Key result
Hemodynamic unloading via left atrial ligation inhibits pectinate muscle formation and slows impulse propagation.
Why the study?
The formation and patterning of pectinate muscles in embryonic atria remain understudied compared to ventricular trabeculae. This study tested whether pectinate muscles are homologous to ventricular trabeculae and depend on hemodynamic loading for their specification.
Does hemodynamic unloading inhibit pectinate muscle formation and alter atrial myocardial differentiation in chick embryos?
Does hemodynamic unloading inhibit pectinate muscle formation and alter atrial myocardial differentiation in chick embryos?
This preclinical study demonstrates that embryonic atrial pectinate muscle formation and electrophysiological differentiation are critically dependent on hemodynamic loading via chamber-specific regulatory mechanisms.
Embryonic chick data extend PM-trabeculae homology; leaves open hemodynamic dependence and mammalian relevance.
BACKGROUND: The formation and patterning of pectinate muscles (PM) in embryonic atria remain understudied compared to ventricular trabeculae. This study tests the hypothesis that PM are homologous to ventricular trabeculae and depend on hemodynamic loading for their specification. RESULTS: PM emerged in chick atria at Hamburger-Hamilton stage 23 (embryonic day 4), expanding to comprise over 50% of atrial myocardial cross-sectional area by embryonic day 8. Unlike the compact ventricular myocardium, atrial free wall remained thin (~5-25 μm) throughout development, with proliferation higher in the PM than in the interpectinate regions. Hemodynamic unloading via in vitro culture or in ovo left atrial ligation (LAL) at stages 21-23 inhibited PM formation, reduced myocyte proliferation, and slowed impulse propagation. LAL induced ectopic pacemaking activity in the ligated region, with upregulated HCN4 and downregulated GJA5 and SCN5A expression. Shear stress-responsive gene expression (KLF2, EDN1) was absent in unloaded LAL endocardium, while NOTCH1 expression persisted. CONCLUSIONS: These findings demonstrate that PM formation and atrial myocardial differentiation are highly sensitive to hemodynamic loading. While the early phases of PM formation share mechanosensitivity with ventricular trabeculae, their subsequent growth and myocardial compartment organization differ, suggesting chamber-specific regulatory mechanisms rather than direct developmental equivalence and reflecting their different myocardial architecture.
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Neradilova et al. (2026) studied Embryonic atrial pectinate muscle development. Hemodynamic unloading via in vitro culture or in ovo left atrial ligation (LAL) vs. Normal hemodynamic loading was evaluated on Atrial pectinate muscle formation, myocyte proliferation, impulse propagation, and gene expression. Hemodynamic unloading via left atrial ligation at stages 21-23 inhibited atrial pectinate muscle formation (which normally expands to >50% of myocardial area by day 8) and slowed impulse propagation.
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