On the Mend: Atrial Tubulogenesis After Tachypacing-Induced Heart Failure

Abstract

The negative inotropic impact of TT loss in the atria is moderate, with Ca2+ handling becoming reminiscent of early development when the TT network is immature and SR Ca2+ release is reliant on diffusion from the periphery. Ca2+ handling in HF atrial cells demonstrates a rise in SR Ca2+ load, despite slower SR Ca2+ reuptake. The authors propose that TT loss separates the L-type Ca2+ channel from the Ca2+ releasing points, promoting SR load due to lower Ca2+–dependent inactivation of the L-type Ca2+ channel current.4 Another contributor to Ca2+ decay, NCX, would also be affected by the lack of TTs and separation from the Ca2+ releasing points. However, the decay of caffeine-induced Ca2+ transient did not show differences between groups, suggesting that general Ca2+ extrusion was not reduced in detubulated cells.