Enhanced myofilament responsiveness upon β-adrenergic stimulation in post-infarct remodeled myocardium.
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22 Citations (Scopus)
Previously we showed that left ventricular (LV) responsiveness to exercise-induced increases in noradrenaline was blunted in pigs with a recent myocardial infarction (MI) [van der Velden et al. Circ Res. 2004], consistent with perturbed β-adrenergic receptor (β-AR) signaling. Here we tested the hypothesis that abnormalities at the myofilament level underlie impaired LV responsiveness to catecholamines in MI. Myofilament function and protein composition were studied in remote LV biopsies taken at baseline and during dobutamine stimulation 3weeks after MI or sham. Single permeabilized cardiomyocytes demonstrated reduced maximal force (F