Author + information
- Published online August 21, 2017.
- Christopher A. Rinaldi, MD∗ ()
- Cardiac Department, Guy’s and St Thomas Hospitals, and King’s College London, London, United Kingdom
- ↵∗Address for correspondence:
Dr. Christopher A. Rinaldi, Cardiac Department. St. Thomas’ Hospital, Westminster Bridge Road, London SE1 7EH, United Kingdom.
Cardiac resynchronization therapy (CRT) is an extremely effective treatment for dyssynchronous heart failure with significant reductions in morbidity and mortality; however, approximately one-third of patients are nonresponders to CRT (1). Nonresponse is multifactorially dependent on many complex patient- and procedural-related factors (2). Left ventricular (LV) lead placement and guidance would appear important in an attempt to target late electrically activating regions and avoiding myocardial scar. The use of echocardiographic surrogates of mechanical activation and/or contraction with speckle tracking in both the TARGET (Targeted Left Ventricular Lead Placement to Guide Cardiac Resynchronization Therapy) (3) and STARTER (Speckle Tracking Assisted Resynchronization Therapy for Electrode Region) trials (4) have been shown to result in better outcomes with CRT by targeting late mechanical activation. CRT is a treatment that aims to correct electrical dyssynchrony, but, to date, the demonstration of the correlation between electrical activation and mechanical timing has been lacking.
In this issue of JACC: Clinical Electrophysiology, Mafi-Rad et al. (5) report their study that compares electrical activation using electroanatomical mapping with echocardiographic strain measures in a cohort of CRT patients. The investigators studied 28 patients who underwent CRT, in whom they performed intraprocedural coronary venous electroanatomical mapping that was compared with peak contraction time of the mapped LV regions, which was determined using speckle tracking indexes of longitudinal strain. The study protocol was successful in 23 of 28 patients, and the investigators found a strong positive correlation between electrical activation and peak contraction times within each individual patient; however, the magnitude of the electrical activation to peak contraction relationship varied greatly among patients. In their study, the regions of latest electrical activation and latest peak contraction corresponded in 19 of 23 (83%) patients and was adjacent in the remaining 4 patients. Based on these results, the investigators concluded that a strategy of determining the latest activated LV region based on speckle tracking echocardiography corresponded to that based on intracardiac measurements of electrical activation.
The extrapolation of the current findings suggests that LV lead targeting strategies that use direct intracardiac measurements of electrical activation or speckle tracking strain echocardiography will most likely target the same myocardial region. The investigators acknowledged that electrical mapping of the coronary veins could extend procedure time and might be cumbersome in routine clinical practice, but that speckle tracking time-to-peak contraction analysis could be performed offline before CRT implantation. This information could then be provided to the implanter during CRT implantation, who could then, after performing invasive coronary venous angiography, match the location of the cardiac veins to the underlying LV myocardial segments and target the LV lead to the segment of latest peak contraction.
The investigators are to be congratulated on their study, which provides important insights into the relationship between electrical activation and mechanical activation. However, there are several important limitations and factors that should be taken into account. The sample size was small, with only 28 patients as acknowledged by the investigators, and notably, 5 patients were excluded from the analysis (4 due to suboptimal echocardiographic imaging and 1 due to frequent ventricular ectopy). Notably, 43% of patients had an intraventricular conduction delay (IVCD) rather than left bundle branch block (LBBB), and only 2 of the patients studied had myocardial scar inferred on echocardiography. It is important to state that this patient population may therefore be unrepresentative of a typical CRT population, most of which will have typical LBBB. Likewise, the small number of patients with myocardial scar limits the extrapolation of the current results to the many ischemic cardiomyopathy patients undergoing CRT who have transmural scar. Furthermore, it is in this ischemic population that CRT is often less effective (6), and a better understanding of the interaction between electrical and mechanical indexes may be important in tailoring CRT in this group.
The findings of a significant correlation with electrical activation and mechanical contraction may direct us to believe that targeting the regions for LV lead placement will result in better CRT outcomes. However, this may not necessarily be the case in all patients, especially in ischemic patients with myocardial scar in whom the latest activating region may not always be the optimal pacing site. In such patients, there may be areas of scarred tissue with late activation that may not necessarily be the optimal target site for lead placement because of slow conduction when pacing from these sites (6). The presence of scar may create late activation; however, pacing in these late activating and/or contracting scarred regions may reduce the effectiveness of CRT instead of improving it. In this respect, the use of multimodality imaging, including cardiac magnetic resonance imaging that is able to delineate both areas of scar and late mechanical contraction, may prove useful to target optimal LV pacing sites (7).
No acute hemodynamic measurements of CRT response were performed in the current study, and there was no randomization to targeted lead placement. This study therefore lacks the correct design to investigate whether a lead targeting strategy combining electrical and mechanical information may improve CRT response, as the investigators acknowledged. Importantly, the electrical activation time of some LV free wall segments could not be assessed because they did not contain any suitable epicardial veins; it is well known that epicardial mapping through the coronary veins is limited by coronary venous anatomy. As such, there may be late activated LV regions that represent the optimal site of LV lead implantation, which could not be mapped via the coronary sinus; in such patients, an endocardial approach to LV mapping and stimulation may be considered.
The current study by Mafi-Rad et al. (5) provides us with important insights into the relationship between electrical activation and mechanical contraction in patients undergoing CRT. At present, it is unclear whether combining such electrical and mechanical information may further improve LV lead targeting and CRT response, and this is likely to be answered only by further evaluation in large prospective randomized studies.
↵∗ Editorials published in JACC: Clinical Electrophysiology reflect the views of the authors and do not necessarily represent the views of JACC: Clinical Electrophysiology or the American College of Cardiology.
Dr. Rinaldi has received research funding received from Abbott Medical, Medtronic, Boston Scientific, and Livanova; and has received speaker fees and sponsorship from Abbott Medical and LivaNova.
The author attests that he is in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Clinical Electrophysiology author instructions page.
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