Abstract 10346: Relationship Between Markers of Bone Remodeling and Coronary Calcification
Background: Vascular calcification is an active process and increased osteoprotegerin (OPG) levels, a marker of bone turnover, have been described in cross-sectional studies of patients with coronary artery disease (CAD). We tested the hypothesis that progression of coronary artery calcification (CAC) is associated with changes in levels of OPG and its ligand, receptor activator of nuclear kappa- B (RANKL).
Methods: Women on the Move through Activity and Nutrition (WOMAN) was a prospective, randomized, clinical trial that studied the effects of intensive lifestyle change versus health education on CAD risk factors in postmenopausal women without known CAD. We measured serum OPG and RANKL levels at baseline and 48 months by ELISA on 86 women in the health education arm and determined the correlation with progression of CAC measured by EBCT.
Results: Mean age of study participants was 57±3 years. Largest change in CAC from baseline to 48 months was seen in those with highest levels of OPG (table). There was no correlation between use of hormone replacement therapy and OPG levels (p=0.7). No correlation was observed between RANKL levels and CAC progression. RANKL/OPG ratios were categorized as tertiles and log-transformed and showed a similar relationship to CAC: 20% of patients in the lowest tertile of RANKL/OPG had progression to CAC>100 vs 9% in the highest tertile (p<0.001). Among other atherosclerosis risk factors, higher frequency of antihypertensive medication use was noted in patients with the highest tertile of OPG levels. C-reactive protein, LDL particle size and interleukin-1a levels correlated with higher OPG levels and lower RANKL/OPG ratios (p=0.005). Table 1: Relationship between progression of CAC and OPG levels
Conclusions: Serum OPG levels correlate significantly with progression of coronary atherosclerosis. High serum OPG levels may represent a proinflammatory milieu leading to further plaque development.
- © 2010 by American Heart Association, Inc.