Left bundle branch pacing from distal His‐bundle region by tricuspid valve annulus angiography

A 78‐year‐old man presenting with amaurosis was admitted to the outpatient clinic 1 week ago. His baseline electrocardiogram showed Mobitz type II atrioventricular block and right bundle branch block. The patient's heart rate from Holter was only 32 bpm and therefore the indication for pacemaker implantation.     

Real‐World Data on the Lifespan of Implantable Cardioverter‐Defibrillators Depending on Manufacturers and the Amount of Ventricular Pacing

Real‐World Data on the Lifespan of ICDs Introduction: Implantable cardioverter‐defibrillator (ICD) longevity is crucial for both patients and public health systems because it determines the number of surgical ICD replacements, which can generally be considered an additional risk factor for complications, and the cost‐effectiveness of ICD therapy. Our objective was to obtain insight into the “real‐world” longevities of implantable cardioverter‐defibrillators, which quite often differ from those stated in the manufacturers’ declarations. Methods and Results: On the basis of a prospective database, we analyzed all ICD implantations performed in our hospital from June 1988 to June 2009. We studied 980 patients (follow‐up 58 ± 51 months) with 1,502 ICDs and all respective data until August 2010. We compared the percentage of still operating ICDs at different points in time in relation to manufacturers, types of device (single chamber 623, dual chamber 588, cardiac resynchronization therapy ICDs [CRT‐D] 291), and amount of right ventricular pacing (VP). We found distinct differences between the mean lifespans of ICDs of different manufacturers (Biotronik 4.3 years, Sorin 4.5 years, Guidant/Boston Scientific 4.7 years, St. Jude Medical 5 years, Medtronic 5.8 years). CRT‐D devices (hazard ratio [HR] 1.778, P = 0.0005) were associated with an elevated annual relative risk for device replacement while a decrease in the proportion of VP (HR 0.934 for each 10% decrease in VP, P < 0.0001) and Medtronic ICDs were associated with a reduced risk of device replacement (HR 0.544, P < 0.0001). Conclusion: CRT‐Ds and an elevated percentage of VP are associated with a significantly elevated risk for device replacement, while Medtronic ICDs showed the longest lifespans. (J Cardiovasc Electrophysiol, Vol. 23, pp. 1336‐1342, December 2012)     

A novel use of cardiac resynchronization therapy‐defibrillator device in hypertrophic cardiomyopathy

Dual‐chamber implantable cardioverter‐defibrillator is generally used in patients with atrioventricular block and hypertrophic cardiomyopathy with preserved left ventricular ejection fraction. In the current case, a cardiac resynchronization therapy‐defibrillator device was implanted in a patient with non‐obstructive hypertrophic cardiomyopathy with preserved ejection fraction and atrioventricular block to achieve both more physiological pacing and life‐threatening ventricular arrhythmia management.     

Comparison of the Acute Hemodynamic Effect of Right Ventricular Apex,Outflow Tract,and Dual‐Site Right Ventricular Pacing

Background: We studied the acute effect of pacing at the right ventricular outflow tract (RVOT), right ventricular apex (RVA) and simultaneous RVA and RVOT—dual‐site right ventricular pacing (DuRV) in random order on systolic function using impedance cardiography. Methods: Seventy‐three patients (46 males), aged 52–89 years (mean 71.4 years) subjected to routine dual chamber pacemaker implantation with symptomatic chronic II or atrioventricular block, were included to the study. Results: DuRV pacing resulted in significantly higher cardiac index (CI) in comparison to RVOT and RVA and CI at RVOT was higher than at RVA pacing (2.46 vs 2.35 vs 2.28; P < 0.001). In patients with ejection fraction >50% significantly higher CI was observed during DuRV pacing when compared to RVOT and RVA pacing and there was no difference of CI between RVOT and RVA pacing (2.53 vs 2.41 vs 2.37; P < 0.001). In patients with ejection fraction <50%, DuRV and RVOT pacing resulted in significantly higher CI in comparison to RVA pacing while no difference in CI was observed between RVOT and DuRV pacing (2.28 vs 2.21 vs 2.09; P < 0.001). Conclusion: Dual‐site right ventricular pacing in comparison to RVA pacing improved cardiac systolic function. RVOT appeared to be more advantageous than RVA pacing in patients with impaired, but not in those with preserved left ventricular function. No clear hemodynamic benefit of DuRV in comparison to RVOT pacing in patients with impaired systolic function was observed. Ann Noninvasive Electrocardiol 2010;15(4):353‐359     

Ventricular force‐frequency relationships during biventricular or multisite pacing in congenital heart disease

