January 14, 2006AJP Heart and Circulatory Physiology
Multimodal functional cardiac MRI in creatine kinase-deficient mice reveals subtle abnormalities in myocardial perfusion and mechanics
Why the study?
Does creatine kinase deficiency alter myocardial perfusion and mechanics in mice at baseline and post-myocardial infarction?
Population
Mice with a combined knockout of mitochondrial and cytosolic creatine kinase (CK) and wild-type mice…
Comparison
Combined knockout of mitochondrial and cytosolic… vs Wild-type mice
Design
Preclinical
Follow-up
4 weeks post-MI
Authors
Discussion
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Member takes
Implication
CK deficiency models reveal early perfusion and mechanical changes; leaves open whether CK modulation affects human post-MI outcomes.
Structured PICO
Does creatine kinase deficiency alter myocardial perfusion and mechanics in mice at baseline and post-myocardial infarction?
P
Population
Mice with a combined knockout of mitochondrial and cytosolic creatine kinase (CK(-/-)) and wild-type mice, evaluated at baseline and 4 weeks after myocardial infarction (MI)
I
Intervention
Combined knockout of mitochondrial and cytosolic creatine kinase (CK(-/-))
C
Comparator
Wild-type mice
O
Outcome
Maximal myocardial velocity (Vmax) and myocardial perfusion measured by MRIsurrogate
Multimodal MRI reveals that creatine kinase-deficient mice have reduced myocardial perfusion and maximal contraction velocity despite normal ejection fraction, indicating subtle functional abnormalities.
Cite This Study
Nahrendorf et al. (2006) studied this question.