R-wave amplitude changes in lead aVL predict outcomes in cardiac resynchronization therapy: Exploring the role of papillary muscle dyssynchrony and mitral regurgitation

Figures

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  Figure 1. A: Example of R-wave amplitude decrease in a patient with 2 grades of mitral regurgitation improvement after cardiac resynchronization therapy. B: Example of R-wave measurement in lead aVL. C: Example of intrinsicoid deflection measurement in lead aVL. Pre = before cardiac resynchronization therapy; Post = after cardiac resynchronization therapy.

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  Figure 2. Boxplots depicting changes in QRS duration (A) and RaVL (B) from baseline electrocardiogram before any conduction abnormality or ventricular pacing (labeled as pre-BBB) to after the onset of conduction delay or ventricular pacing but before CRT implantation (labeled as BBB before CRT) and after CRT. BBB = bundle branch block; CRT = cardiac resynchronization therapy; MR = mitral regurgitation; RaVL = R-wave amplitude in lead aVL.

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  Figure 3. ROC curves for different logistic regression models including predictors of MR response. AUC = area under the curve; CI = confidence interval; MR = mitral regurgitation; MRpre = mitral regurgitation severity before cardiac resynchronization therapy; OR = odds ratio; RaVLpre = R-wave amplitude in lead aVL before cardiac resynchronization therapy; ROC = receiver operating characteristic; TRpre = tricuspid regurgitation severity before cardiac resynchronization therapy.

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  Figure 4. Kaplan-Meier survival estimates after CRT. A: Comparison between patients with a post-CRT reduction in QRS duration and those with unchanged or prolonged QRS duration. B: Comparison between patients with a reduction in aVL R-wave amplitude after CRT and those with unchanged or increased amplitude. CRT = cardiac resynchronization therapy.

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  Figure 5. Proposed mechanism of functional mitral regurgitation (MR) owing to electrical dyssynchrony in patients with IVCD. A: In normal conduction, left ventricular and papillary muscle (PM) depolarization occurs synchronously via the anterior and posterior fascicles, resulting in no MR. Electrical activation of both PMs occurs simultaneously (moment t1). Owing to significant cancellation of electrical forces in the frontal plane, the overall Depol is angled away from lead aVL, resulting in a relatively low R-wave amplitude in lead aVL. B: In the presence of LBBB, left ventricular depolarization is delayed, leading to asynchronous activation of the PMs. The posteromedial PM activates earlier (t1), whereas the anterolateral PM activates later (t2). This temporal disparity contributes to functional MR. The Depol in the frontal plane shifts leftward, becoming more aligned with lead aVL, which increases the R-wave amplitude in lead aVL. The delay in electrical activation between the PMs leads to mechanical dyssynchrony, impairing mitral leaflet coaptation and resulting in MR. Depol = depolarization vector; IVCD = intraventricular conduction delay; LBBB = left bundle branch block.