title: Impaired coronary microvascular function and increased intima-media thickness in rheumatoid arthritis.
abstract: BACKGROUND
  Rheumatoid arthritis (RA) is associated with excessive cardiovascular mortality. Recently, some studies have shown endothelial dysfunction in RA patients with high inflammatory activity. In addition, it has been suggested that the chronic inflammatory state of RA contributes to accelerated atherosclerosis. Therefore, we aimed to evaluate whether coronary microvascular dysfunction and increased carotid artery intima-media thickness exist in patients with a long history and well controlled disease activity of RA lacking traditional cardiovascular risk factors.
  
  
  METHODS
  Thirty RA patients (22 women; mean age 43.7+/-9.0) and 52 healthy volunteers (38 women; mean age 45.3+/-5.4) were included into the study. Using transthoracic echocardiography, each subject underwent echocardiographic examination including coronary flow reserve (CFR) and carotid intima-media thickness (IMT) measurement.
  
  
  RESULTS
  CFR values were statistically reduced for RA patients as compared to controls (2.4+/-0.5 vs. 2.7+/-0.4, P=0.002) whereas IMT values were significantly increased (0.6+/-0.1 vs. 0.5+/-0.1, P=0.001). In RA patients, CFR positively correlated with lateral Em/Am ratio (r=0.399, P=0.029), and negatively correlated with lateral isovolumic relaxation time (IVRT) (r=-0.744, P=0.005), IMT (r=-0.542, P=0.002) and RA disease duration (r=-0.495, P=0.005). Reflecting LV diastolic function, mitral E-wave deceleration time and isovolumic relaxation time were borderline significant between the groups, however lateral Em/Am ratio and lateral IVRT were statistically different.
  
  
  CONCLUSIONS
  Patients with RA had impaired CFR and increased carotid IMT, and these injurious effects correlated significantly with disease duration.
authors.affiliation: Baskent University Medicine Faculty Cardiology, Ankara, Turkey. ozgurciftci@baskent-kon.edu.tr
authors.forename: Ozgur
authors.initials: O
authors.lastname: Ciftci
authors.forename: Sema
authors.initials: S
authors.lastname: Yilmaz
authors.forename: Semra
authors.initials: S
authors.lastname: Topcu
authors.forename: Mustafa
authors.initials: M
authors.lastname: Caliskan
authors.forename: Hakan
authors.initials: H
authors.lastname: Gullu
authors.forename: Dogan
authors.initials: D
authors.lastname: Erdogan
authors.forename: Baris O
authors.initials: BO
authors.lastname: Pamuk
authors.forename: Aylin
authors.initials: A
authors.lastname: Yildirir
authors.forename: Haldun
authors.initials: H
authors.lastname: Muderrisoglu
mesh_terms: D000328:Adult; D001172:Arthritis, Rheumatoid / Q000150:complications / Q000473:pathology* / Q000503:physiopathology*; D002196:Capillaries / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D002339:Carotid Arteries / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology*; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology*; D003971:Diastole; D015150:Echocardiography, Doppler; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D017539:Tunica Intima / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D017540:Tunica Media / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000473:pathology / Q000503:physiopathology