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Calcification is a common feature of abdominal aortic aneurysm (AAA), but its role in the pathogenesis of the disease remains incompletely understood. While heavy arterial macrocalcification is thought be a marker of disease stability, earlier stages in osteogenic remodelling of AAAs marked by microcalcification represent active disease associated with a healing response to inflammation and carry a greater risk of aneurysm expansion. Whether tracking changes in calcification using 18F-sodium fluoride (NaF) positron emission tomography (PET) after therapeutic intervention can improve risk stratification in AAA is the thought-provoking topic of the proof-of-concept study by Debono et al published in Heart (figure 1).1
AAA is a potentially life-threatening condition caused by medial degeneration with smooth muscle cell death and degradation of collagen and elastin in the extracellular matrix. AAAs occur most often in older men who smoke tobacco, have hypertension or a family history of the disease. The prevalence of AAA is 1%–2% in men aged 65 years and 0.5% in women aged 70 years. While the risk of AAA rupture is directly related to size, growth is non-linear and difficult to predict. For AAAs ≥5.0 cm, rupture risk is 1.5% annually. This risk must be balanced against the 2%–10% risk of mortality following elective surgery for …
Contributors JMT and MMC wrote and edited the article.
Funding JMT is supported by a Wellcome Trust Clinical Research Career Development Fellowship (211100/Z/18/Z), the British Heart Foundation and the Cambridge BHF Centre for Research Excellence (18/1/34212). MMC is supported by an NIHR Clinical Lectureship.
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.