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原文 A clear cause-and-effect
relationship between excessive myocardial MMP-1 activity,
increased mysial collagen degradation, and progression to
systolic HF has been shown experimentally through the use
of transgenic models and the use of pharmacological MMP
activators.53,54 In addition, experimental evidence has
been provided showing that following chronic neurohormonal
activation, increased synthesis and release of MMPs
into the local extracellular matrix of the cardiomyocyte
occurs,55 which in turn could contribute to endomysial and
perimysial collagen degradation and disruption.
In this context, we have reported recently that the
volume of myocardial tissue occupied by perimysial and
endomysial collagen was lower in hypertensive patients
with HF and depressed ejection fraction (systolic HF), than
in hypertensive patients with HF and preserved ejection
fraction (diastolic HF) and normotensive sub

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