV block, especially Mobitz type II second-degree AV block. The widespread use of numerous disparate definitions of type II block appears primarily responsible for many of the diagnostic problems surrounding second-degree AV block. Adherence to the correct definitions provides a logical and simple framework for clinical evaluation. Type II second-degree AV block describes what appears to be an all-or-none conduction without visible changes in the AV conduction time before and after the blocked impulse. Although the diagnosis of type II block requires a stable sinus rate, absence of sinus slowing is an important criterion of type II block because a vagal surge (generally a benign condition) can cause simultaneous sinus slowing and AV nodal block, which can superficially resemble type II block. Furthermore, type II block has not yet been reported in inferior myocardial infarction (MI) and in young athletes where type I block may be misinterpreted as type II block. The diagnosis of type II block cannot be established if the first postblock P wave is followed by a shortened PR interval or the P wave is not discernible. A narrow QRS type I block is almost always AV nodal, whereas a type I block with bundle branch block barring acute MI is infranodal in 60-70 % of cases. A 2:1 AV block cannot be classified in terms of type I or type II block, but it can be nodal or infranodal. A pattern resembling a narrow QRS type II block in association with an obvious type I structure in the same recording (e.g., Holter) effectively rules out type II block because the coexistence of both types of narrow QRS block is exceedingly rare. Concealed (nonpropagated) His bundle or ventricular extrasystoles may mimic both type I and/or type II block (pseudo AV block). All correctly defined type II blocks are infranodal. Infranodal block presenting with either type I or II manifestations requires pacing regardless of QRS duration or symptoms. © 2012 Springer-Verlag Berlin Heidelberg.


Barold S.S.,Florida Heart Rhythm Institute | Kucher A.,Biotronik
PACE - Pacing and Clinical Electrophysiology | Year: 2014

Some devices used for cardiac resynchronization therapy (CRT) can sense from the left ventricular (LV) lead as in Biotronik CRT devices (Biotronik GmbH, Berlin, Germany), whose special LV timing cycles form the basis of this report. LV sensing (LVs) was designed to prevent competitive pacing outside the LV myocardial absolute refractory period. LVs works by inhibiting the release of an LV pacemaker stimulus (LVp) in the vulnerable period of the LV during a programmable period. LVs with stored LV electrograms may also provide recordings of diagnostic value in tachyarrhythmias. LVs has added a new dimension to the evaluation of the function of CRT devices, because it is manifested by unfamiliar timing cycles. In this respect, Biotronik devices can initiate an LV upper rate interval (URI) upon sensing a right-sided event when LVs is turned off. An inhibited LVp can also initiate an LVURI. The LVURI should generally be programmed to a relatively short duration and shorter than the right ventricular URI to prevent a special form of desynchronization arrhythmia sustained by LVs. This arrhythmia is characterized by recurring delayed LVs events in sequences associated with RV pacing followed by LVs events with loss of LVp. © 2014 Wiley Periodicals, Inc.


Serge Barold S.,Florida Heart Rhythm Institute | Herweg B.,Florida Heart Rhythm Institute
Cardiology Journal | Year: 2011

The interval from the pacemaker stimulus to the onset of the earliest paced QRS complex (latency) may be prolonged during left ventricular (LV) pacing. Marked latency is more common with LV than right ventricular (RV) pacing because of indirect stimulation through a coronary vein and higher incidence of LV pathology including scars. During simultaneous biventricular (BiV) pacing a prolonged latency interval may give rise to an ECG dominated by the pattern of RV pacing with a left bundle branch block configuration and commonly a QS complex in lead V1. With marked latency programming the V-V interval (LV before RV) often restore the dominant R wave in lead V1 representing the visible contribution of the LV to overall myocardial depolarization. When faced with a negative QRS complex in lead V1 during simultaneous BiV pacing especially in setting of a relatively short PR interval, the most likely diagnosis is ventricular fusion with the intrinsic rhythm. Fusion may cause misinterpretation of the ECG because narrowing of the paced QRS complex simulates appropriate BiV capture. The diagnosis of fusion depends on temporary reprogramming a very short atrio-ventricular delay or an asynchronous BiV pacing mode. Sequential programming of various interventricular (V-V) delays may bring out a diagnostic dominant QRS complex in lead V1 that was previously negative with simultaneous LV and RV apical pacing even in the absence of an obvious latency problem. The emergence of a dominant R wave by V-V programming strongly indicates that the LV lead captures the LV from the posterior or the posterolateral coronary vein and therefore rules out pacing from the middle or anterior coronary vein. In some cardiac resynchronization systems LV pacing is achieved with the tip electrode of the LV lead as the cathode and the proximal electrode of the bipolar RV as the anode. This arrangement creates a common anode for both RV and LV pacing. RV anodal capture can occur at a high LV output during BiV pacing when it may cause slight ECG changes. During LV only pacing (RV channel turned off) RV anodal pacing may also occur in a more obvious form so that the ECG looks precisely like that during BiV pacing. RV anodal stimulation may complicate threshold testing and ECG interpretation and should not be misinterpreted as pacemaker malfunction. Programming the V-V interval (LV before RV) in the setting of RV anodal stimulation cancels the V-V timing to zero.© 2011 Via Medica.


