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Proteomic analysis of cardiac tissue of endomyocardial fibrosis patients

Grant number: 10/04943-9
Support type:Scholarships in Brazil - Master
Effective date (Start): August 01, 2010
Effective date (End): June 30, 2012
Field of knowledge:Biological Sciences - Immunology - Cellular Immunology
Principal Investigator:Edecio Cunha Neto
Grantee:Aline Siqueira Bossa
Home Institution: Instituto do Coração Professor Euryclides de Jesus Zerbini (INCOR). Hospital das Clínicas da Faculdade de Medicina da USP (HCFMUSP). Secretaria da Saúde (São Paulo - Estado). São Paulo , SP, Brazil

Abstract

Endomyocardial fibrosis (EMF) is an idiopathic restrictive cardiomyopathy with malignant course, characterized by the deposition of fibrous tissue in the endocardial surface and to a lesser extent in the myocardial, with or without calcification, causing diastolic dysfunction and heart failure.The disease is present in tropical and subtropical regions of the world and is endemic in sub-Saharan Africa and is often observed in children and young adults. In Brazil, the disease has a predilection for females and usually affects individuals in the fourth decade of life. There are many theories to explain the etiology, which includes several factors, such as viral infections, parasitic infections, autoimmunity and nutritional deficiencies. The most accepted theory is related to helminth infections and hypereosinophilia, since eosinophilia is observed in approximately 20% of the biopsies of cardiac tissue of patients with EMF, and the morphological lesions are similar to those seen in the hypereosinophilic syndrome caused by helminths. In addition, areas where EMF is endemic also have a high prevalence of parasites.EMF has an insidious onset, his symptoms are late and involve dysfunction of specific chambers and valves. Since there is no specific drugs for treatment, the main alternative consists of surgical resection of fibrosis. However, reports of recurrence suggest that this intervention is only palliative. Moreover, the mortality is high (15-20%) and survival of patients undergoing this treatment is only 50% in four years. Studies indicate that the EMF is the result of a chronic inflammatory process that contributes to the fibrosis of the endocardium and heart damage due to causes probably multifactorial, but unknown. If clarified the roles of possible inducing factors related to EMF, we could elucidate the pathogenesis of the disease and suggests new measures of treatment for these patients. Therefore, we think of fundamental importance to study which proteins are expressed in heart tissue of patients with EMF, as this analysis indicates that the metabolic pathways are altered, allowing to know which of these changes also contribute to the fibrosing process in the EMF and what factors could be related to recurrence of fibrosis compared to patients without recurrence.