During a heart beat, an electrical impulse leads to the contraction of the upper part of the heart: the atria. The electrical impulse slows down through the atrioventricular junction (AVJ) before resuming rapid propagation to induce contraction of the lower part of the heart: the ventricles. This contraction delay, combined with the presence of cardiac valves, is crucial for unidirectional blood flow in the heart and is altered in various heart diseases. How is this slow conducting property established and restricted to the AVJ? On p. , Takashi Mikawa and colleagues discover that, contrary to the current hypothesis, the AVJ does not maintain juvenile slow conduction; instead, AVJ conduction velocity is plastic and determined by its proximity to the endocardium (the inner lining of the heart). They further show that the cardiac jelly (an extracellular martix-rich deposit that accumulates during valve formation) acts as a crucial physical barrier separating the AVJ from endocardial signals that induce a fast conduction phenotype. The authors thus uncover an exciting mechanism whereby valve formation and the delay in chamber contraction are developmentally linked, and open new perspectives for understanding heart development and congenital diseases.
