Thoracic aortic dilation more common in patients with giant cell arteritis
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Thoracic aortic dilation is more common among patients with giant cell arteritis, but the subsequent risk for aortic repair, rupture or dissection is low, according to data published in Seminars in Arthritis and Rheumatism.
“While the 1990 ACR classification criteria have emphasized the importance of cranial arteries, newer imaging studies indicate that extracranial large arteries, and particularly the aorta, are frequently involved,” Philipp Jud, MD, of the Medical University of Graz, in Austria, and colleagues wrote. “Indeed, GCA patients have been reported to be at an increased risk for the development of aortic damage including aortic dilatation (AD), aortic aneurysms (AA), aortic rupture and/or dissection.”
“Furthermore, GCA patients with AA have a higher mortality compared to GCA patients without AA and the general population,” they added. “Previous data are controversial concerning the incidence of AA in GCA patients ranging from 3.2 to 30.5/1,000 person-years, which is mainly caused by the different populations studied and divergent methods applied to detect AA. Another unresolved question is which biomarkers best correlate with AD in GCA.”
To analyze the prevalence of aortic dilation among patients with giant cell arteritis, and identify its possible predictors, Jud and colleagues identified and recruited 144 individuals diagnosed between 1993 and 2010 at the Medical University of Graz and the rheumatology outpatient clinic of the Styrian State hospital Muerzzuschlag. An additional 115 participants without giant cell arteritis were enrolled as a control group. All participants underwent aortic contrast enhanced computed tomography. Aortic dilation was defined based on aortic diameter adjusted to age, gender and body surface area.
In addition, the researchers performed pulse-wave velocity, intima-media thickness and laboratory studies that included lymphocyte subsets to identify potential factors associated with aortic dilation. Clinical and laboratory parameters at disease onset, and the occurrence of aortic rupture or dissection prior to, and up to 5 years after, study visit, were accessed through chart review.
According to the researchers, patients with giant cell arteritis more frequently demonstrated aortic dilation of the ascending aorta (OR = 2.6; P = .016) and the thoracic descending aorta (OR = 3.65; P = .005), compared with the control group. Factors associated with aortic dilation of the thoracic descending aorta, but not of the ascending aorta, were higher percentages of circulating CD3+CD4+ cells, a higher CD4-CD8 ratio, the presence of polymyalgia rheumatica, and increased carotid intima-media thickness at disease onset (OR range = 1.1-3.11; P < .05).
No patients with giant cell arteritis required surgical aortic repair, or suffered aortic rupture or dissection, during the follow-up period.
“GCA is associated with a higher risk of dilatation of the thoracic aorta, especially if AD is defined according to values adjusted for age, gender and BSA, and selected lymphocyte subsets as well as initial present PMR are independent predictors for AD development,” Jud and colleagues wrote. “Different aortic regions may be variably susceptible for AD and initial vascular injury. Further studies are needed to elucidate underlying mechanisms of the development of AD in GCA, especially the role of lymphocyte subsets needs to be proven in non-disease controls.”
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