Key result
Pulmonary vein cardiomyocytes are longer and thinner than left atrial cells and lack length-shortening correlation.
Why the study?
Pulmonary vein myocardial sleeves are a major source of ectopic activity causing atrial arrhythmias, but the mechanical function of pulmonary vein cardiomyocytes had not yet been studied.
Myocardial sleeves of the pulmonary veins (PV) extending from the left atrium (LA) are the major source of ectopic activity causing atrial arrhythmias. The structural and electrophysiological characteristics of the PV myocardium differ from those of the LA. The mechanical activity of cardiomyocytes (CM) impacts cardiac excitation-contraction coupling, however, the mechanical function of PV CM has not been studied yet. We compared the characteristics of the actin-myosin interaction and sarcomere length (SL) dynamics in mechanically non-loaded single CM between the PV and LA in the guinea pig heart. We found that the functional properties of myosin from the PV and LA are not different, while the phosphorylation levels of sarcomeric proteins in the PV and LA are different. End-diastolic SL, sarcomere shortening amplitude, and velocities of sarcomere shortening and relengthening of PV and LA CM do not differ, while PV CM are longer and thinner than LA CM. The amplitude of sarcomere shortening increased with an increase in CM length in the LA but not in the PV. We assume that an absence of correlation between the morphometric parameters of CM and the amplitude of sarcomere shortening together with the electrophysiological features of the PV myocardium may contribute to the occurrence and development of atrial fibrillation.
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Butova et al. (2024) studied Atrial fibrillation. Pulmonary vein cardiomyocytes vs. Left atrial cardiomyocytes was evaluated on Characteristics of actin-myosin interaction and sarcomere length dynamics. Pulmonary vein cardiomyocytes are longer and thinner than left atrial cardiomyocytes and lack a correlation between cell length and sarcomere shortening amplitude.
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