title: Early atherosclerosis in systemic sclerosis and its relation to disease or traditional risk factors.
abstract: BACKGROUND
  Several systemic autoimmune diseases are associated with an increased prevalence of atherosclerosis which could not be explained by traditional risk factors alone. In systemic sclerosis (SSc), microvascular abnormalities are well recognized. Previous studies have suggested an increased prevalence of macrovascular disease as well. We compared patients with SSc to healthy controls for signs of early atherosclerosis by measuring intima-media thickness (IMT) of the common carotid artery in relation to traditional risk factors and markers of endothelial activation.
  
  
  METHODS
  Forty-nine patients with SSc, of whom 92% had limited cutaneous SSc, and 32 healthy controls were studied. Common carotid IMT was measured by using B-mode ultrasound. Traditional risk factors for cardiovascular disease were assessed and serum markers for endothelial activation were measured.
  
  
  RESULTS
  In patients with SSc, the mean IMT (median 0.69 mm, interquartile range [IQR] 0.62 to 0.79 mm) was not significantly increased compared with healthy controls (0.68 mm, IQR 0.56 to 0.75 mm; P = 0.067). Also, after correction for the confounders age, high-density lipoprotein (HDL) cholesterol, and low-density lipoprotein cholesterol (P = 0.328) or using a different model taking into account the confounders age, HDL cholesterol, and history of macrovascular disease (P = 0.474), no difference in IMT was present between SSc patients and healthy controls. Plaques were found in three patients and not in healthy controls (P = 0.274). In patients, no correlations were found between maximum IMT, disease-related variables, and markers of endothelial activation. Endothelial activation markers were not increased in SSc patients compared with controls.
  
  
  CONCLUSIONS
  SSc is not associated with an increased prevalence of early signs of atherosclerosis.
authors.affiliation: Department of Internal Medicine, Division of Rheumatology and Clinical Immunology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, PO Box 30,001, 9700 RB Groningen, The Netherlands. m.e.hettema@int.umcg.nl
authors.forename: Martha E
authors.initials: ME
authors.lastname: Hettema
authors.forename: Dan
authors.initials: D
authors.lastname: Zhang
authors.forename: Karina
authors.initials: K
authors.lastname: de Leeuw
authors.forename: Ymkje
authors.initials: Y
authors.lastname: Stienstra
authors.forename: Andries J
authors.initials: AJ
authors.lastname: Smit
authors.forename: Cees G M
authors.initials: CG
authors.lastname: Kallenberg
authors.forename: Hendrika
authors.initials: H
authors.lastname: Bootsma
mesh_terms: D050197:Atherosclerosis / Q000150:complications* / Q000453:epidemiology*; D002340:Carotid Artery Diseases / Q000150:complications / Q000453:epidemiology; D017536:Carotid Artery, Common / Q000473:pathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D012307:Risk Factors; D012595:Scleroderma, Systemic / Q000150:complications*; D018180:Thrombomodulin / Q000378:metabolism; D017539:Tunica Intima / Q000473:pathology*; D017540:Tunica Media / Q000473:pathology*; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D018180:Thrombomodulin; D019010:Vascular Cell Adhesion Molecule-1; D014841:von Willebrand Factor