Relationship of serum osteoprotegerin levels with coronary artery disease severity, left ventricular hypertrophy and C-reactive protein.
OPG (osteoprotegerin) is an inhibitor of osteoclastogenesis and recent work suggests it has a role in atherosclerosis. Therefore we measured serum OPG levels in patients with coronary artery disease, compared the serum OPG levels among the different groups according to the number of stenotic vessels and determined whether there was any correlation with aortic calcification, LV (left ventricular) mass index and serum CRP (C-reactive protein) levels. Subjects (n=100; mean age, 57 years) who underwent coronary angiograms were enrolled. Blood pressure, body mass index, fasting blood glucose, lipid profiles and CRP levels were measured and the LV mass indices were calculated using ECGs. Serum OPG levels were measured by ELISA. The presence of calcification in the aortic notch was checked by a chest X-ray. The subjects were divided into four groups according to the number of stenotic vessels. The mean serum OPG levels increased significantly as the number of stenotic vessels increased, and the mean serum OPG levels were higher in the group with three-vessel disease compared with the groups with no- or one-vessel disease. The mean serum CRP level was significantly higher in the group with three-vessel disease compared with the groups with no-, one- and two-vessel disease. Age and LV mass index showed significant positive correlations with serum OPG levels, although significance was lost after an adjustment for age. Serum CRP levels were positively correlated with serum OPG levels even after an adjustment for age. There were no differences in serum OPG levels according to the presence of fasting hyperglycaemia or aortic calcification. In conclusion, serum OPG level was related to the severity of stenotic coronary arteries and serum CRP levels. LV mass indices showed no significant correlation with OPG levels. The precise mechanism for the role of OPG in atherosclerosis needs to be investigated further.
Rhee
Eun-Jung
EJ
Department of Internal Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Pyung-dong, Seoul 110-746, South Korea.
Lee
Won-Young
WY
Kim
Se-Yeon
SY
Kim
Byung-Jin
BJ
Sung
Ki-Chul
KC
Kim
Bum-Su
BS
Kang
Jin-Ho
JH
Oh
Ki-Won
KW
Oh
Eun-Sook
ES
Baek
Ki-Hyun
KH
Kang
Moo-Ii
MI
Woo
Hee-Yeon
HY
Park
Hyo-Soon
HS
Kim
Sun-Woo
SW
Lee
Man-Ho
MH
Park
Jung-Roe
JR
D000368:Aged; D001027:Aortography; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism*; D002114:Calcinosis / Q000097:blood / Q000150:complications / Q000000981:diagnostic imaging; D017023:Coronary Angiography; D003327:Coronary Disease / Q000097:blood* / Q000150:complications / Q000000981:diagnostic imaging; D018450:Disease Progression; D004562:Electrocardiography; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D006023:Glycoproteins / Q000097:blood*; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000097:blood* / Q000150:complications / Q000000981:diagnostic imaging; D008875:Middle Aged; D053244:Osteoprotegerin; D018160:Receptors, Cytoplasmic and Nuclear / Q000097:blood*; D018124:Receptors, Tumor Necrosis Factor
D015415:Biomarkers; D006023:Glycoproteins; D053244:Osteoprotegerin; D018160:Receptors, Cytoplasmic and Nuclear; D018124:Receptors, Tumor Necrosis Factor; C506030:TNFRSF11B protein, human; D002097:C-Reactive Protein