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Ongoing inflammation in children with rheumatic heart disease

Published online by Cambridge University Press:  08 February 2011

Nevin M. M. Habeeb  and
Iman S. Al Hadidi
Nevin M. M. Habeeb*
Affiliation:
Pediatric Cardiology Department and Clinical Pathology Department, Ain Shams University, Cairo, Egypt
Iman S. Al Hadidi
Affiliation:
Pediatric Cardiology Department and Clinical Pathology Department, Ain Shams University, Cairo, Egypt
*
Correspondence to: Dr N. M. M. Habeeb MD, 15 A Saraya Al Kobba Square, Cairo, Egypt. Tel: 00966 0508057325 ext: 0020101912490; Fax: 00202 (22597453); E-mail: [email protected]
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Abstract

Aim of the work

To elucidate the hypothesis of ongoing inflammation in children with chronic rheumatic heart disease, and its possible consequences.

Subjects and methods

This study was conducted on 36 patients with a mean age of 12.63 years: six with acute rheumatic carditis, and 30 with chronic rheumatic heart disease. There were 15 age- and sex-matched children who served as a control group. All subjects underwent echocardiographic assessment of valvular involvement and left ventricular function. Laboratory investigations comprised lipid profile, high-sensitivity C-reactive protein, and homocysteine assay.

Results

High-sensitivity C-reactive protein was significantly elevated in patients with acute rheumatic carditis and in patients with chronic rheumatic heart disease (mean and standard deviation of 78.33, 156 micrograms per millilitre and 78.33, 23.17 micrograms per millilitre, respectively) as compared to the control group (mean and standard deviation of 5.83 and 2.79 micrograms per millilitre). High-sensitivity C-reactive protein correlated with the grade of mitral regurgitation (p less than 0.05). Homocysteine was significantly elevated in patients with acute carditis and patients with rheumatic heart disease as compared to the control group (their mean and standard deviation were 2.96, 0.476 nanograms per decilitre, 2.99, 1.48 nanograms per decilitre, and 1.717, 0.733 nanograms per decilitre, respectively), but did not show significant difference between the two studied groups of patients. Neither C-reactive protein nor homocysteine correlated with any of the studied parameters of lipid profile.

Conclusion

There is evidence of ongoing inflammation in children with rheumatic heart disease, which correlates with the degree of valvular involvement. This ongoing inflammation may put those children at risk for premature atherosclerosis.

Keywords

Rheumatic mitral regurgehighly sensitive C-reactive proteinhomocysteineatherosclerosis
Type
Original Articles
Information
Cardiology in the Young , Volume 21 , Issue 3 , June 2011 , pp. 334 - 339
Copyright
Copyright © Cambridge University Press 2011

