Discussion
Rheumatic heart disease is one of the major causes of cardiac mortality and morbidity in school age children specifically in developing countries. The estimates show 15 million cases worldwide, 233.000 of them dying every year [12]. Therefore, the diagnosis, the treatment and the pathophysiology of the disease is of utmost importance.
Although some investigators suggest that RHD always presents as pancarditis, it is generally accepted as a disease of the endocardium and the valves, and it rarely involves the myocardium [13]. Clinical findings such as tachycardia and tachypnea indicate heart failure for which valvular regurgitation is the main reason, although myocardial involvement can also contribute to that process [14, 15]. Narula et al. found no myocyte necrosis, but non-specific changes were frequently observed in the right ventricle biopsy specimens [3]. Several recent studies questioned myocardial involvement contributing to myocardial dysfunction and they proposed that RHD is only a disease of the endocardium and that myocardial influences are due to valve regurgitation [16, 17]. For patients with rheumatic heart disease, the postmortem microscopic examination of the cardiac muscle showed lymphocyte infiltration during acute stage and fibrosis during chronic stage and functional disorders of the heart muscle were reported due to these changes [18, 19]. Myocardial biopsies demonstrated mononuclear cells and fibrin degeneration while myocardial necrosis was not reported [3]. Cross reactivity between cardiac myosin and group A beta hemolytic Streptococcal M protein has also been demonstrated [19].
Two dimensional STE can detect myocardial contraction abnormalities long before decreases in left ventricle ejection fraction are observed [20, 21]. Moreover, STE is less angle dependent than Doppler based methods [21]. In this study, patients were analyzed before and after the treatment and compared to healthy controls by STE.
In the present study, significantly reduced left ventricle global longitudinal and circumferential strain and strain rates, and right ventricle global longitudinal strain and strain rates were found in patients with preserved left ventricular ejection fraction and fractional shortening in acute phase of RHD compared to healthy controls. Our results showed no statistically significant correlation with strain and strain rates and the severity of the valvular involvement. This made us think that decreases in strain were related to effects on myocardial tissue than heart failure. Supporting this view, Ozdemir et al. found higher Troponin T levels in 28 patients with active rheumatic carditis compared to healthy controls and they commend that all patients have minimal myocardial involvement especially near the endocardium by the spread of the inflammation in the connective tissue [2]. We also found recovery in left ventricle global longitudinal and circumferential and right ventricle global longitudinal strain and strain rates after treatment in patients when we used paired samples T test. After the treatment, all strain and strain rates increased.
In the literature, there are a limited number of studies analysing rheumatic heart disease and myocardial strain. In one of such studies, in adults with rheumatic mitral stenosis, left ventricular global longitudinal and global circumferential strain values were lower than those of the controls and recovery was seen after balloon mitral valvuloplasty. This was not due to myopathic processes but due to a tethering effect caused by the secondary restriction of the basal myocardium from mitral stenosis [22]. In another study similar to this one, 60 adult patients with rheumatic mitral stenosis having preserved ejection fraction left ventricle global longitudinal strain and strain rate values were low [23]. In a rare study by Beaton et. al. analyzing the correlation between myocardial strain and RHD in children, in latent RHD patients with normal systolic functions, left ventricle global longitudinal strain values were found to be lower than those of the controls and myocardial strain was thought to play a role in understanding the pathophysiology of latent rheumatic heart disease [24]. In this study, similar to ours, a pediatric patient group without systolic dysfunction was analyzed and the only difference was the inclusion of patients in the study during the latent stage. In our study, different from this study, global longitudinal strain values were different than those of the healthy controls only during the acute stage. This difference disappeared after the treatment, the treatment also resulted in an increase in right ventricular strain values, the difference with healthy children during the acute stage disappeared after the treatment. In pediatric patients with latent rheumatic heart disease, normal heart muscle function was demonstrated with conventional methods; a new technique, 3D strain echocardiography found normal strain values during latent stage supporting our study [25].