P4.35 LARGE ARTERY DYSFUNCTION DOES NOT EXPLAIN OSTEOARTHRITIC BONE MARROW LESIONS
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- 10.1016/j.artres.2012.09.182How to use a DOI?
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Background: The pathogenesis of osteoarthritis (OA) has been linked to microvascular abnormalities. Since this is preceded by large artery dysfunction, there remains the possibility that adverse large artery function could play a role in OA. This study aimed to determine the relationship between central haemodynamic indices of large artery function and bone marrow lesions (BMLs) in patients with OA.
Methods: Study sample included 207 participants with OA (63 ± 7 years; 48% male) who underwent magnetic resonance imaging of their dominant leg for determination of tibia and femoral BMLs. Large artery haemodynamics were assessed by aortic stiffness (pulse wave velocity) and central blood pressure (including augmentation index) by radial tonometry. Brachial blood pressure was recorded by automated oscillometric device.
Results: BMLs were present in 145 participants. There was no significant difference between participants with and without BMLs for aortic stiffness (9.3 ± 2.3 vs 9.0 ± 2.3 m/s; P=0.49), central pulse pressure (43 ± 11 vs 43 ± 12 mmHg; P=0.89), augmentation index (25 ± 10 vs 26 ± 9 %; P=0.46) or brachial pulse pressure (56 ± 12 vs 55 ± 12 mmHg; P=0.65). Similarly, there were no significant relationships between BML size and any central or brachial haemodynamic measure (P>0.05 for all).
Conclusions: BMLs in patients with OA are not related to central or peripheral large artery haemodynamics. This suggests that although microvascular abnormalities may play a role in OA, there appears to be minimal contribution by large artery function.
Cite this article
TY - JOUR AU - G. Goldsmith AU - D. Dore AU - C. Ding AU - G. Jones AU - J. Sharman PY - 2012 DA - 2012/11/17 TI - P4.35 LARGE ARTERY DYSFUNCTION DOES NOT EXPLAIN OSTEOARTHRITIC BONE MARROW LESIONS JO - Artery Research SP - 193 EP - 193 VL - 6 IS - 4 SN - 1876-4401 UR - https://doi.org/10.1016/j.artres.2012.09.182 DO - 10.1016/j.artres.2012.09.182 ID - Goldsmith2012 ER -