Processos patojenicos da tripanozomiase americana

Chagas, Carlos

doi:10.1590/s0074-02761916000200002

Cited by 82 publications

(48 citation statements)

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“…In 1916, in addition to giving a lecture in Buenos Aires (Chagas 1916a), he published two important articles, one on the pathogeny (Chagas 1916b) and the other on the acute phase of the disease (Chagas 1916c). In these papers, Chagas systematized his observations, justified his concepts and emphasized some points.…”

Section: Early Studies Of Chagas Disease In Lassancementioning

confidence: 99%

“…The limits of the chronic nervous form of Chagas disease have not yet been defined. Chagas (1916b) mentioned that acute or subacute symptoms appeared in some patients with chronic heart disease, with a worsened prognosis. He called this form chronic heart disease with acute exacerbations.…”

Section: Enlargement Of Knowledges On Chagas Diseasementioning

confidence: 99%

“…For this reason, this clinical form, as suggested by Chagas (1916b), started to be referred to as chronic form with acute reactivation.…”

Section: Enlargement Of Knowledges On Chagas Diseasementioning

confidence: 99%

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Evolution of the clinical and epidemiological knowledge about Chagas disease 90 years after its discovery

Prata

1999

Mem. Inst. Oswaldo Cruz

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Section: Early Studies Of Chagas Disease In Lassancementioning

confidence: 99%

Section: Enlargement Of Knowledges On Chagas Diseasementioning

confidence: 99%

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Evolution of the clinical and epidemiological knowledge about Chagas disease 90 years after its discovery

Prata

1999

Mem. Inst. Oswaldo Cruz

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“…A literatura sobre a doença de Chagas crônica humana, anterior aos estudos citados acima, registra apenas as referências ao parasitismo pelo T. cruzi em células da cortical das supra-renais, feitas por Chagas12 13 14 15 16 17, geralmente citando observações de Vianna43.…”

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Comparação do parasitismo da veia central da supra-renal com o de outros tecidos em chagásicos crônicos

P¹,

Reis²,

Mb³

et al. 1991

Rev. Soc. Bras. Med. Trop.

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Nos últimos anos descrevemos a existência de células musculares lisas na veia central das suprarenais parasitadas pelo T. cruzfi, o que foi confirmado por Barbosa Jr. e Andrade9. A literatura sobre a doença de Chagas crônica humana, anterior aos estudos citados acima, registra apenas as referências ao parasitismo pelo T. cruzi em células da cortical das supra-renais, feitas por Chagas12 13 14 15 16 17, geralmente citando observações de Vianna43.Em trabalho posterior3 9 mostramos ainda que 55% dos chagásicos crônicos falecidos em decorrên cia de insuficiência cardíaca congestiva (ICC) apre sentavam leiomiócitos da veia central da supra-renal parasitados pelo T. cruzi. Embora esta cifra seja bastante superior ao que a literatura registra sobre o encontro de parasitas no miocárdio8 23 44 (de 30 a 55% para a veia supra-renálica e de 18 a 36% para o coração), esta diferença pode não ser real por duas razões básicas: a) Os chagásicos nos quais se estuda ram as supra-renais e o miocárdio são diferentes e residiam em locais diversos, por isso as divergências entre nossos dados para as supra-renais e os de Koberle23; Widmer e Azevedo44; Andrade e Andra de® para o miocárdio podem ser interpretadas como Recebido para publicação em 13/12/90. devido a comportamentos variáveis das populações de chagásicos no que se refere à ocorrência de parasitas no seu organismo; b) nossa experiência tem mostrado que a quantidade de tecido examinado influi decisiva mente na freqüência do parasitismo, o que pode ser facilmente compreendido quando se leva em conta que a intensidade do parasitismo dos tecidos no chagásico crônico é, geralmente, baixa, exigindo, às vezes, o exame de centenas de cortes para o encontro de uma única célula parasitada.Tentando esclarecer tais questões'procuramos, em um mesmo grupo de chagásicos crônicos, compa rar a freqüência e a intensidade do parasitismo no parênquima e na veia supra-renálica com o no miocár dio, nos valendo de métodos histométricos. Além disso, utilizando a mesma metodologia estudamos o parasitismo da parede da veia cava, para avaliar eventual tropismo para tecido muscular venoso com concentração mais baixa de hormônios supra-rená-licos.

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New predictors of malignant ventricular arrhythmias in Chagas disease: searching for the holy grail

Barros

2015

Rev. Soc. Bras. Med. Trop.

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(Carlos Chagas, 1916) (1) Since the fi rst descriptions of Chagas disease (ChD), sudden death is considered one of the characteristics and responsible for >50% of the mortality in chagasic patients with heart failure. In this issue of RSBMT, Barbosa et al (2) . highlight several important aspects of the pathogenesis, prognosis, and treatment of ventricular arrhythmias in ChD (2) . Chagas disease has an essentially arrhythmogenic nature characterized by dense and complex ventricular arrhythmias; therefore, ventricular fi brillation likely constitutes the terminal event in most cases of sudden death, which accounts for the majority of deaths in ChD. Chagas cardiomyopathy gives rise to the most intense fi brous reaction amongst all causes of myocarditis, leading to severe disorganization of the myocardial architecture and structure. In addition to the fi brotic substrate, electrical dispersion plays an important role in arrhythmogenesis, and it is caused by areas of slow conduction leading to electrical instability. Myocardial fi brosis and areas of slow electrical conduction result in mechanical alterations in both timing and function. With the development of therapeutic strategies to prevent death from ventricular fi brillation, particularly the use of implantable cardioverter-defi brillators (ICDs), accurate patient stratifi cation based on the future risk of arrhythmic events has become very relevant in ChD (3) .A major therapeutic goal in the management of Chagas cardiomyopathy is prevention of sudden cardiac death. While ICD therapy is the standard treatment for secondary prevention of cardiac arrest, the strategy for primary prevention of cardiac arrest in Chagas cardiomyopathy is much more controversial. Although several clinical features have been assessed as possible risk factors for the development of fatal arrhythmias, the sensitivity and specifi city of any single test to predict fatal arrhythmias are limited. For example, left ventricular dysfunction is recognized as a strong general risk predictor, particularly for arrhythmic death in ChD (4) ; however, the mere presence of a depressed left ventricular ejection fraction (LVEF) is not sensitive or specifi c enough to stratify the risk of sudden death. Most patients with ChD that have an ICD for secondary prevention and thus have experienced a potentially fatal arrhythmic event have an LVEF >30%. Electrocardiographic techniquesIn the last few years, several new electrocardiographic methods have been used to predict mortality in ChD including measurement of the length of the QRS and QT intervals from a standard 12-lead ECG, which is a simple and inexpensive method of risk assessment in ChD. QT dispersion is associated with left ventricular (LV) systolic dysfunction, and both increased QT dispersion and QT interval are related to a higher risk of death in ChD patients (5) . Moreover, in another study performed in the same study sample, T-wave axis deviation was a strong and independent predictor of mortality risk. Furthermore,

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Processos patojenicos da tripanozomiase americana

Cited by 82 publications

References 0 publications

Evolution of the clinical and epidemiological knowledge about Chagas disease 90 years after its discovery

Evolution of the clinical and epidemiological knowledge about Chagas disease 90 years after its discovery

Comparação do parasitismo da veia central da supra-renal com o de outros tecidos em chagásicos crônicos

New predictors of malignant ventricular arrhythmias in Chagas disease: searching for the holy grail

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