Barold S.S.,Florida Heart Rhythm Institute | Herweg B.,Florida Heart Rhythm Institute
Europace | Year: 2014

In patients with pacemakers, hyperkalaemia causes three important abnormalities that usually become manifest when the K level exceeds 7 mEq/L: (i) widening of the paced QRS complex from delayed intraventricular conduction velocity, (ii) Increased atrial and ventricular pacing thresholds that may cause failure to capture. In this respect, the atria are more susceptible to loss of capture than the ventricles, and (iii) Increased latency (usually with ventricular pacing) manifested by a greater delay of the interval from the pacemaker stimulus to the onset of depolarization. First-degree ventricular pacemaker exit block may progress to second-degree Wenckebach (type I) exit block characterized by gradual prolongation of the interval from the pacemaker stimulus to the onset of the paced QRS complex ultimately resulting in an ineffectual stimulus. The disturbance may then progress to 2: 1, 3: 1 pacemaker exit block, etc., and eventually to complete exit block with total lack of capture. Ventricular undersensing is uncommonly observed because of frequent antibradycardia pacing. During managed ventricular pacing, hyperkalaemia-induced marked first-degree atrioventricular block may induce a pacemaker syndrome. With implantable cardioverter-defibrillators (ICDs) oversensing of the paced or spontaneous T-wave may occur. The latter may cause inappropriate shocks. A raised impedance from the right ventricular coil to the superior vena cava coil may become an important sign of hyperkalaemia in the asymptomatic or the minimally symptomatic ICD patient. © The Author 2014.


Barold S.S.,Florida Heart Rhythm Institute | Stroobandt R.X.,Ghent University
Europace | Year: 2012

This report describes the de novo occurrence of pacemaker-mediated tachycardia (PMT) in a patient with a dual-chamber implantable cardioverter-defibrillator and stable retrograde ventriculoatrial conduction time. The same rate-adaptive post-ventricular atrial refractory period (PVARP) duration had previously prevented PMT. Oversensing of atrial false signals from a defective lead shortened the PVARP with consequent sensing of retrograde conduction. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2012.2012 © Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2012.


Barold S.S.,Florida Heart Rhythm Institute | Stroobandt R.X.,Ghent University
Journal of Electrocardiology | Year: 2012

We report the initiation of pacemaker-mediated tachycardia by a St Jude implantable cardioverter-defibrillator with a programmed Ventricular Intrinsic Preference algorithm used for minimizing or inhibiting right ventricular pacing. This feature prolongs the atrioventricular (AV) delay periodically to determine if ventricular sensed events follow atrial events. Retrograde ventriculoatrial conduction and pacemaker-mediated tachycardia were initiated by long extended AV delays of 300 and 400 milliseconds. The 400-millisecond AV delay consisted of the programmed sensed AV delay (100 milliseconds) plus the Ventricular Intrinsic Preference increment (200 milliseconds) plus 100 milliseconds imposed by the AutoCapture algorithm when it detected loss of ventricular capture. © 2012 Elsevier Inc. All rights reserved.


Barold S.S.,Florida Heart Rhythm Institute | Israel C.W.,Klinik fur Innere MedizinKardiologie
Herzschrittmachertherapie und Elektrophysiologie | Year: 2015

A number of trials have shown that irrespective of baseline QRS duration, left ventricular (LV) dysfunction and heart failure are more common in patients with right ventricular (RV) than in those with biventricular (BiV) pacing. By contrast, preliminary results of the BIOPACE trial (follow-up 5.6 years) yielded a disappointing comparison of RV vs. BiV pacing. Pacemaker-induced cardiomyopathy (PIC) may occur in patients with normal and abnormal LV ejection fractions (LVEF) and tends to occur if there is RV pacing more than 40 % of the time. Yet, some pacemaker-dependent patients do not develop LV dysfunction. PIC can be improved in about two thirds of patients by upgrading to a BiV system and the results are comparable to de novo BiV pacing in patients with a wide QRS complex. The findings of the BLOCK HF trial (2013) suggested that patients requiring pacing virtually 100 % of the time might benefit from BiV pacing irrespective of the LVEF (< 50 %), manifestations of heart failure, QRS duration, or functional class. These characteristics would generate many patients for BiV pacing. However, these recommendations should now be weighed against a more conservative approach based on the recently announced results of the BIOPACE trial. Organizational guidelines recommend BiV pacing for bradycardia irrespective of QRS duration for patients with LVEF < 35 %. At this time, BiV pacing for antibradycardia therapy (irrespective of QRS duration) has to be individualized in the setting of a normal or decreased LVEF (> 35 %) and according to the expected percentage of RV pacing. The benefit of BiV pacing should be considered against procedural complications, which are more frequent than with traditional RV pacing. © 2014, Springer-Verlag Berlin Heidelberg.


Zanon F.,General Hospital | Barold S.S.,Florida Heart Rhythm Institute
Annals of Noninvasive Electrocardiology | Year: 2012

The success rate of direct His bundle pacing (DHBP) and paraHisian pacing has improved remarkably in the last 3-5 years with the advent of dedicated fixation systems that have reduced procedural duration, dislodgement rate, and fluoroscopy time. The methodology of DBHP remains still more complex than paraHisian pacing and is associated with high-pacing thresholds. Thus, DHBP entails greater battery current drain and reduced device longevity. A shift toward paraHisian pacing (which is fusion pacing of myocardium and His bundle) has occurred because its implementation is easier and the electrical parameters are superior to those of DBHP. Currently, an additional safety lead is inserted at the RV apex or outflow tract to prevent asystole, especially in patients with pure DHBP. It is often possible to avoid a safety lead with paraHisian pacing because ventricular pacing is virtually assured on a long-term basis via myocardial capture. DBHP and paraHisian pacing can be achieved in a substantial proportion of patients with varying grades of narrow QRS AV block or after AV junctional ablation and in some patients with the ECG manifestation of bundle branch block caused by an intraHisian lesion. Preliminary observations suggest that DHBP may be useful in some patients requiring cardiac resynchronization if it produces a narrow QRS complex because the site of an intraHisian lesion responsible for left bundle branch block is above the site of DHBP. © 2012, Wiley Periodicals, Inc.

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