By Michael V. Orlov, MD, PhD & Timothy McIntyre, MSBME
Published in HeartRhythm, the Official Journal of the Heart Rhythm Society, The Cardiac Electrophysiology Society, and the Pediatric & Congenital Electrophysiology Society
Left bundle branch area pacing (LBBAP) has rapidly gained popularity, replacing His bundle pacing for both bradycardia and cardiac resynchronization therapy (CRT) indications.1 Initial impressions of a simpler implantation procedure, better capture thresholds, and hopes for efficacy comparable to His bundle pacing have created the perception that the electrophysiology community has finally found the “holy grail” of conduction system pacing. Subsequent investigation has called for more detail in many aspects that are presently being defined and debated.
Strength-duration curves (SDCs) are not well understood and are infrequently used in a clinical setting. Yet our under standing of safe and energy-efficient stimulation programming is based on the value of the chronaxie, a characteristic of the SDC. The SDC typically takes the form of a hyperbolic equation relating stimulation intensity to the stimulus pulse duration. In cardiac pacing, the SDC is a plot of the capture threshold in volts as a function of the stimulation pulse duration in milliseconds. The rheobase is defined as the lowest intensity that captures the tissue with indefinitely long pulse duration—the flat portion of the SDC. The chronaxie is the pulse duration at which the threshold is twice the rheobase.
Furthermore, chronaxie reflects the excitability of the tis sue at the pacing electrode and hence the conduction velocity; specialized conducting myocardium has lower chronaxie. Tissue-electrode interface plays a significant role in these electrical measurements; electrode sizes and materials matter—chronaxie may vary between different electrodes.
SDCs have previously been characterized for the right ventricular endocardium, left ventricular (LV) epicardium, and His bundle. Conduction velocities were also measured in other parts of the heart, including LV septal superficial subendocardial muscle cells,2 which were found to have faster conduction velocities, competing with specialized conduction tissue.
In this issue of Heart Rhythm, Kie1basa and colleagues3 present well-collected data on SDCs in 141 patients with permanent LBBAP. This is the first calculation of left bundle branch–specific chronaxie and rheobase presented in comparison to LV septal endocardium and prior His bundle pacing data by the same group.4 Chronaxie and rheobase were almost identical for LBBP and LV septal pacing (LVSP). Chronaxie for His bundle pacing was significantly higher, corresponding to a steeper SDC, probably reflecting a more insulated nature of the His bundle tissue. Furthermore, the authors describe 3 different transition patterns during threshold testing (their Figure 2), namely, between the nonselective, selective LBBP, and pure LVSP capture. Interestingly, the individual SDCs for LBBP and LVSP mirror each other for 2 different transition patterns. This results in a significantly lower LVSP rheobase for the transition from nonselective to pure LVSP and, consequently, a real possibility of conduction system pacing loss during follow-up at programmed lower out puts and shorter pulse widths.
Inadvertent loss of conduction system capture with pure LVSP in follow-up at programmed output is reported in >10% of patients. This is a clinically important observation that may result in loss of resynchronization and a clinical deterioration in the CRT population.3
The last part of the data concerns battery longevity and current drain at different pulse widths. The lowest current drain occurred when pacing at chronaxie at the traditional (twice the threshold) output voltage.
These observations have important clinical implications far beyond the first in vivo calculation of LBBP and LVSP chronaxie. The reported inadvertent loss of conduction system capture in >10% of patients during follow-up is worrisome, particularly for patients receiving LBBAP for CRT indications.
Moreover, the transition from nonselective LBBP to LVSP may be subtle (the authors’ Figure 2B), and the diagnostic criteria defining different variants of conduction system and septal capture are still in flux. Unless a detailed review of a 12-lead electrocardiogram is performed in follow-up, loss of conduction system capture may be easy to miss.
Further difficulties emerge in comparing the results of LVSP (ie, capturing the rapidly conducting LV endocardium) and deep septal pacing (DSP; capturing the septum at lesser depths). Conflicting evidence indicates superiority of LBBP to LVSP5 or their equivalence, but a better outcome compared with DSP.6 Animal data2 showed a significantly slower con duction velocity of deeper layers compared with superficial endocardium, suggesting an improved resynchronization with LVSP compared with DSP. This theory is further sup ported by similar chronaxies between LBBP and LVSP in this study.3 Interestingly, a study by Vijayaraman and coworkers7 also suggested that in some patients with non-LBBB intraventricular conduction delay, cardiac resynchronization can be achieved, presumably secondary to left septal endomyocardial capture with faster conduction to the LV lateral wall. The exact interaction between the rapidly conducting septal endocardium and the diffusely diseased conduction system needs further investigation.
Two novel programming strategies to achieve safe con duction system pacing and to minimize battery current drain are presented. Thresholds at short pulse width values of 0.03 ms, 0.06 ms, 0.1 ms, and 0.2 ms emerge as a new “best practice” to achieve these goals. All current pace makers have pulse widths of 0.1 ms; only Medtronic devices provide 0.03 ms and 0.06 ms and Abbott, 0.05 ms. This minimizes applicability of lower pulse width settings. Fixed safety margins are the key to success at short pulse widths, but Figure 3C illustrates that these short pulse width values require higher output where the slope of the SDC is steep.
Battery drain involves the extra step of computing the mean voltage between the leading edge and trailing edge of the pacing pulse. Despite this high degree of fidelity, the authors do not assess the impact of “voltage boosting,” and their formula does not include such a term. An inspection of Figure 3A–3C indicates that the thresholds at 0.03 ms and 0.06 ms are at least 2.0 V. Hence, adding a safety margin of 1.0 V or 1.5 V will require programming above 2.5 V, which invokes the voltage-boosting circuitry of every pacemaker. All voltage-boosting topologies consume extra current, whether
a charge pump or less efficient voltage multiplier is used. Voltage boosting may add up to 30% more current to pace at 5.0 V compared with 2.5 V.
The paper by Kie1basa and colleagues3 is the first to describe chronaxie of LBBP and LV septal endocardium and to compare them with His bundle and surrounding right ventricular endocardium. Left bundle branch and LV septal endocardium have similar SDC characteristics that may account for some of the difficulties in differentiating between the conduction system and septal capture. SDC data provide an important aid to safe device programming for LBBAP. Maintenance of conduction system capture (and potential switch to pure septal capture at programmed outputs that was observed in >10% of patients) is important for better cardiac resynchronization, particularly in the CRT population. This may require a detailed analysis of a 12-lead electrocardiogram and intracardiac electrograms. Programming a shorter pulse width while maintaining conduction system capture may provide added battery life but will require further studies.
Funding Sources: The authors have no funding sources to disclose.
Disclosures: The authors have no conflicts of interest to disclose.
Address reprint requests and correspondence: Dr Michael V. Orlov, St Elizabeth’s Medical Center, 736 Cambridge St, Bos ton, MA 02135. E-mail address: michael.orlov@steward.org
References
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