Myocardial fibrosis and increased passive stiffness are key factors in the transition from compensated hypertrophy to heart failure in spontaneously hypertensive rats.
Does not support clinical practice changes in hypertensive heart disease; leaves open antifibrotic targets for human HF progression.
The development of heart failure in the aging SHR is associated with marked myocardial fibrosis, increased passive stiffness, and impaired contractile function relative to age-matched nonfailing SHR and nonhypertensive control animals. These data suggest that fibrosis or events underlying the connective tissue response are important in the transition from compensated hypertrophy to failure in the SHR.
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Conrad et al. (1995) studied this question.
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