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Year : 2004  |  Volume : 50  |  Issue : 4  |  Page : 266-267

Cardiac function in juvenile rheumatoid arthritis


Division of Pediatric Cardiology, University of Texas-Houston Medical School, 6431 Fannin, MSB 3.130, Houston, TX 77030, USA

Correspondence Address:
Monesha Gupta
Division of Pediatric Cardiology, University of Texas-Houston Medical School, 6431 Fannin, MSB 3.130, Houston, TX 77030
USA
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Source of Support: None, Conflict of Interest: None


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How to cite this article:
Gupta M, Syamasundar Rao P. Cardiac function in juvenile rheumatoid arthritis . J Postgrad Med 2004;50:266-7

How to cite this URL:
Gupta M, Syamasundar Rao P. Cardiac function in juvenile rheumatoid arthritis . J Postgrad Med [serial online] 2004 [cited 2019 Nov 15];50:266-7. Available from: http://www.jpgmonline.com/text.asp?2004/50/4/266/13643


Cardiac dysfunction is seen with many of the collagen vascular diseases including systemic lupus erythematosis, rheumatoid arthritis (RA), dermatomyositis, and systemic sclerosis. Juvenile rheumatoid arthritis (JRA) is the most common rheumatic disease in childhood with a very variable course. The second major cause of mortality in this disease is from cardiac involvement.[1] This occurs in about 4.5% cases[2] and includes pericarditis, aortitis, coronary vasculitis, valvulitis (endocarditis), conduction system involvement, pulmonary hypertension and myocarditis.



Proinflammatory cytokines, in particular tumor necrosis factor (TNF- ) and interleukin 6 (IL-6) play an important role in this disease and may be responsible for the damage seen with arthritis, rash, fever and serositis. Therapy includes pain management and reduction of the inflammatory process. Non steroidal anti-inflammatory drugs (NSAID) including COX-1 and COX-2 inhibitors, corticosteroids, methotrexate, sulfasalazine and other disease-modifying anti-rheumatic drugs are used with varying success. Newer anti-cytokine agents such as leflunomide[3],[4] and etanercept[5],[6] have been found to be effective in reducing disease progression in adult rheumatoid arthritis.



In most cases of RA, the cardiac disease is subclinical with early diastolic dysfunction followed by insidious onset of symptoms with increasing systolic dysfunction and cardiac failure which is a late finding. Abnormal diastolic function of the left ventricle has been reported in adult RA[7] and JRA.[8],[9] In this issue of the Journal, Bharti et al[10] studied systolic and diastolic function of the left ventricle in 35 patients and compared the data with age and sex matched controls. They demonstrate a higher blood pressure, higher heart rate, larger left ventricular dimension, lower left ventricular systolic function, and decreased diastolic function in JRA patients, compared to control population. The study did not find any differences in the left ventricular wall thickness or pericardial involvement. They conclude that there are significant systolic and diastolic functional abnormalities in asymptomatic juvenile rheumatoid arthritis patients and suggest monitoring the patients. The manuscript is reasonably well-written and has some merits, particularly documentation of left ventricular diastolic function abnormalities. But, there are several limitations in the study: The age range of study subjects is 7 to 28 years, and as such, many subjects are not truly children. Blood pressures are said to be higher, but indeed they are within normal range. Furthermore, all patients are receiving NSAID which may account for hypertension. The report also does not mention drugs other than NSAIDs taken by the study population. At the time of the study a sedimentation rate or C-reactive protein level may reflect the inflammatory status of the disease although many studies in adults have failed to correlate the degree of inflammation with the amount of diastolic or systolic dysfunction in RA.[7],[11],[12],[13] Large left ventricular size and volume may be related to lower hemoglobin levels. Ejection fraction and fractional shortening are indeed within normal range of established values; should they be called abnormal? The effect of increasing size of the child with time should be accounted for before concluding that increase in LV dimension is the effect of the disease. Despite all these limitations, we believe that this study supplements the limited literature available on cardiac involvement in JRA.



