Prevalence and prognostic factors for aortic dilatation in giant cell arteritis - a longitudinal study.

OBJECTIVES: Predictive data for the development of aortic dilatation (AD) in giant-cell arteritis (GCA) are controversial. The aim was to investigate by computed tomography (CT) the prevalence of AD in a consecutive cohort of GCA patients and controls, and to identify possible predictors for AD. METHODS: GCA patients and controls were identified by electronic search and underwent aortic contrast enhanced CT defining AD by aortic diameter adjusted to age, gender and body surface area. Pulse-wave velocity, intima-media thickness (IMT) and laboratory studies including lymphocyte subsets were conducted identifying potential factors associated with AD. Clinical and laboratory parameters at disease onset, occurrence of aortic rupture/dissection before and up to five years after study visit were retrieved by chart review. RESULTS: 144 GCA patients and 115 controls were included. GCA patients developed more frequently AD of the ascending and thoracic descending aorta compared to controls (OR 2.60, p = 0.016; OR 3.65, p = 0.005, respectively). Factors associated with AD development of thoracic descending aorta, but not of the ascending aorta, were higher percentages of circulating CD3+CD4+ cells, higher CD4/CD8 ratio, presence of polymyalgia rheumatica and increased carotid IMT at disease onset (OR range 1.10-3.11, all with p < 0.05). During follow-up, no GCA patient required surgical aortic repair or suffered aortic rupture/dissection. CONCLUSIONS: Thoracic but not abdominal ADs occur more commonly in GCA patients, however, the subsequent risk for aortic repair, rupture or dissection is low. Changes of T-cell subsets, presence of polymyalgia rheumatica and increased carotid IMT at disease onset are associated with AD development.

Endothelial dysfunction and brachial intima-media thickness: long term cardiovascular risk with claudication related to peripheral arterial disease: a prospective analysis.

OBJECTIVE: Endothelial dysfunction plays a key role in the development, progression, and clinical manifestation of atherosclerosis, and in symptomatic peripheral arterial disease, endothelial dysfunction and enlarged intima-media thickness might be associated with increased cardiovascular risk. Flow-mediated dilatation and serologic parameters are used to evaluate individual endothelial function. Brachial intima-media thickness, a less recognized parameter of cardiovascular risk, is independently associated with coronary artery disease. The aim of this study was to evaluate the prognostic value of ultrasound and serologic parameters of endothelial function in relation to cardiovascular mortality in peripheral arterial disease. DESIGN: monocentric, prospective cohort study. METHODS: Flow mediated dilatation and brachial intima-media thickness were assessed in 184 (124 male) patients with peripheral arterial disease (Rutherford stages 2-3). Serologic parameters of endothelial function included asymmetric dimethylarginine (ADMA), symmetric dimethylarginine (SDMA), and L-homoarginine. Cardiovascular events were recorded during a follow-up of 99.1±11.1 months. Subjects who died of noncardiovascular causes were excluded from further analysis. RESULTS: Eighty-two patients (44.6%) died during follow-up after a mean duration of 49.7±28.3 months. There were 49 cardiovascular deaths (59.8%) and 33 other deaths (40.2%). Flow mediated dilatation was associated with cardiovascular death [1.17% (0.0, 4.3) vs. 4.1% (1.2, 6.4), p<0.001]. Intima-media thickness was greater in patients who succumbed to cardiovascular disease [0.37 mm (0.30, 0.41)] than in survivors [0.21 mm (0.15, 0.38), p<0.001]. Brachial intima-media thickness above 0.345 mm was most predictive of cardiovascular death, with sensitivity and specificity values of 0.714 and 0.657, respectively (p<0.001). Furthermore, ADMA levels above 0.745 µmol/l and SDMA levels above 0.825 µmol/l were significantly associated with cardiovascular death (p<0.001 and 0.030). CONCLUSION: In symptomatic peripheral arterial disease, decreased flow mediated dilatation, enlarged intima-media thickness, and elevated levels of ADMA and SDMA were associated with increased cardiovascular risk.

Endothelial function and carotid intima-media thickness in giant-cell arteritis.

BACKGROUND: Vascular endothelial dysfunction and intima-media thickness are characteristic aspects of several vasculitides. We investigated retrospectively the impact of steroid treatment on endothelial dysfunction and intima-media thickness in giant-cell arteritis. METHODS: Forty-one patients with giant-cell arteritis (28 female and 13 male) underwent flow-mediated dilatation, a marker of endothelial function, and carotid intima-media thickness within 24 h after diagnosis and 6 months thereafter. Both parameters were investigated in 41 patients of an age- and gender-matched control group. RESULTS: Brachial flow-mediated dilatation response at baseline was 3.4% (0.2, 8.0) and 1.7% (0.2, 4.8) in giant-cell arteritis patients and control group, respectively. After 6 months treatment, flow-mediated dilatation response was 2.8% (0.4, 4.8) in patients with giant-cell arteritis (P = 0.066) and 1.4% (0.1, 5.5) in the control group (P = 0.741). In contrast, mean carotid intima-media thickness of giant-cell arteritis patients improved significantly between baseline [1.0 mm (0.79, 1.2)] and 6-month follow-up [0.82 mm (0.7, 1.04), P < 0.001]. Subjects with additional symptoms of polymyalgia rheumatica had a notable enlargement of carotid intima-media thickness [1.23 mm (1.14, 2.09)] compared to giant-cell arteritis patients without polymyalgia rheumatica at baseline [0.91 mm (0.76, 1.04), P = 0.001] and 6-month follow-up [1.16 mm (0.80, 1.26) vs. 0.77 mm (0.68, 0.88), P = 0.009]. CONCLUSION: Steroid therapy has no influence on endothelial function but does significantly improve carotid intima-media thickness in giant-cell arteritis. This divergence of endothelial function and intima-media thickness reflects the specifity of giant-cell arteritis for cerebrovascular arteries thereby sparing the brachial arteries.