Key result
CAD linked to impaired mitochondrial oxidative phosphorylation and lower adiponectin in EAT.
Why the study?
Epicardial adipose tissue is metabolically active and produces adipokines, but the role of its mitochondria in CAD has not been established.
Observational (n=25)
Yes
p-value: p=<0.05
Impaired mitochondrial oxidative phosphorylation in epicardial adipose tissue is associated with decreased adiponectin levels and greater severity of coronary atherosclerosis, suggesting a local pathophysiological role of EAT in CAD.
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Should not change practice; hypothesis-generating for epicardial adipose tissue mitochondrial impairment in CAD.
Nakajima et al. (2019) conducted an observational in Coronary artery disease (n=25). Coronary artery disease vs. Non-coronary artery disease was evaluated on Mitochondrial oxidative phosphorylation (OXPHOS) capacity in epicardial adipose tissue (p=<0.05). Coronary artery disease is associated with significantly impaired mitochondrial oxidative phosphorylation capacity and decreased adiponectin concentration in epicardial adipose tissue.
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