我的表妹在读医学研究生，发了一篇她写的医学文章让我帮忙修正语法和修辞，因为她小时候很崇拜我的英文，长大了还把我看做偶像，呵呵呵~~~看样子我这个姐姐做的很成功，但遗憾的是对她那么专业的医学文章我头都看晕了，所以请英文高手帮忙修正此篇文章是否有语法和修辞方面的错误。

非常感谢！



Idophilic Hypereosinophilic Syndrome with Loffler’s Endomyocarditis: complete resolution after bioprosthetic mitral valve replacement


Loffler’s endocarditis is an uncommon myocardial disease, thought to be secondary to eosinophil damage, due to idiopathic hypereosinophilic syndrome. Loffler’s endocarditis is a major source of the morbidity and mortality of idiopathic hypereosinophilic syndrome (IHES). Typical cardiac findings include endomyocardial thickening, left and right ventricular apical thrombus formation, and posterior mitral leaflet involvement[1]. There are often progressive features of a restrictive cardiomyopathy with regurgitation of the atrioventricular valves secondary to subvalvular damage [2]. We herein describe a case of a man in whom loffler’s endocarditis was identified. He had a unique echocardiography manifestation with severe endomyocardial fibrosis. His symptoms were complete relieved after bioprosthetic mitral valve replacement and appears excellent result after bioprosthetic mitral valve replacement.


Idiophilic hypereosinophilic syndrome (IHES) is classically defined as prolonged, unexplained peripheral eosinophilia in a patient presenting with evidence of end-organ damage. Cardiac involvement is a major cause of death in the IHES. Echocardiography is a adjunct in the cardiac evaluation of patients with the IHES. Thickening of the posterobasal wall is usually associated with impairment of posterior mitral leaflet function, resulting in mitral regurgitation, mitral valvuar displacement by a prosthetic valve may be important at that time.


Case Description
A 36-year-old male presented with 1 year of tachypnea and fatigue, 2 months of progressive dyspnea on exertion. On auscultation a 4/6 apical systolic murmur were heard. Blood investigations revealed a persistent increase in the eosinophil count in the peripheral blood with the absolute eosinophil count ranging from 2400-14800 cells/cu mm in the last 1 year. Bone-marrow biopsy revealed hypercellular marrow with predominant eosinophil precursors. His electrocardiogram showed auricular tachycardia with non-complete right bundle branch block and right ventricular hypertrophy. Chest computerized tomography (CT) scan revealed a left-sided pleural effusion. Echocardiography reviewed an area of increased echo density denotes fibrosis along the basal posterior wall of the left ventricle which also involves the posterior leaflet of the mitral valve, and moderate mitral valve regurgitation was evident. Although the systolic function of the left ventricule was preserved, diastolic dysfunction was present. Besides, there were small amounts of pericardial effusion around the atrioventricular ring. Because we found no clues for an allergic cause or a parasitic infection on examination of blood and stool, so the diagnosis consistent with loffler’s endomyocarditis due to IHES.
The patient was started on steroids (prednisolone 60 mg daily) for three months and ciclosporin (150 mg daily) for two months. On follow-up, the absolute eosinophil count was down to 500 cells/cu, but the symptoms was severer than before and repetitive echocardiography showed severe mitral valve regurgitation.
He underwent a bioprosthetic mitral valve replacement one month later because of mitral valve regurgitation. At the operation the inner posterior wall of the left ventricular cavity was covered with grey fibrotic tissue, which totally encapsulated the posterior mitral valve leaflet with its chordae and papillary muscles. The histopathologic findings include fibrotic thickening of the endocardium which was made up of collagen without elastic fibers and few fiborcytes.
At follow up, the patient appears a good chance for one year survival.
Comments
IHES is classically defined as prolonged, unexplained peripheral eosinophilia in a patient presenting with evidence of end-organ damage. Loffler’s endocarditis was first described as a nosologic entity by Loffler in 1936, who called it “syndrome of eosinophilia and chronic heart failure due to constrictive pericarditis with endocardial fibrosis” [3]. It is the most characteristic abnormalities in the IHES. Earlier studies reported that up to 84% of IHES patients have signs and symptoms of cardiac disease, more recent reports suggest that the frequency is closer to 40%~50%[4-5].
Endocardial-mediated cardiac damage generally evolves in three stages. First stage is an acute necrotic stage which involves the endomyocardium is often asymptomatic and echocardiographic examination can be normal. The stage is followed by a thrombotic stage in which thrombi develop in the cardiac chambers and can be determined with echocardiography. In the final fibrotic stage, endomyocardial fibrosis results in irreversible restrictive cardiomyopathy, the stage involves progressive scarring which may lead mitral and/or tricuspid valve regurgitation due to entrapment of choradae tendineae. Thickening of the posterior mitral valve leaflet and the endomyocardial fibrosis areas that are characterized with increased in intensities of endomyocardial echoes.
Two-dimensional echocardiography is beneficial in recognizing the abnormalities of loffler’s endocarditis. These include structural alterations such as endomyocardial fibrosis, cavity obliteration, or thrombi, and functional abnormalities directly resulting from myocardial involvement or secondary to atrioventricular valvular regurgitation. M-mode echocardiography was not specific but can provide additional information about the effects of mitral valve involvement and left ventricular systolic and diastolic function.
Our patient showed a localized area of echo-dense material on the posterior wall beneath the mitral valve and a total posterior mitral valve destruction and a endomyocardial thickening without any thrombosis. Extensive endocardial fibrosis are relate to the occurrence of restrictive cardiomyopathy and mitral valvular abnormalities (particularly mitral regurgitation). In many other cases, mural thrombosis in the both apices of the both ventricles may be dominated.
Surgical intervention secondary to progressive valvular dysfunction may become necessary. But the experience with valve replacement in HES patients is very limited due to the rarity of the disease. Our patient has done well after bioprosthetic mitral valve replacement.

Figure1. two-dimensional echocardiography shows the thickend posterobasal left ventricular wall and impaired absent mitral leaflet motion.
Figure 2.
Two-dimensional echocardiograp shows the bioprosthetic mitral valve.


References
1. Ommen SR, Seward JB, Tajik AJ. Clinical and echocardiographic features of hypereosinophilic syndromes. Am J Cardiol. 2000 Jul 1;86(1):110–113
2. Zientek DM, King DL, Dewan SJ, Harford PH, Youman DJ, Hines TR. Hypereosinophilic syndrome with rapid progression of cardiac involvement and early echocardiographic abnormalities. Am Heart J. 1995 Dec;130(6):1295–1298.
3. Loffler W. Endocarditis parietalis fibroplastica mit Bluteosinophilie, eineigenartiges Krankheitsbild. Schweiz Med Wochenschr. 1936;17:817
4. Parrillo JE, Borer JS, Henry WL, Wolff SM, Fauci AS. The cardiovascular manifestations of the hypereosinophilic syndrome. Prospective study of 26 patients, with review of the literature. Am J Med. 1979 Oct;67(4):572–582
5.Weyman AE, Rankin R, King H. Loeffler's endocarditis presenting as mitral and tricuspid stenosis. Am J Cardiol 1977; 40: 438-44