Anatomical and electrical remodeling with incomplete left atrial appendage ligation: Results from the LAALA‐AF registry

    loading  Checking for direct PDF access through Ovid

Excerpt

To the Editor:
We thank Drs. Alsagheir and Whitlock1 for their interest in our manuscript entitled “Anatomical and electrical remodeling with incomplete left atrial appendage (LAA) ligation: Results from the LAALA‐AF Registry.”2
The authors comment that the non‐vitamin K antagonist oral anticoagulants (NOACs) can potentially cause less major bleeding in high‐risk groups of patients and may be an alternative in warfarin ineligible patients. We disagree with this comment. The AVERROES included patients that were relatively low risk with a CHADS2 score of 2.1 ± 1.1 and 14% with prior stroke/TIA.3 Our study consists of patients with a higher CHA2DS2VASC score of 3.2 ± 1.3 and 33% had a prior stroke/transient ischemic attack.2 Furthermore, our recent real‐world experience including 263 patients also demonstrated that NOACs are not the “holy grail” for patients who are warfarin ineligible as the majority (two‐thirds) of them suffered major rebleeding with NOACs.4 NOACs are also associated with poor physician prescription rates, drug adherence, and high discontinuation rates exposing a large number of patients to risk of stroke and systemic embolism.5 Our recent analysis from the MarketScan® administrative claims for U.S. patients with private or Medicare supplemental insurance including 158,325 patients followed for 300,614 patient‐years demonstrated that higher adherence (>80%) was only achieved in 69% of patients prescribed NOACs and 52% with warfarin. Low adherence further increased risk of stroke and systemic embolism by 46% [HR, 1.46 (P < 0.001)] with warfarin and 68% [1.68 (P < 0.001)] with NOACs when compared with those with higher adherence.6
The authors also comment that 1 year of follow‐up is not considered long term and raised concerns regarding the short‐ and long‐term safety of the procedure and stopping oral anticoagulation. We have already acknowledged this in our limitations that despite the majority of our patients were able to discontinue oral anticoagulation for 1 year, due to a relatively modest sample size, we are unable to demonstrate a definitive interaction between LAA ligation and stroke risk from this study. This study was mainly designed to demonstrate the electrical and morphological remodeling that accompanies Lariat LAA ligation and understanding its indirect impact on atrial fibrillation (AF) burden and stroke.
We would also like to point out that there were no major complications in this study that required percutaneous or surgical intervention and this procedure can be a relatively low‐risk procedure in experienced hands where the risks of exposing a high‐risk patient to stroke and systemic thromboembolism is higher than the procedural complications itself.
The authors also mention that the surgical LAA ligation trial, LAAOS III, will provide reliable estimates about the risks and benefits of LAA ligation.7 Several studies to date have demonstrated very poor outcomes in patients undergoing surgical LAA ligation. Kanderian et al. reported that surgical LAA exclusion rates have been very dismal, as low as 40%, with high rates of thrombus formation with incomplete closure (suture 46% and stapler 67%) resulting in high rates of stroke and systemic embolism.8
Finally, we would like to remind the authors that >80% of patients in this study had persistent AF with limited treatment options in whom LAA Lariat ligation has demonstrated a significant reduction in AF burden at 1‐year follow‐up.9 We agree with their comment that this current study is a prospective nonrandomized trial without a control group and is prone to inherent selection bias. A randomized controlled trial is necessary to demonstrate the impact of LAA exclusion on reduction of ischemic stroke and AF burden.
    loading  Loading Related Articles