Abstract-In the present study, we examined the expression of regulators of bone formation and osteoclastogenesis in human atherosclerosis because accumulating evidence suggests that atherosclerotic calcification shares features with bone calcification. The most striking finding of this study was the constitutive immunoreactivity of matrix Gla protein, osteocalcin, and bone sialoprotein in nondiseased aortas and the absence of bone morphogenetic protein (BMP)-2, BMP-4, osteopontin, and osteonectin in nondiseased aortas and early atherosclerotic lesions. When atherosclerotic plaques demonstrated calcification or bone formation, BMP-2, BMP-4, osteopontin, and osteonectin were upregulated. Interestingly, this upregulation was associated with a sustained immunoreactivity of matrix Gla protein, osteocalcin, and bone sialoprotein. The 2 modulators of osteoclastogenesis (osteoprotegerin [OPG] and its ligand, OPGL) were present in the nondiseased vessel wall and in early atherosclerotic lesions. In advanced calcified lesions, OPG was present in bone structures, whereas OPGL was only present in the extracellular matrix surrounding calcium deposits. The observed expression patterns suggest a tight regulation of the expression of bone matrix regulatory proteins during human atherogenesis. The expression pattern of both OPG and OPGL during atherogenesis might suggest a regulatory role of these proteins not only in osteoclastogenesis but also in atherosclerotic calcification. (Arterioscler Thromb Vasc Biol.

Moving-bed infusion-tracking MR angiography can be used to image all peripheral arteries in 4 minutes by using a small amount of contrast material and a conventional 1.5-T MR imager.

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Background— Abdominal aortic aneurysms (AAA) are characterized by extensive transmural inflammation and C-reactive protein (CRP) has emerged as an independent risk factor for the development of cardiovascular disease. Therefore, we evaluated a possible association between serum CRP and aneurysm dimension in patients with asymptomatic AAA. Furthermore, the possibility of CRP production by aneurysmal tissue has been examined. Methods and Results— Serum CRP was determined highly sensitive ( hs CRP) and aneurysmal size was measured in 39 patients with AAA. The presence of CRP mRNA was assessed in the aneurysmal tissue of 16 patients. Mean (SD) hs CRP was 3.23 (2.96) mg/L. After log-transformation, hs CRP correlated significantly with aneurysmal size ( r =0.477, P =0.002). When the patients were divided into 3 equally sized groups according to hs CRP level, aortic diameter increased from lowest to upper hs CRP-tertile (49 mm, 61 mm, and 67 mm, respectively; P <0.05 for 3rd versus 1st tertile). This association persisted after correction for risk factors. CRP mRNA was found in 25% of aneurysmal aortic tissues. Conclusions— This is the first report showing that serum hs CRP is associated with aneurysmal size and that—in at least some patients—CRP may be produced by aneurysmal tissue. These data underscore the inflammatory nature of AAA formation, suggesting that serum hs CRP may serve as a marker of AAA disease and that CRP produced in vascular tissue might contribute to aneurysm formation.

These observations suggest that the reduction in mean wall shear stress with age results from the concomitant increase in diameter in an attempt of the arterial system to limit the reduction in storage capacity of the arterial system with increasing age.