Increasing diastolic dysfunction has been found with increased duration of the disease but the etiology of this diastolic dysfunction is still unclear. The abnormal relaxation of the myocardium may be due to thickened and stiff pericardium, left ventricular hypertrophy, interstitial fibrosis, ischemic changes (resulting in abnormal relaxation of the ventricle) and/or amyloid infiltration. Thus, the cause of abnormal diastolic parameters may be multiple and may be a cumulative effect of several factors such as pericarditis with or without pericardial effusion, hypertension,[14] left ventricular hypertrophy, therapy with cardiotoxic agents such as cyclosporine, gold salts,[15] d-penicillamine,[15] chroloquine,[16],[17] and hydrochloroquine, hypertension due to steroid therapy, secondary amyloidosis,[18] and vascular stiffness from vasculitis.[19] The abnormal echocardiographic diastolic parameters may not be so much reflective of "myocarditis" because such myocarditis in JRA is a rare phenomenon and seen in only 1 to 10% cases,[2],[20],[21] especially when there is severe active systemic disease.[20] However, pericardial involvement can be seen in almost 45 % of the cases at autopsy[22] and collagen fiber involvement with endocarditis and pericarditis is more prevalent.



In conclusion, children with JRA are at risk for cardiac dysfunction. Routine cardiac evaluation, possibly yearly may be one way to monitor these children, as implied by the authors. Blood pressure measurement, electrocardiogram and echocar-diogram may be performed. On an echocardiogram, evaluation of left ventricular wall thickness, pulmonary artery pressure, pericardial effusion, pericardial thickening, left ventricular diastolic and systolic function, left ventricular dilatation, valvular thickening with insufficiency or stenosis, aortic root diameter and coronary artery involvement should be performed.

