Cardiomyocyte stiffness in diastolic heart failure is associated with reduced phosphorylation of sarcomeric proteins and can be corrected by PKA.
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Cardiomyocyte stiffness may underlie diastolic dysfunction in DHF; animal data leaves open PKA modulation for clinical translation.
DHF patients had stiffer cardiomyocytes, as evident from a higher F(passive) at the same sarcomere length. Together with CVF, F(passive) determined in vivo diastolic LV dysfunction. Correction of this high F(passive) by PKA suggests that reduced phosphorylation of sarcomeric proteins is involved in DHF.
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Borbély et al. (2005) studied this question.
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