Abdominal aortic calcification: A reappraisal of epidemiological and pathophysiological data

- Semiquantitative assessment of abdominal aortic calcification (AAC) on X-rays and DXA scans is rapid, easy, and inexpensive.
- Severe AAC is associated with increased cardiovascular morbidity and mortality and higher risk of fragility fracture.
- Many factors (lifestyle, health status, hormones, cytokines, matrix vesicles) determine initiation and progression of AAC.
- Osteoblastic differentiation of vascular smooth muscle cells and circulating osteoprogenitors is essential for AAC formation.

In men and women, there is a significant association between the risk of cardiovascular event (myocardial infarction, stroke) and risk of major fragility fracture (hip, vertebra). Abdominal aortic calcification (AAC) can be assessed using semiquantitative scores on spine radiographs and spine scans obtained by DXA. Severe AAC is associated with higher risk of major cardiovascular event. Not only does severe AAC reflect poor cardiovascular health status, but also directly disturbs blood flow in the vascular system. Severe (but not mild or moderate) AAC is associated with lower bone mineral density (BMD), faster bone loss and higher risk of major fragility fracture. The fracture risk remains increased after adjustment for BMD and other potential risk factors. The association between severe AAC and fracture risk was found in both sexes, mainly in the follow-ups of less than 10 years.Many factors contribute to initiation and progression of AAC: lifestyle, co-morbidities, inorganic ions, dyslipidemia, hormones, cytokines (e.g. inflammatory cytokines, RANKL), matrix vesicles, microRNAs, structural proteins (e.g. elastin), vitamin K-dependent proteins, and medications (e.g. vitamin K antagonists). Osteogenic transdifferentiation of vascular smooth muscle cells (VSMC) and circulating osteoprogenitors penetrating into vascular wall plays a major role in the AAC initiation and progression. Vitamin K-dependent proteins protect vascular tunica media against formation of calcified deposits (matrix GLA protein, GLA-rich protein) and against VSMC apoptosis (Gas6).Further studies are needed to investigate clinical utility of AAC for the assessment of fracture and cardiovascular risk at the individual level and develop new medications permitting to prevent AAC progression.