 
 :: References Top

1.Hull RG. Outcome in juvenile arthritis. Br J Rheumatol 1988;27:66-71  Back to cited text no. 1  [PUBMED]  
2.Svantesson H, Bjorkhem G, Elborgh R. Cardiac involvement in juvenile rheumatoid arthritis. A follow-up study. Acta Paediatr Scand 1983;72:345-50.  Back to cited text no. 2  [PUBMED]  
3.Smolen JS, Kalden JR, Scott DL, Rozman B, Kvien TK, Larsen A, et al. Efficacy and safety of leflunomide compared with placebo and sulphasalazine in active rheumatoid arthritis: a double-blind, randomized, multicentre trial. European Leflunomide Study Group. Lancet 1999;353:259-66.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]
4.Strand V, Cohen S, Schiff M, Weaver A, Fleischmann R, Cannon G, et al. Treatment of active rheumatoid arthritis with leflunomide compared with placebo and methotrexate. Leflunomide Rheumatoid Arthritis Investigators Group. Arch Intern Med 1999;159:2542-50.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Weinblatt ME, Kremer JM, Bankhurst AD, Bulpitt KJ, Fleischmann RM, Fox RI, et al. A trial of etanercept, a recombinant tumor necrosis factor receptor:Fc fusion protein, in patients with rheumatoid arthritis receiving methotrexate. N Engl J Med 1999;340:253-9.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]
6.Moreland LW, Schiff MH, Baumgartner SW, Tindall EA, Fleischmann RM, Bulpitt KJ, et al. Etanercept therapy in rheumatoid arthritis. A randomized, controlled trial. Ann Intern Med 1999;130:478-86.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]
7.Di Franco M, Paradiso M, Mammarella A, Paoletti V, Labbadia G, Coppotelli L, et al. Diastolic function abnormalities in rheumatoid arthritis. Evaluation By echo Doppler transmitral flow and pulmonary venous flow: relation with duration of disease. Ann Rheum Dis 2000;59:227-9.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]
8.Huppertz H, Voigt I, Muller-Scholden J, Sandhage K. Cardiac manifestations in patients with HLA B27-associated juvenile arthritis. Pediatr Cardiol 2000;21:141-7.  Back to cited text no. 8  [PUBMED]  [FULLTEXT]
9.Oguz D, Ocal B, Ertan U, Narin H, Karademir S, Senocak F. Left ventricular diastolic functions in juvenile rheumatoid arthritis. Pediatr Cardiol 2000;21:374-7.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.Bharti BB, Kumar S, Kapoor A, Agarwal A, Mishra R, Sinha N. Assessment of left ventricular systolic and diastolic function in juvenile rheumatoid arthritis. J Postgrad Med 2004;50:262-7.  Back to cited text no. 10  [PUBMED]  
11.Levendoglu F, Temizhan A, Ugurlu H, Ozdemir A, Yazici M. Ventricular function abnormalities in active rheumatoid arthritis: a Doppler echocardiographic study. Rheumatol Int 2004;24:141-6. Epub 2003 Jun 19  Back to cited text no. 11    
12.Montecucco C, Gobbi G, Perlini S, Rossi S, Grandi AM, Caporali R, et al. Impaired diastolic function in active rheumatoid arthritis. Relationship with disease duration. Clin Exp Rheumatol 1999;17:407-12.  Back to cited text no. 12  [PUBMED]  
13.Cindas A, Gokce-Kutsal Y, Tokgozoglu L, Karanfil. A QT dispersion and cardiac involvement in patients with rheumatoid arthritis. Scand J Rheumatol 2002;31:22-6.  Back to cited text no. 13    
14.Yamamoto T, Abe T, Mastuya M, Kobayashi K, Akaike J, Ikeda Y, et al. A case with juvenile rheumatoid arthritis who developed cerebral vasculitis and venovascular hypertension. Ryumachi 2000;40:818-23.  Back to cited text no. 14  [PUBMED]  
15.Qasim FJ, Thiru S, Gillespie K. Gold and D-penicillamine induce vasculitis and up-regulate mRNA for IL-4 in the Brown Norway rat: support for a role for Th2 cell activity. Clin Exp Immunol 1997;108:438-45.  Back to cited text no. 15  [PUBMED]  
16.Iglesias Cubero G, Rodriguez Reguero JJ, Rojo Ortega JM. Restrictive cardiomyopathy caused by chloroquine. Br Heart J 1993;69:451-2  Back to cited text no. 16  [PUBMED]  
17.Ratliff NB, Estes ML, McMahon JT, Myles JL. Chloroquine-induced cardiomyopathy. Arch Pathol Lab Med 1988;112:578.  Back to cited text no. 17  [PUBMED]  
18.Husby G. Amyloidosis and rheumatoid arthritis. Clin Exp Rheumatol 1985;3:173-80.   Back to cited text no. 18  [PUBMED]  
19.Klocke R, Cockcroft JR, Taylor GJ, Hall IR, Blake DR. Arterial stiffness and central blood pressure, as determined by pulse wave analysis, in rheumatoid arthritis. Ann Rheum Dis 2003;62:414-8.  Back to cited text no. 19  [PUBMED]  [FULLTEXT]
20.Miller JJ 3rd, French JW. Myocarditis in juvenile rheumatoid arthritis. Am J Dis Child 1977;131:205-9.  Back to cited text no. 20  [PUBMED]  
21.Bernstein B, Takahashi M, Hanson V. Cardiac involvement in juvenile rheumatoid arthritis. J Pediatr 1974;85:313-7.  Back to cited text no. 21  [PUBMED]  
22.Lietman PS, Bywaters EG. Pericarditis in juvenile rheumatoid arthritis. Pediatrics 1963;32:855-60.  Back to cited text no. 22  [PUBMED]  




 

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Online since 12th February '04
2004 - Journal of Postgraduate Medicine
Official Publication of the Staff Society of the Seth GS Medical College and KEM Hospital, Mumbai, India
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