title: Long-term evaluation of cardiac function in juvenile idiopathic arthritis under anti-TNF therapy.
abstract: OBJECTIVE
  This paper aims to perform global assessment of long-term cardiac function in juvenile idiopathic arthritis (JIA) patients under TNF blockage therapy.
  
  
  METHODS
  Twenty-five polyarticular-course JIA patients pre-anti-TNF and 22 healthy controls underwent conventional/tissue Doppler echocardiography and cardiac biomarkers measurements (N-terminal pro-brain natriuretic peptide [NT-pro-BNP] and troponin T) at baseline (BL). Twenty-one JIA patients completed six evaluations during two consecutive years. Clinical/laboratorial evaluations were assessed before and during TNF blockage therapy.
  
  
  RESULTS
  JIA patients and controls were comparable regarding current age (p=0.898) and female gender (p=0.38). At BL isovolumetric relaxation time of left ventricle (p=0.03), ventricular septum (VS), E' wave (p=0.014) and VS S wave velocity (p=0.03) were significantly reduced in JIA patients compared to controls. Frequencies of elevated NT-pro-BNP and troponin T levels were similar in JIA and controls (p=0.297 and p=0.756) and levels remained within normal range throughout the study, except for one patient with mild troponin T elevation. During TNF blockage therapy, none of the 21 participants had heart failure, ejection fraction or other parameters alterations in conventional and tissue Doppler. Only one had mild pulmonary hypertension. Further analysis revealed that JIA patients with elevated levels of NT-pro-BNP at BL had significantly more active joints (p=0.025) and higher ESR (p=0.034).
  
  
  CONCLUSIONS
  Long-term TNF blockage safety was demonstrated in JIA patients in spite of the observed subclinical diastolic involvement. Elevated cardiac biomarker in these patients was associated with inflammatory parameters reinforcing the need for a careful interpretation of this finding in patients with active disease.
authors.affiliation: Radiology Unit, Faculdade de Medicina da Universidade de Sao Paulo, Brazil. ac.lianza@me.com.
authors.forename: Alessandro C
authors.initials: AC
authors.lastname: Lianza
authors.forename: Nadia E
authors.initials: NE
authors.lastname: Aikawa
authors.forename: Julio C B
authors.initials: JC
authors.lastname: Moraes
authors.forename: Gabriela N
authors.initials: GN
authors.lastname: Leal
authors.forename: Samira S
authors.initials: SS
authors.lastname: Morhy
authors.forename: Jose L
authors.initials: JL
authors.lastname: Andrade
authors.forename: Eloisa
authors.initials: E
authors.lastname: Bonfa
authors.forename: Clovis A
authors.initials: CA
authors.lastname: Silva
mesh_terms: D000293:Adolescent; D000893:Anti-Inflammatory Agents / Q000009:adverse effects / Q000627:therapeutic use*; D001171:Arthritis, Juvenile / Q000150:complications / Q000175:diagnosis / Q000188:drug therapy* / Q000276:immunology; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D015150:Echocardiography, Doppler; D005260:Female; D006331:Heart Diseases / Q000097:blood / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology; D006801:Humans; D008297:Male; D020097:Natriuretic Peptide, Brain / Q000097:blood; D010446:Peptide Fragments / Q000097:blood; D011446:Prospective Studies; D012307:Risk Factors; D013997:Time Factors; D016896:Treatment Outcome; D020107:Troponin T / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000378:metabolism; D016277:Ventricular Function, Left / Q000187:drug effects
chemical_list: D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D010446:Peptide Fragments; D020107:Troponin T; D014409:Tumor Necrosis Factor-alpha; C109794:pro-brain natriuretic peptide (1-76); D020097:Natriuretic Peptide, Brain