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Circulating serum adiponectin levels in patients with coronary artery disease: relationship to atherosclerotic burden and cardiac function
Author(s) -
Patel J. V.,
Abraheem A.,
Dotsenko O.,
Creamer J.,
Gunning M.,
Hughes E. A.,
Lip G. Y. H.
Publication year - 2008
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/j.1365-2796.2008.02007.x
Subject(s) - adiponectin , medicine , cardiology , coronary artery disease , ejection fraction , myocardial infarction , cardiac function curve , risk factor , heart failure , obesity , insulin resistance
. Background. Abnormal adipocyte function is implicated in both the pathophysiology of coronary heart disease (CHD) and cardiac function, where adiponectin provides a putative link. However, the utility of adiponectin as a discriminator of CHD severity is unclear and may be confounded by cardiac function. We hypothesized that plasma adiponectin would relate to indices of coronary artery disease severity (coronary atheroma scores, CAS), ejection fraction (EF) and regional wall motion abnormalities (RWMA) therein. Method. We measured adiponectin using a cross‐sectional approach, we measured plasma adiponectin enzyme‐linked immunosorbent assay in 204 consecutive patients (aged 34–81 years) undergoing elective coronary angiography. Results. Levels of adiponectin decreased in an ordinal fashion across tertiles of increasing CAS ( P = 0.047), but were nonsignificantly correlated to absolute values of CAS ( P = 0.06). Adiponectin levels were unrelated to left ventricular dysfunction related measures of RWMA or EF. On multivariate analysis, (including factors relating to CHD risk, history and medication) adiponectin levels were independently inversely associated with triglycerides ( P = 0.001), CAS tertiles ( P = 0.01) and positively with age ( P < 0.001). Conclusion. Levels of adiponectin decreased with coronary artery disease severity, without impact from systolic dysfunction, but levels may be moderated through established CHD risk factors such as smoking and triglycerides. Further work is warranted as to the clinical prognostic utility of this marker amongst CHD patients.