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].