March 11, 2004Cardiovascular ResearchOpen Access

Does the loss of transverse tubules contribute to dyssynchronous Ca2+ release during heart failure?

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Structured PICO

Population

Cultured pig ventricular myocytes and failing human ventricular myocytes (discussed from Louch et al.)

Outcome

T-tubule density and synchrony of Ca2+ releasesurrogate

Limitations

Enzymatic isolation procedures may yield predominantly healthy myocytes
Small cardiac specimens may not be representative of the different myocyte populations of the ventricular wall
Detubulation may predominate in distinct pathological areas such as the border zone of myocardial infarction or hibernating myocardium

Discussion

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Implication

This editorial discusses findings that challenge the hypothesis that T-tubule loss and asynchronous calcium release are primary drivers of defective excitation-contraction coupling in end-stage heart failure.

Cite This Study

Stéphane Hatem (2004) studied this question.

synapsesocial.com/papers/6a777b343da069e66cbdaa7a https://doi.org/10.1016/j.cardiores.2004.01.037

Topics

Heart failure HFrEF treatment

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Does the loss of transverse tubules contribute to dyssynchronous Ca2+ release during heart failure?

Structured PICO

Limitations

Discussion

Implication

Cite This Study

Topics

Does the loss of transverse tubules contribute to dyssynchronous Ca2+ release during heart failure?

Structured PICO

Limitations

Discussion

Implication

Cite This Study

Also Consider

Topics

Also Consider