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Published on: May 31, 2016
Aortic and coronary calcifications in Takayasu arteritis
Emire Seyahi1, Ayca Ucgul, Deniz Cebi Olgun
1Division of Rheumatology, Department of Medicine, Cerrahpasa Medical Faculty, University of Istanbul, Istanbul, Turkey. eseyahi@yahoo.com
Insights
Takayasu arteritis (TAK) and SLE show increased atherosclerosis. Arterial calcification in TAK, particularly in the thoracic aorta, suggests local inflammation, while coronary calcification may indicate systemic effects.
Area of Science:
- Cardiovascular Medicine
- Rheumatology
- Vascular Biology
Background:
- Atherosclerosis is common in Takayasu arteritis (TAK), often localized to inflamed arterial segments.
- Arterial wall calcification patterns may differentiate systemic from local inflammation in TAK.
Purpose of the Study:
- To investigate arterial wall calcification in TAK patients compared to SLE patients and healthy controls.
- To determine if coronary artery calcification reflects systemic inflammation and thoracic aorta calcification reflects local inflammation in TAK.
Main Methods:
- Multi-detector computed tomography (MDCT) assessed coronary artery and thoracic aorta calcifications (ToAC) in 47 TAK, 43 SLE, and 70 healthy controls.
- B-mode ultrasound screened for atherosclerotic plaques in carotid arteries.
Main Results:
- Coronary artery calcification was increased in SLE but not significantly in TAK compared to controls.
- TAK patients showed significantly more ToAC (45%) than SLE patients (23%).
- Circumferential calcification was common in TAK (67%), unlike SLE and controls. Atherosclerotic plaques and calcifications in TAK often occurred at sites of vasculitis.
Conclusions:
- Both TAK and SLE exhibit increased atherosclerosis.
- Vessel wall inflammation plays a significant role in TAK-associated atherosclerosis.
Objectives:
Atherosclerosis is well recognized in Takayasu arteritis (TAK) and the associated plaques tend to be more common in areas of arteritis. We now report arterial wall calcification in a large group of TAK patients and controls. We hypothesized that the degree of coronary artery calcification would point to a systemic effect of inflammation while that in the thoracic aorta more of local inflammation.
Methods:
A total of 47 patients with TAK, 43 patients with SLE and 70 healthy controls (HC) were studied. The presence of coronary artery and thoracic aorta calcifications (ToAC) was investigated by multi-detector computed tomography (MDCT). Atherosclerotic plaques in the carotid arteries were screened using B mode ultrasound.
Results:
The frequency of coronary artery calcification was significantly increased among patients with SLE as compared to the healthy controls while the increase in TAK did not reach statistical significance. There were more TAK patients with ToAC among the TAK as compared to the SLE patients [21/47 (45%) vs 10/43 (23%), P = 0.033]. In addition, a circumferential type of calcification, vs a punctuate or linear type, was the more common type in 67% of patients with TAK whereas only the linear or punctuate type was seen in SLE patients and HC. SLE and TAK patients were found to have increased risk for carotid artery plaques. Among TAK patients, coronary artery calcification, ToAC and carotid artery plaques tend to be at sites of primary vasculitic involvement.
Conclusions:
There is increased atherosclerosis in TAK and SLE. Vessel wall inflammation seems to be also important in the atherosclerosis associated with TAK.
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