Key result
Porcine left atrial tissue generated significantly less force than left ventricular tissue at maximal calcium activation (61.04 vs 88.47 mN/mm2) and exhibited a structurally distinct resting state.
Why the study?
Each cardiac chamber has distinct properties tailored to its circulatory role, but whether this results in chamber-specific differences in myofilament structure and regulation between atria and ventricles was unknown.
Absolute Event Rate: 61.04% vs 88.47%
p-value: p=<0.01
This study demonstrates that atrial myosin thick filaments adopt a distinct resting configuration and lack direct calcium-dependent activation, suggesting evolutionary optimization for rapid, burst-like contractions compared to the sustained force generation of the ventricle.
Porcine atrial-ventricular differences may reflect chamber-specific regulation; leaves open translation to human atrial function or therapies.
The heart maintains systemic perfusion through the coordinated function of its four chambers: the left and right atria and ventricles. Each chamber has distinct structural, functional, and molecular properties tailored to its role in circulation, which may result in chamber-specific differences in myofilament structure and regulation between atria and ventricles. To test this hypothesis, we employed muscle mechanics and X-ray diffraction to investigate functional and structural differences in porcine left atrial (LA) and left ventricular (LV) tissue. Here, we report the first X-ray diffraction study of atrial tissue, demonstrating that under resting conditions, myosin filaments in LA adopted a more ON-like, structurally distinct configuration compared with those in LV. Under contracting conditions, LV generated greater force and exhibited higher sinusoidal stiffness than LA across multiple calcium concentrations. LA showed faster k TR than in LV, with no calcium-dependence, in contrast to the calcium-dependence of k TR seen in LV. Structurally, the distinct myosin head configuration seen in the relaxed LA persisted during contraction. Furthermore, using the troponin inhibitor MYK-7660 to inhibit active contraction, we showed that, unlike LV, LA showed no direct calcium-dependent thick filament activation, reconciling discrepancies between fast rat and slow porcine ventricular myocardium regarding calcium’s role in thick filament regulation. Altogether, our study reveals that LA myosin filaments adopt a molecular architecture and regulatory mechanism distinct from their LV counterparts, suggesting that myosin filament structure and regulation have evolved differently to meet the unique functional demands of each cardiac chamber. Moreover, atrial disease is often associated with cardiomyopathy-related genetic variants, highlighting the atrial myocardium as an important therapeutic target and understanding atrial-specific regulatory mechanisms provides new insights into therapeutic strategies for atrial diseases.
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Qi et al. (2026) studied this question. Left atrial myocardium vs. Left ventricular myocardium was evaluated on Steady-state isometric force generation at maximal calcium activation (pCa 4.3) (p=<0.01). Porcine left atrial tissue generated significantly less force than left ventricular tissue at maximal calcium activation (61.04 vs 88.47 mN/mm2) and exhibited a structurally distinct resting state.
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