Key result
In renovascular hypertensive rats, impaired diastolic function is related to interstitial fibrosis rather than myocardial hypertrophy, as ramipril regressed myocyte mass but maintained stiffness.
Why the study?
Does myocardial fibrosis or hypertrophy drive diastolic dysfunction in renovascular hypertensive rats?
Does myocardial fibrosis or hypertrophy drive diastolic dysfunction in renovascular hypertensive rats?
In a rat model of renovascular hypertension, impaired diastolic function is driven by interstitial fibrosis rather than myocardial hypertrophy.
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Implicates fibrosis over hypertrophy in experimental diastolic dysfunction; leaves open human translation.
Matsubara et al. (1997) studied Renovascular hypertension (n=40). Ramipril vs. Untreated renovascular hypertensive rats and unoperated/untreated controls was evaluated on Diastolic myocardial function (myocardial passive stiffness) and myocardial fibrosis. In renovascular hypertensive rats, impaired diastolic function is related to interstitial fibrosis rather than myocardial hypertrophy, as ramipril regressed myocyte mass but maintained stiffness.
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