Ongoing release of myosin fragments could also be explained by proteolytic degradation of myofibrils by such enzymes as Ca2+ -activated proteinases, cathepsins B and D, and possibly cathepsins H and L. Thus, following myocardial infarction the free myosin is degraded by proteolytic enzymes or dissociated by the pH shift liberating more myosin fragments into circulation where they remain up to the