Effect of long-term treatment with risedronate on arterial compliance in osteoporotic patients with cardiovascular risk factors.
Accumulating evidence suggests that osteoporosis and coronary artery disease have epidemiologic similarities. Moreover, the anti-atherogenic effects of bisphosphonates have been observed in vitro and in animal models. The present study investigated the effect of risedronate on indices of arterial compliance, serum osteoprotegerin (OPG) level, inflammatory and metabolic parameters in osteoporotic women with cardiovascular risk factors. In an open label, prospective study 68 postmenopausal osteoporotic women were evaluated for the study. Patients received risedronate orally in a dose of 35 mg per week, daily supplements of calcium and cholecalciferol during 6month treatment period. Patients were evaluated for lipid profile, HbA1C, insulin, C-peptide, fibrinogen, hs-CRP and plasma osreoprotegerin. Arterial elasticity was evaluated using pulse wave contour analysis (HDI CR 2000, Eagan, Minnesota). Large artery elasticity index (LAEI) increased from 9.86+/-3.66 to 11.54+/-">+/-3.16 ml/mm HgX10 (p<0.0001) during treatment period. Small artery elasticity index (SAEI) increased from 2.64+/-1.10 to 3.28+/-1.16 ml/mm HgX100 (p<0.0001). Systemic vascular resistance (SVR) decreased from 1876.12+/-457.72 to 1646.12+/-260.17 dyn/s/cm(- 5) (p<0.013). Metabolic parameters did not change during the treatment period. Plasma osteoprotegerin was significantly, positively correlated to SVR at baseline (r=0.36, p=0.045). At the final visit, OPG was marginally inversely associated with LAE (r=- 0.312, p=0.09), and significantly, positively associated with total vascular impedance (r=0.43, p=0.015). In conclusion, prolonged treatment with risedronate improved arterial elasticity of small and large arteries, and decreased SVR. These beneficial vascular effects were not related to changes in cardiovascular risk factors and may be attributed to direct effects of risedronate on the vascular wall.
Department of Internal Medicine, Holon, 58100, Israel.
A
A
Luckish
Department of Nephrology, Holon, 58100, Israel.
R
R
Cernes
Department of Epidemiology and Statistics, Holon, 58100, Israel.
M
M
Boaz
Department of Internal Medicine, Holon, 58100, Israel; The Brunner Institute for Cardiovascular Research, Holon, 58100, Israel; E. Wolfson Medical Center; and Sackler School of Medicine, Tel Aviv University, Israel.
D
D
Gavish
Department of Biochemistry, Holon, 58100, Israel.
Z
Z
Matas
Department of Biochemistry, Holon, 58100, Israel.
A
A
Fux
Endocrinology Unit, Holon, 58100, Israel; The Brunner Institute for Cardiovascular Research, Holon, 58100, Israel; E. Wolfson Medical Center; and Sackler School of Medicine, Tel Aviv University, Israel. Electronic address: marinas@wolfson.health.gov.il.
M
M
Shargorodsky
D000368:Aged; D001158:Arteries / Q000187:drug effects / Q000503:physiopathology*; D015415:Biomarkers / Q000378:metabolism; D050071:Bone Density Conservation Agents / Q000627:therapeutic use*; D002318:Cardiovascular Diseases / Q000150:complications*; D003187:Compliance / Q000187:drug effects; D003710:Demography; D004548:Elasticity / Q000187:drug effects; D012968:Etidronic Acid / Q000031:analogs & derivatives* / Q000627:therapeutic use; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D007249:Inflammation; D010024:Osteoporosis / Q000150:complications* / Q000188:drug therapy* / Q000503:physiopathology; D000068296:Risedronic Acid; D012307:Risk Factors; D013997:Time Factors
D015415:Biomarkers; D050071:Bone Density Conservation Agents; D000068296:Risedronic Acid; D012968:Etidronic Acid