Background. Rheumatic heart disease (RHD) is a leading cause of heart failure in children and young adults worldwide. B-type natriuretic peptide (BNP) is a useful marker of critical pediatric heart disease, and its N-terminal peptide, NT-proBNP, is elevated in congenital and acquired heart disease in children. Aim. To measure NT-proBNP levels as a marker of carditis in children with acute rheumatic carditis, as compared to children with quiescent RHD and healthy controls. Methods. 16 children with acute rheumatic carditis, 33 children with quiescent RHD, and a cohort of 30 healthy children were studied. Transthoracic echocardiography was performed to assess valve and cardiac function. Tissue Doppler echocardiography was performed for E/E′ (ratio between mitral inflow E wave and lateral mitral annulus E′ wave) and systolic strain. Results. NT-proBNP levels were significantly higher in children with acute rheumatic carditis and dropped with its resolution. Strain and E/E′ values were comparable among the three groups. Conclusion. NT-proBNP is significantly elevated in children with acute rheumatic carditis in the acute stage compared to children with quiescent RHD and healthy subjects, in the presence of comparable echocardiographic indices of LV systolic and diastolic function. 1. Introduction Acute rheumatic fever (ARF) and rheumatic heart disease (RHD) continue to be a major health problem in developing countries, and RHD is the leading cause of heart failure in children and young adults worldwide, resulting in disability and premature death [1]; 80–85% of children younger than 15 years live in areas where rheumatic heart disease is endemic [2]. Late diagnosis is prejudicial since a bout of ARF is a therapeutic emergency. While polyarthritis is the initial and most common major manifestation, carditis is the most serious manifestation of ARF [3] and occurs in around a half of patients [4–9] within 3 weeks of onset of ARF [3]. Although the initial attack can lead to severe valvular disease, ARF might be insidious at onset, and RHD most often results from cumulative valve damage due to recurrent episodes of ARF with a paucity of clinical symptoms [1, 10, 11]. Given that the efficacy and safety of antibiotic prophylaxis are well established and should lead to near complete eradication of advanced RHD when combined with broader changes such as improved living conditions, education, and awareness [12–14], early detection of acute rheumatic carditis will allow appropriate initiation of secondary prophylaxis. No diagnostic method exists that detects onset of
References
[1]
J. R. Carapetis, A. C. Steer, E. K. Mulholland, and M. Weber, “The global burden of group A streptococcal diseases,” The Lancet Infectious Diseases, vol. 5, no. 11, pp. 685–694, 2005.
[2]
Population Reference Bureau, “world population data sheet,” 2008, http://www.prb.org/Publications/Datasheets/2008/2008wpds.aspx.
[3]
C. Weil-Olivier, “Rheumatic fever. Orphanet encyclopedia,” 2004, http://www.orpha.net/data/patho/GB/uk-RF.pdf.
[4]
Z. M. A. Meira, E. M. A. Goulart, E. A. Colosimo, and C. C. C. Mota, “Long term follow up of rheumatic fever and predictors of severe rheumatic valvar disease in Brazilian children and adolescents,” Heart, vol. 91, no. 8, pp. 1019–1022, 2005.
[5]
á. M. Caldas, M. T. R. A. Terreri, V. A. Moises et al., “What is the true frequency of carditis in acute rheumatic fever? A prospective clinical and doppler blind study of 56 children with up to 60 months of follow-up evaluation,” Pediatric Cardiology, vol. 29, no. 6, pp. 1048–1053, 2008.
[6]
S. K. Sanyal, M. K. Thapar, and S. H. Ahmed, “The initial attack of acute rheumatic fever during childhood in North India. A prospective study of the clinical profile,” Circulation, vol. 49, no. 1, pp. 7–12, 1974.
[7]
P. Vardi, W. Markiewicz, and Y. Weiss, “Clinical-echocardiographic correlations in acute rheumatic fever,” Pediatrics, vol. 71, no. 5, pp. 830–834, 1983.
[8]
R. S. Vasan, S. Shrivastava, M. Vijayakumar, R. Narang, B. C. Lister, and J. Narula, “Echocardiographic evaluation of patients with acute rheumatic fever and rheumatic carditis,” Circulation, vol. 94, no. 1, pp. 73–82, 1996.
[9]
F. E. Figueroa, P. Valdés, F. Carrión et al., “Prospective comparison of clinical and echocardiographic diagnosis of rheumatic carditis: long term follow up of patients with subclinical disease,” Heart, vol. 85, no. 4, pp. 407–410, 2001.
[10]
J. R. Carapetis, M. McDonald, and N. J. Wilson, “Acute rheumatic fever,” The Lancet, vol. 366, no. 9480, pp. 155–168, 2005.
[11]
K. Sliwa, M. Carrington, B. M. Mayosi, E. Zigiriadis, R. Mvungi, and S. Stewart, “Incidence and characteristics of newly diagnosed rheumatic heart disease in Urban African adults: insights from the Heart of Soweto Study,” European Heart Journal, vol. 31, no. 6, pp. 719–727, 2010.
[12]
M. Markowitz, E. Kaplan, R. Cuttica et al., “Allergic reactions to long-term benzathine penicillin prophylaxis for rheumatic fever,” The Lancet, vol. 337, no. 8753, pp. 1308–1310, 1991.
