Abstract

Objective: We aimed to investigate the changes in left atrial stiffness (LASt) in children with acute rheumatic fever (ARF) and its impact on clinical outcome. Patients and methods: 64 children presented with first attack of ARF, were enrolled and studied, using standard, tissue Doppler and speckle tracking echocardiography. They were compared with 36 matched controls. Left atrial (LA) volumes, mitral annular velocities, and global longitudinal LA strain were measured. The ratio of E/e′ to LA strain was used as an index of LA stiffness. Results: LA maximal, minimal and pre-A volume indexes were significantly higher in children with ARF compared to controls (P<0.001). The E/e“ ratio was significantly elevated (P<0.001), whilst the global LA strain was significantly decreased (P<0.001). LASt was greater in children with ARF than in the controls (p<0.001). Follow-up data showed that children with adverse clinical outcomes had a significantly greater LASt (P<0.003). ROC analysis showed that the predictive value of LASt in predicting adverse clinical outcome in children with ARF is corresponding to a good test with a cut off value ≥ 0.63 with area under the curve = 0.91 (P<0.0001), with a sensitivity of 81.5% and a specificity of 94.7%. Conclusions: Children with first attack ARF have increased LASt in comparison with that of the matched controls. Meanwhile LASt is a good predictor adverse events of children of first attack of ARF. LASt could be a valuable parameter of subclinical carditis and ARF risk stratification.

Highlights

  • Acute rheumatic fever (ARF) is an inflammatory and autoimmune disease, occurs as a sequel of delayed group A β-hemolytic streptococcal pharyngitis [1]

  • While the global Left atrial (LA) strain was significantly decreased (P

  • The results showed that children with carditis had a significant lower global left atrial peak strain% (P

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Summary

Introduction

Acute rheumatic fever (ARF) is an inflammatory and autoimmune disease, occurs as a sequel of delayed group A β-hemolytic streptococcal pharyngitis [1]. The exact pathophysiologic and genetic determinants of ARF and rheumatic heart disease remain undefined. The autoimmunelike reaction on exposure to group A Streptococci, leads to myocarditis and endocarditis with eventually rheumatic heart disease. The antigenic mimicry hypothesis was claimed to be the underlying cause of autoimmune reaction [2]. Spite of advances in preventing medicine ARF remains a major and endemic health problem, among school-age children in developing nations. The initial attack of ARF is usually associated with nearly 50% of cardiac involvement. This serious sequel may affect endocardium, myocardium and rarely pericardium [3]

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