ADP-stimulated contraction: A predictor of thin-filament activation in cardiac disease
Population
Cardiac samples from patients with idiopathic dilated cardiomyopathy, hypertrophic cardiomyopathy harboring…
Comparison
ADP-stimulated force development, protein kinase… vs Nonfailing donor samples and baseline conditions
Design
Preclinical
Authors
Discussion
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Member takes
Implication
Animal data implicate ADP sensitivity in relaxation defects; hypothesis-generating for PKA-targeted therapies in human cardiomyopathies.
Structured PICO
P
Population
Cardiac samples from patients with idiopathic dilated cardiomyopathy (IDCM), hypertrophic cardiomyopathy (HCM) harboring thick-filament (MYH7mut, MYBPC3mut) and thin-filament (TNNT2mut, TNNI3mut) mutations, sarcomere mutation-negative HCM (HCMsmn), and nonfailing donors.
I
Intervention
ADP-stimulated force development (without Ca2+), protein kinase A (PKA) treatment, troponin exchange, and cMyBP-C antibody incubation
C
Comparator
Nonfailing donor samples and baseline conditions
O
Outcome
Myofilament ADP sensitivity and actin-myosin blockadesurrogate
ADP-stimulated contraction reveals that pathologic ADP levels, low PKA-phosphorylation, and high actin-myosin formation contribute to impaired myocardial relaxation in cardiomyopathies.
Cite This Study
Sequeira et al. (2015) studied this question.