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References

1. Rajamannan, NM, Antonini-Canterin, F, Moura, L, et al. Medical therapy for rheumatic heart disease: is it time to be proactive rather than reactive? Indian heart J 2009; 61: 14–23.Google ScholarPubMed
2. Essop, MR, Nkomo, VT. Rheumatic and non rheumatic valvular heart disease: epidemiology, management, and prevention in Africa. Circulation 2005; 112: 3584–3591.CrossRefGoogle Scholar
3. Chopra, P, Gulwani, H. Pathology and pathogenesis of rheumatic heart disease. Indian J Pathol Microbiol 2007; 50: 685–697.Google ScholarPubMed
4. Ridker, PM, Buring, JE, Shih, J, Matias, M, Hnnekens, CH. Prospective study of C-reactive protein and the risk of future cardiovascular events among apparently healthy women. Circulation 1998; 98: 731–733.CrossRefGoogle ScholarPubMed
5. Ferrieri, P. Jones criteria working group. Proceedings of the Jones criteria workshop. Circulation 2002; 106: 2521–2523.CrossRefGoogle Scholar
6. Golbasi, Z, Ucar, O, Keles, T, et al. Increased levels of sensitive C-reactive protein in patients with chronic rheumatic valve disease: evidence of ongoing inflammation. Eur J Heart Fail 2002; 4: 593–595.CrossRefGoogle ScholarPubMed
7. Chiu-Braga, UU, Hayashi, SY, Schafranski, M, Messias-Reason, IJ. Further evidence of inflammation in chronic rheumatic valve disease (CRVD): high levels of advanced oxidation protein products (AOPP) and high sensitive C-reactive protein (hs-CRP). Int J Cardiol 2006; 1109: 275–276.CrossRefGoogle Scholar
8. Davutoglu, V, Celik, A, Aksoy, M. Contribution of selected serum inflammatory mediators to the progression of chronic rheumatic valve disease, subsequent valve calcification and NYHA functional class. J Heart Valve Dis 2005; 14: 251–256.Google Scholar
9. Krasuski, RA, Bush, A, Kay, JE, et al. C-reactive protein elevation independently influences the procedural success of percutaneous balloon mitral valve commissurotomy. Am Heart J 2003; 146: 146–151.CrossRefGoogle ScholarPubMed
10. Hingorani, AD, Shah, T, Casas, JP, Humphries, SE, Talmud, PJ. C-reactive protein and coronary heart disease: predictive test or therapeutic target? Clin Chem 2009; 55: 239–255.CrossRefGoogle ScholarPubMed
11. Zhang, YX, Cliff, WJ, Schoefi, GI, Higgins, G. Coronary C-reactive protein distribution: its relation to development of atherosclerosis. Atherosclerosis 1999; 145: 375–379.CrossRefGoogle ScholarPubMed
12. de Beer, FC, Soutar, AK, Baltz, ML, Trayner, I, Feinstein, A, Pepys, MB. Low density and very low density lipoproteins are selectively bound by aggregated C-reactive protein. J Exp Med 1982; 156: 230–242.CrossRefGoogle ScholarPubMed
13. Bhakdi, S, Torzewski, M, Klouche, M, Hemmes, M. Complement activation and atherogenesis. Binding of CRP to degraded, nonoxidised LDL enhances complement activation. Arterioscler Thromb Vasc Biol 1999; 19: 2348–2354.CrossRefGoogle Scholar
14. Li, BL, Li, L, Hou, XL, et al. Prevalence of coronary artery disease in patients with rheumatic heart disease in China. Zhonghua Yi Xue Za Zhi 2007; 87: 3313–3316.Google ScholarPubMed
15. Panamonta, M, Settasatinan, N, Kaplan, EL, Chaikitpinyo, A. Serum cholesterol levels in patients with acute rheumatic fever. Am J Dis Child 1993; 147: 732–736.Google ScholarPubMed
16. Yilmaz, MB, Demirkan, B, Caldir, V, et al. Association of lipid profile with echocardiographic Wilkins score in patients with moderate to severe mitral stenosis: possible impact on prognosis. J Am Coll Cardiol 2009; 53: 1874–1879.Google Scholar
17. Antonini-Canteri, F, Leiballi, E, Enache, R, et al. Hydroxymethylglutaryl coenzyme-a reductase inhibitors delay the progression of rheumatic aortic valve stenosis. A long-term echocardiographic study. J Am Coll Cardiol 2009; 53: 1874–1879.CrossRefGoogle Scholar
18. Kurban, S, Mehmetoglu, I, Oran, B, Kiyici, A. Homocysteine levels and total antioxidant capacity in children with acute rheumatic fever. Clin Biochem 2007; 10: 26–29.Google Scholar
19. Wald, DS, Law, M, Marris, KJ. Homocyseine and cardiovascular disease: evidence of causality from a meta-analysis. BMJ 2002; 325: 1202.CrossRefGoogle Scholar
20. Cleophas, TJ, Hornstra, N, van Hoogstraten, B, van der Meulen, J. Homocysteine, a risk factor for coronary artery disease or not? A meta-analysis. J Am Coll Cardiol 2000; 86: 1005–1009.CrossRefGoogle ScholarPubMed