Exercise after myocardial infarction improves contractility and decreases myofilament Ca2+ sensitivity.

Abstract

Impaired Myofilament Function After Myocardial Infarction While myocardial infarction (MI) is the major cause of heart failure, there are conflicting data over the roles of abnormal calcium handling and myofilament function. The acute injury leads to the activation of neurohormones and cytokines, subsequent myocardial remodelling, further decline in heart function, and finally overt heart failure. Depressed myocyte contractility in the remodelled myocardium can largely be explained by Ca handling abnormalities.1 Abnormalities in myofilament function are less well understood. A seminal study in pigs demonstrated that impaired pump function three weeks after MI can also be attributed to decreased maximal isometric tension in skinned cardiomyocytes in areas remote from the ischemic border zone.2 Somewhat paradoxically, the impairment occurred in the context of increased Ca sensitivity of the myofilaments. The authors attributed the increased Ca sensitivity following MI to reduced protein kinase A-mediated troponin I (TnI) phosphorylation.2 Increased myofilament Ca sensitivity has also been reported for end-stage human heart failure, apparently largely because of a reduction of TnI phosphorylation.3

Cite this paper

@article{Schober2007ExerciseAM, title={Exercise after myocardial infarction improves contractility and decreases myofilament Ca2+ sensitivity.}, author={Tilmann Schober and Bj{\"{o}rn C Knollmann}, journal={Circulation research}, year={2007}, volume={100 7}, pages={937-9} }