Key result
T-tubule disruption in failing dog ventricles increases the incidence of triggered Ca2+ waves and is a critical component of abnormal Ca2+ cycling in heart failure.
T-tubule loss alone is a critical component of abnormal calcium cycling in the development of heart failure.
T-tubule loss may promote arrhythmogenic Ca2+ waves in HF; hypothesis-generating in animal models and requires human validation.
Three-dimensional analysis of t-tubule density showed t-tubule disruption throughout the whole myocyte in failing dog ventricle. A double-linear relationship between Ca 2+ release and t-tubule density displays a steeper slope at t-tubule densities below a threshold value (∼1.5%) above which there is little effect on Ca 2+ release (T-tubule reserve). T-tubule loss increases incidence of triggered Ca 2+ waves. Chemically induced t-tubule disruption suggests that t-tubule loss alone is a critical component of abnormal Ca 2+ cycling in heart failure.
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Yamakawa et al. (2021) studied Heart failure. T-tubule disruption was evaluated on Ca 2+ release and triggered Ca 2+ waves. T-tubule disruption in failing dog ventricles increases the incidence of triggered Ca2+ waves and is a critical component of abnormal Ca2+ cycling in heart failure.
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