Subclinical left ventricular dysfunction in childhood-onset systemic lupus erythematosus: a two-dimensional speckle-tracking echocardiographic study

Carregando...
Imagem de Miniatura
Citações na Scopus
18
Tipo de produção
article
Data de publicação
2016
Título da Revista
ISSN da Revista
Título do Volume
Editora
TAYLOR & FRANCIS LTD
Citação
SCANDINAVIAN JOURNAL OF RHEUMATOLOGY, v.45, n.3, p.202-209, 2016
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Objectives: The main purpose of the study was to investigate left ventricular (LV) subclinical systolic and diastolic dysfunction in childhood-onset systemic lupus erythematosus (c-SLE) patients using two-dimensional speckle-tracking (2DST) echocardiography. We also interrogated possible correlations between impairment of myocardial deformation and the SLE Disease Activity Index 2000 (SLEDAI-2K), as well as the presence of traditional and disease-related cardiovascular risk factors (CRFs).Method: A total of 50 asymptomatic patients and 50 controls (age 14.74 vs. 14.82years, p=0.83) were evaluated by standard and 2DST echocardiography.Results: Despite a normal ejection fraction (EF), there was reduction in all parameters of LV longitudinal and radial deformation in patients compared to controls: peak longitudinal systolic strain (PLSS) [-20.3 (-11 to -26) vs. -22 (-17.8 to -30.4)%, p<0.0001], PLSS rate [-1.190.21 vs. -1.3 +/- 0.25s(-1), p=0.0005], longitudinal strain rate in early diastole [1.7 (0.99-2.95) vs. 2 (1.08-3.00) s(-1), p=0.0034], peak radial systolic strain [33.09 +/- 8.6 vs. 44.36 +/- 8.72%, p<0.0001], peak radial systolic strain rate [1.98 +/- 0.53 vs. 2.49 +/- 0.68s(-1), p<0.0001], and radial strain rate in early diastole [-2.31 +/- 0.88 vs. -2.75 +/- 0.97s(-1), p=0.02]. Peak circumferential systolic strain [-23.67 +/- 3.46 vs. -24.6 +/- 2.86%, p=0.43] and circumferential strain in early diastole [0.37 +/- 0.17 vs. 0.41 +/- 0.15, p=0.27] were similar between patients and controls, although peak circumferential systolic strain rate [-1.5 +/- 0.3 vs. -1.6 +/- 0.3s(-1), p=0.036] was reduced in c-SLE. Further analysis of patients revealed a negative correlation between LV PLSS and SLEDAI-2K (r= -0.52, p<0.0001), and also between LV PLSS and the number of CRFs per patient (r= -0.32, p=0.024).Conclusions: 2DST echocardiography has identified subclinical LV deformation impairment in c-SLE patients. Disease activity and cumulative exposure to CRFs contribute to myocardial compromise.
Palavras-chave
Referências
  1. Dokainish H, 2008, AM J CARDIOL, V101, P1504, DOI 10.1016/j.amjcard.2008.01.037
  2. Harambat J, 2012, PEDIATR NEPHROL, V27, P363, DOI 10.1007/s00467-011-1939-1
  3. Sozeri B, 2013, PEDIATR NEPHROL, V28, P471, DOI 10.1007/s00467-012-2342-2
  4. Pons-Estel GJ, 2009, RHEUMATOLOGY, V48, P817, DOI 10.1093/rheumatology/kep102
  5. Jain D, 2009, J CLIN PATHOL, V62, P584, DOI 10.1136/jcp.2009.064311
  6. Silva CA, 2012, ARTHRIT CARE RES, V64, P1787, DOI 10.1002/acr.21757
  7. Hochberg MC, 1997, ARTHRITIS RHEUM, V40, P1725, DOI 10.1002/art.1780400928
  8. Tucker LB, 2008, LUPUS, V17, P314, DOI 10.1177/0961203307087875
  9. Daniels SR, 2008, PEDIATRICS, V122, P198, DOI 10.1542/peds.2008-1349
  10. Eidem BW, 2004, J AM SOC ECHOCARDIOG, V17, P212, DOI 10.1067/j.echo.2003.12.005
  11. Boros CA, 2011, CLIN EXP RHEUMATOL, V29, P575
  12. Khoury PR, 2009, J AM SOC ECHOCARDIOG, V22, P709, DOI 10.1016/j.echo.2009.03.003
  13. HAYCOCK GB, 1978, J PEDIATR-US, V93, P62, DOI 10.1016/S0022-3476(78)80601-5
  14. Gladman D, 1996, ARTHRITIS RHEUM, V39, P363, DOI 10.1002/art.1780390303
  15. Knight JS, 2013, CURR OPIN RHEUMATOL, V25, P597, DOI 10.1097/BOR.0b013e328363eba3
  16. Canpolat N, 2013, PEDIATR NEPHROL, V28, P305, DOI 10.1007/s00467-012-2317-3
  17. Magder LS, 2012, AM J EPIDEMIOL, V176, P708, DOI 10.1093/aje/kws130
  18. Pieretti J, 2007, CIRCULATION, V116, P419, DOI 10.1161/CIRCULATIONAHA.106.673319
  19. Lopez L, 2010, J AM SOC ECHOCARDIOG, V23, P465, DOI 10.1016/j.echo.2010.03.019
  20. Mor-Avi V, 2011, EUR J ECHOCARDIOGR, V12, P167, DOI 10.1093/ejechocard/jer021
  21. Nagueh SF, 2009, EUR J ECHOCARDIOGR, V10, P165, DOI 10.1093/ejechocard/jep007
  22. Barbosa JAA, 2013, EUR HEART J-CARD IMG, V14, P882, DOI 10.1093/ehjci/jes294
  23. Ardoin SP, 2010, LUPUS, V19, P1315, DOI 10.1177/0961203310373937
  24. Gidding SS, 2013, CIRC-CARDIOVASC IMAG, V6, P769, DOI 10.1161/CIRCIMAGING.112.000450
  25. Kavey REW, 2006, CIRCULATION, V114, P2710, DOI 10.1161/CIRCULATIONAHA.106.179568
  26. Wislowska M, 2009, RHEUMATOL INT, V29, P1469, DOI 10.1007/s00296-009-0889-4
  27. Ardoin SP, 2014, ANN RHEUM DIS, V73, P557, DOI 10.1136/annrheumdis-2012-202315
  28. Geyer H, 2010, J AM SOC ECHOCARDIOG, V23, P351, DOI 10.1016/j.echo.2010.02.015
  29. Gazarian M, 1998, J PEDIATR-US, V132, P109, DOI 10.1016/S0022-3476(98)70494-9
  30. Buss SJ, 2010, J RHEUMATOL, V37, P79, DOI 10.3899/jrheum.090043
  31. Gladman DD, 2002, J RHEUMATOL, V29, P288
  32. Bussadori C, 2009, CARDIOVASC ULTRASOUN, V7, DOI 10.1186/1476-7120-7-8
  33. Huang BT, 2014, ECHOCARDIOGR-J CARD, V31, P1085, DOI 10.1111/echo.12515
  34. LEVY D, 1990, NEW ENGL J MED, V322, P1561, DOI 10.1056/NEJM199005313222203
  35. Mavrogeni Sophie, 2015, Inflamm Allergy Drug Targets, V13, P371
  36. Russo C, 2014, EUR J HEART FAIL, V16, P1301, DOI 10.1002/ejhf.154
  37. Sinicato Nailú Angélica, 2013, Curr Cardiol Rev, V9, P15
  38. Skamra C, 2010, INT J CLIN RHEUMATOL, V5, P75, DOI 10.2217/ijr.09.73