Key result
Action potential prolongation may initially serve as a compensatory response to support cardiac output, but chronic activation may trigger maladaptive gene expression and progression to heart failure.
This review proposes a mechanistic hypothesis linking chronic action potential prolongation and altered calcium handling to maladaptive gene expression and heart failure progression.
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Hypothesis-generating for action potential-targeted therapies in heart failure; leaves open need for prospective validation before clinical consideration.
Alan Wickenden (1998) conducted a review in Heart failure and cardiac hypertrophy. Action potential prolongation and altered intracellular calcium handling was evaluated. Action potential prolongation may initially serve as a compensatory response to support cardiac output, but chronic activation may trigger maladaptive gene expression and progression to heart failure.
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