Clarifies potential mechanisms linking β-adrenergic stimulation and mechanical stretch to arrhythmogenesis in heart failure to identify novel therapeutic targets.
microdomains during the remodeling process associated the HF may contribute to the increased disposition for β-adrenergic or stretch induced arrhythmogenic triggers. Finally, the potential mechanisms linking β-adrenergic stimulation and mechanical stretch will be clarified, with the aim of finding common modalities of arrhythmogenesis that could be targeted by novel therapeutic agents in the setting of HF.
Johnson et al. (Mon,) studied this question.
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