In a sheep model, LBBB-like activation induced by pacing led to a 29% decrease in septal thickness and a 24% increase in lateral wall thickness over 16 weeks (p<0.05).
Does LBBB-like conduction delay alter wall stress distribution and trigger regional remodeling in a sheep model?
LBBB-like activation causes an acute reduction in septal wall stress at the onset of shortening, triggering differential regional remodeling that rebalances initial stress but worsens peak wall stress distribution.
p-value: p=<0.05
Abstract Introduction A left bundle branch block (LBBB) induces an early activation of the septal wall and late activation of the lateral wall of the left ventricle. This mechanical dyssynchrony causes the septal wall to shorten against low left ventricular (LV) pressure, whereas the lateral wall will shorten against higher LV pressure. This loading asymmetry has been hypothesized as the trigger for compensatory remodeling – septal thinning and lateral thickening – which has been suggested to rebalance wall stresses in the left ventricle. Yet, empirical measurements of wall stress during chronic LBBB are sparse. Purpose This study aimed to investigate how wall stress distribution within the left ventricle relates to regional remodelling in an animal model with chronic exposure to LBBB. Methods Fifteen sheep underwent DDD pacing of the right ventricle at 180 bpm to induce LBBB-like conduction delay and accelerate remodeling. Echocardiography allowed to measure septal and lateral wall thickness; speckle-tracking provided septal and lateral strain and curvature; and LV pressure was recorded via a Millar catheter. Dynamic wall stress was assessed by the Law of Laplace – wall stress = pressure x (radius of curvature / 2 x wall thickness) – and was measured at the onset of regional shortening and at peak. All measurements were performed at baseline, 8 weeks, and 16 weeks. A "control" setting was recorded at baseline without pacing. Results LBBB induced mechanical dyssynchrony (Fig. A vs. B). By week 16, septal thickness decreased by 29% (p0.05) and lateral wall thickness increased by 24% (p0.05). Mechanical dyssynchrony worsened progressively, with amplifying early-systolic septal shortening and septal rebound stretch and lateral wall pre-stretch (Fig. B-D). At baseline control, no differences in wall stress were observed (Fig. F). After induction of LBBB, at the onset of shortening, initial septal wall stress was significantly lower than lateral wall stress (all p0.01) (Fig. G-I), but this difference narrowed from 41±7 mmHg at baseline, to 25±9 mmHg at week 8 and 11±2 mmHg at week 16 (all p0.05) (Fig. E), reflecting increased septal stress (due to thinning) and reduced lateral stress (due to thickening). In contrast, peak septal stress remained higher than lateral stress (all p0.01), and the difference further widened over 16 weeks from 9±8 mmHg over 24±12 mmHg to 43±14 mmHg (all p0.05) (Fig. J). Conclusions LBBB-like LV activation leads to an acute reduction in septal wall stress at onset of shortening of the respective wall, which is then re-balanced through differential regional remodelling of the left ventricle. This remodelling, however, leads to an increasingly unfavourable peak wall stress distribution. Our data suggest that regional loading conditions at onset of shortening rather than peak stress trigger adaptive processes of the myocardium.
Duchenne et al. (2026) studied Left bundle branch block (LBBB) (n=15). DDD pacing of the right ventricle to induce LBBB vs. Baseline control (without pacing) was evaluated on Septal and lateral wall thickness and wall stress distribution (p=<0.05). In a sheep model, LBBB-like activation induced by pacing led to a 29% decrease in septal thickness and a 24% increase in lateral wall thickness over 16 weeks (p<0.05).