Background: Traditional indices to evaluate biventricular (BiV) pacing are load dependent, fail to assess dynamic changes, and may not be appropriate in patients with congenital heart disease (CHD). We therefore measured the force‐frequency relationship (FFR) using tissue Doppler‐de‐ rived isovolumic acceleration (IVA) to assess the dynamic adaption of the myocardium and its vari‐ ability with different ventricular pacing strategies.
Methods: This was a prospective pilot study of pediatric and young adult CHD patients with biventricular or multisite pacing systems. Color‐coded myocardial velocities were recorded at the base of the systemic ventricular free wall. IVA was calculated at resting heart rate and with incremental pacing. FFR curves were obtained by plotting IVA against heart rate for different ventricular pacing strategies.
Results: Ten patients were included (mean: 22 ± 7 years). The FFR identified a best and worst ventricular pacing strategy for each patient, based on the AUC at baseline, submaximal, and peak heart rates (P < .001). However, there was no single best ventricular pacing strategy that was optimal for all patients. Additionally, the best ventricular pacing strategy often differed within the same patient at different heart rates.
Conclusion: This novel assessment demonstrates a wide variability in optimal ventricular pac‐ ing strategy. These inherent differences may play a role in the unpredictable clinical response to BiV pacing in CHD, and emphasizes an individualized approach. Furthermore, the optimal ventricular pacing varies with heart rate within individuals, suggesting that rate‐responsive ventricular pacing modulation may be required to optimize ventricular performance.     

Electrocardiographic Follow‐Up of Biventricular Pacemakers

Multisite pacing for the treatment of heart failure has added a new dimension to the electrocardiographic evaluation of device function. During left ventricular (LV) pacing from the appropriate site in the coronary venous system, a correctly positioned lead V1 registers a right bundle branch block pattern with few exceptions. During biventricular stimulation associated with right ventricular (RV) apical pacing, the QRS is often positive in lead V1. The frontal plane QRS axis is usually in the right superior quadrant and occasionally in the left superior quadrant. Barring incorrect placement of lead V1 (too high on the chest), lack of LV capture, LV lead displacement or marked latency (exit block or delay from the stimulation site), ventricular fusion with the spontaneous QRS complex, a negative QRS complex in lead V1 during biventricular pacing involving the RV apex probably reflects different activation of an heterogeneous biventricular substrate (ischemia, scar, His‐Purkinje participation in view of the varying patterns of LV activation in spontaneous left bundle branch block) and does not necessarily indicate a poor (electrical or mechanical) contribution from LV stimulation. In this situation, it is imperative to rule out the presence of coronary venous pacing via the middle cardiac vein or even unintended placement of two leads in the RV. During biventricular pacing 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). In patients with sinus rhythm and a relatively short PR interval, ventricular fusion with competing native conduction during biventricular pacing may cause misinterpretation of the ECG because narrowing of the paced QRS complex simulates appropriate biventricular capture. This represents a common pitfall in device follow‐up. Elimination of ventricular fusion by shortening the AV delay, is often associated with clinical improvement. Anodal stimulation may complicate threshold testing and should not be misinterpreted as pacemaker malfunction. One must be cognizant of the various disturbances that can disrupt 1:1 atrial tracking and cause loss of ventricular resynchronization. (1) Upper rate response. The upper rate response of biventricular pacemakers differs from the traditional Wenckebach upper rate response of conventional antibradycardia pacemakers because heart failure patients generally do not have sinus bradycardia or AV junctional conduction delay. The programmed upper rate should be sufficiently fast to avoid loss of resynchronization in situations associated with sinus tachycardia. (2) Below the programmed upper rate. This may be caused by a variety of events (especially ventricular premature complexes and favored by the presence of first‐degree AV block) that alter the timing of sensed and paced events. In such cases, atrial events become trapped into the postventricular atrial refractory period at atrial rates below the programmed upper rate in the presence of spontaneous AV conduction. Algorithms are available to restore resynchronization by automatic temporary abbreviation of the postventricular atrial refractory period.     

Apparent Acute Reversible Right Ventricular Pacing‐Induced Left Ventricular Dysfunction

Apparent Acute Reversible Right Ventricular Pacing‐Induced Left Ventricular Dysfunction . We report the case of a 70‐year‐old Caucasian male with a dual chamber (right atrium/right ventricle) pacemaker implanted for sinus node dysfunction and not pacemaker (PM) dependent who was found to have an apparent acute worsening of left ventricular (LV) function with right ventricular (RV) apical pacing caused by the mode switch to VVI pacing as battery depletion occurred. LV dysfunction resolved immediately with RV pacing turned off. To our knowledge, this is the first report of this phenomenon. (J Cardiovasc Electrophysiol, Vol. 24, pp. 224‐226, February 2013)