[13]
P. Nordet, R. Lopez, A. Due?as, and L. Sarmiento, “Prevention and control of rheumatic fever and rheumatic heart disease: the Cuban experience (1986–1996–2002),” Cardiovascular Journal of Africa, vol. 19, no. 3, pp. 135–140, 2008.
[14]
A. Arguedas and E. Mohs, “Prevention of rheumatic fever in Costa Rica,” Journal of Pediatrics, vol. 121, no. 4, pp. 569–572, 1992.
[15]
National Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand, “Diagnosis and management of acute rheumatic fever and rheumatic heart disease in Australia: an evidence-based review,” 2006, http://www.heartfoundation.org.au/SiteCollectionDocuments/Diagnosis-Management-Acute-Rheumatic-Fever.pdf.
[16]
J. R. Carapetis, J. Paar, and T. Cherian, “Standardization of epidemiologic protocols for surveillance of post-streptococcal sequelae: acute rheumatic fever, rheumatic heart disease and acute post-streptococcal glomerulonephritis,” 2006, http://www.niaid.nih.gov/topics/strepThroat/Documents/groupasequelae.pdf.
[17]
B. Reméanyi, N. Wilson, A. Steer et al., “World Heart Federation criteria for echocardiographic diagnosis of rheumatic heart disease-an evidence-based guideline,” Nature Reviews Cardiology, vol. 9, no. 5, pp. 297–309, 2012.
[18]
E. A. Espiner, A. M. Richards, T. G. Yandle, and M. G. Nicholls, “Natriuretic hormones,” Endocrinology and Metabolism Clinics of North America, vol. 24, no. 3, pp. 481–509, 1995.
[19]
A. Luchner, T. L. Stevens, D. D. Borgeson et al., “Differential atrial and ventricular expression of myocardial BNP during evolution of heart failure,” American Journal of Physiology, vol. 274, no. 5, pp. H1684–H1689, 1998.
[20]
R. J. Rodeheffer, “Measuring plasma B-type natriuretic peptide in heart failure: good to go in 2004?” Journal of the American College of Cardiology, vol. 44, no. 4, pp. 740–749, 2004.
[21]
A. Nir, B. Bar-Oz, Z. Perles, R. Brooks, A. Korach, and A. J. J. T. Rein, “N-terminal pro-B-type natriuretic peptide: reference plasma levels from birth to adolescence. Elevated levels at birth and in infants and children with heart diseases,” Acta Paediatrica, International Journal of Paediatrics, vol. 93, no. 5, pp. 603–607, 2004.
[22]
V. Davutoglu, A. Celik, M. Aksoy, Y. Sezen, S. Soydinc, and N. Gunay, “Plasma NT-proBNP is a potential marker of disease severity and correlates with symptoms in patients with chronic rheumatic valve disease,” European Journal of Heart Failure, vol. 7, no. 4, pp. 532–536, 2005.
[23]
G. Koerbin, W. P. Abhayaratna, J. M. Potter, S. Apostoloska, R. D. Telford, and P. E. Hickman, “NTproBNP concentrations in healthy children,” Clinical Biochemistry, vol. 45, pp. 1158–1160, 2012.
[24]
A. Maisel, C. Mueller, K. Adams Jr. et al., “State of the art: using natriuretic peptide levels in clinical practice,” European Journal of Heart Failure, vol. 10, no. 9, pp. 824–839, 2008.
[25]
S. R. Ommen, R. A. Nishimura, C. P. Appleton et al., “Clinical utility of Doppler echocardiography and tissue Doppler imaging in the estimation of left ventricular filling pressures: a comparative simultaneous Doppler-catheterization study,” Circulation, vol. 102, no. 15, pp. 1788–1794, 2000.
[26]
L. Sundereswaran, S. F. Nagueh, S. Vardan et al., “Estimation of left and right ventricular filling pressures after heart transplantation by tissue doppler imaging,” American Journal of Cardiology, vol. 82, no. 3, pp. 352–357, 1998.
[27]
C. Bruch, M. Grude, J. Müller, G. Breithardt, and T. Wichter, “Usefulness of tissue Doppler imaging for estimation of left ventricular filling pressures in patients with systolic and diastolic heart failure,” American Journal of Cardiology, vol. 95, no. 7, pp. 892–895, 2005.
[28]
D. Y. Leung and A. C. T. Ng, “Emerging clinical role of strain imaging in echocardiography,” Heart Lung and Circulation, vol. 19, no. 3, pp. 161–174, 2010.
[29]
K. O. Maher, H. Reed, A. Cuadrado et al., “B-type natriuretic peptide in the emergency diagnosis of critical heart disease in children,” Pediatrics, vol. 121, no. 6, pp. e1484–e1488, 2008.
[30]
J. Kamblock, L. Payot, B. Iung et al., “Does rheumatic myocarditis really exists? Systematic study with echocardiography and cardiac troponin I blood levels,” European Heart Journal, vol. 24, no. 9, pp. 855–862, 2003.
[31]
G. V. Herdy, R. S. Gomes, A. E. Silva, L. S. Silva, and V. G. Lopes, “Follow-up of rheumatic carditis treated with steroids,” Cardiology in the Young, vol. 22, pp. 263–269, 2012.