{"title":"New proposals for diagnosis and treatment of the chronic period without demonstrable pathology of Chagas disease","authors":"L. Giménez, J. Mitelman","doi":"10.15406/JCCR.2018.11.00409","DOIUrl":null,"url":null,"abstract":"Introduction Pathophysiology Intervening factors in the development of cardiomyopathy 1. Intrensic myocardial damage during the acute and chronic phase because of: a) Direct parasitic action. b) Immunological disturbances. c) Neurological damage. 2. Induced disorders due to the host immune response. 3. Alterations in the automatic nervous system. 4. Microvascular lesions with alterations in the microcirculation and subsequent myocytolysis.1 Our research group proposes a score of clinical outcomes, with validated studies and proposed treatment for subclinical lesions (autonomic, endothelial anatomical) early to prevent the development of Chagas cardiomyopathy. Integrated Score is to detect early alterations that would lead to the development of cardiac complications in chronic patients without proven pathology. Risk analysis With the approach of the disease using tools and diagnostic tests sufficiently validated and according to the association between them, it is determined to follow up the most committed patients and use different therapies according to the damage found. It is important to note that other studies may be used to detect subclinical lesions that have the same kind of recommendation and the same level of evidence used in this score. We believe that the persistence of the parasite in the infected organism would not be the only mechanism that would have a determinate role in the development of the pathogenesis of the illness and consequently even a successful etiological treatment would not be able to avoid the development of the terminal lesions characterized by the disease (Table 1).2,3","PeriodicalId":15200,"journal":{"name":"Journal of Cardiology & Current Research","volume":"11 1","pages":"243-244"},"PeriodicalIF":0.0000,"publicationDate":"2019-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Cardiology & Current Research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.15406/JCCR.2018.11.00409","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Introduction Pathophysiology Intervening factors in the development of cardiomyopathy 1. Intrensic myocardial damage during the acute and chronic phase because of: a) Direct parasitic action. b) Immunological disturbances. c) Neurological damage. 2. Induced disorders due to the host immune response. 3. Alterations in the automatic nervous system. 4. Microvascular lesions with alterations in the microcirculation and subsequent myocytolysis.1 Our research group proposes a score of clinical outcomes, with validated studies and proposed treatment for subclinical lesions (autonomic, endothelial anatomical) early to prevent the development of Chagas cardiomyopathy. Integrated Score is to detect early alterations that would lead to the development of cardiac complications in chronic patients without proven pathology. Risk analysis With the approach of the disease using tools and diagnostic tests sufficiently validated and according to the association between them, it is determined to follow up the most committed patients and use different therapies according to the damage found. It is important to note that other studies may be used to detect subclinical lesions that have the same kind of recommendation and the same level of evidence used in this score. We believe that the persistence of the parasite in the infected organism would not be the only mechanism that would have a determinate role in the development of the pathogenesis of the illness and consequently even a successful etiological treatment would not be able to avoid the development of the terminal lesions characterized by the disease (Table 1).2,3