Chagas Heart Failure in Patients from Latin America

Bestetti, Reinaldo B.

doi:10.15420/cfr.2016:14:2

Cited by 11 publications

(18 citation statements)

References 60 publications

(64 reference statements)

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“…CD is classified evolutionary into two phases: an initial acute phase, followed by a chronic phase. Each phase has distinct clinical characteristics, diagnostic parameters, and treatment [72][73][74][75][76]. The acute phase is characterized by intense parasitism related with nonspecific symptoms, including fever, eyelid edema (denominated Chagoma), edema, and myocarditis.…”

Section: Symptomatic Treatment Of Chronic Phasementioning

confidence: 99%

“…Chronic Chagas cardiomyopathy (CCC) is associated with high rates of morbidity and mortality, and it is categorized into stages of cardiac impairment (A, B, C, and D) according to the manifestations, electrocardiograph, radiological alterations, and changes in ventricular function [72,74,75,82,83]. Approximately 20-40% of patients with the indeterminate form will develop CCC.…”

Section: Chronic Chagas Cardiomyopathy (Ccc)mentioning

confidence: 99%

“…The efficacy and tolerability of these drugs in patients with CCC is extrapolated from the results obtained for other etiologies. Therefore, the CCC treatment is suggested to be performed in accordance with the general guidelines for HF treatment and should consist of the combination of three therapeutic classes: angiotensin-converting enzyme inhibitors (ACEI) or angiotensin receptor blockers (ARB), diuretics, and adrenergic beta blockers (BB) [40,72,82].…”

Section: Chronic Chagas Cardiomyopathy (Ccc)mentioning

confidence: 99%

“…Angiotensin-converting enzyme inhibitors (ACEI) or angiotensin receptor blockers (ARB) have an essential role in adverse cardiac remodeling and ventricular dysfunction progression of HF [40,72,82]. In experimental studies reported in the literature, captopril and enalapril demonstrated to diminish myocarditis and fibrosis of CCC [85][86][87][88].…”

Section: Chronic Chagas Cardiomyopathy (Ccc)mentioning

confidence: 99%

“…Moreover, digoxin and diuretics are considered a pharmacological option in CCC, justifying the use of digoxin for patients with symptomatic LVEF ≤45%, principally in the presence of atrial fibrillation when the ventricular frequency is increased and diuretics to improve congestive symptoms and signs. For advanced HF stages, the combination of thiazides with loop diuretics has been proven to be more effective [25,72,73,79,83].…”

Section: Chronic Chagas Cardiomyopathy (Ccc)mentioning

confidence: 99%

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Efficacy and Safety of Chagas Disease Drug Therapy and Treatment Perspectives

Kawaguchi¹,

Cerqueira²,

MillanFachi³

et al. 2018

Chagas Disease - Basic Investigations and Challenges

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Chagas disease, also known as American trypanosomiasis, is a neglected disease caused by the protozoan parasite Trypanosoma cruzi. The disease affects about 6-7 million people worldwide, mostly in Latin America. Although Chagas disease was discovered more than 100 years ago, and the first treatments over 40, only 2 drugs were used to treat this pathology, it is still considered one of the neglected diseases. In this chapter, the subjects related to conventional etiological therapies, benznidazole and nifurtimox, such as the drug, the mechanism of action, the therapy schedule for treatment, efficacy and safety and their adverse effects will be discussed. Additionally, it will address alternative therapies of comorbidities related to the progression of Chagas' disease in patients with chronic disease, such as heart disease and dysfunction of the digestive system. Finally, novel pharmacological strategies and their related compounds will be reviewed accounting for their progression in pharmacological studies and their success rate.

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Section: Symptomatic Treatment Of Chronic Phasementioning

confidence: 99%

Section: Chronic Chagas Cardiomyopathy (Ccc)mentioning

confidence: 99%

Section: Chronic Chagas Cardiomyopathy (Ccc)mentioning

confidence: 99%

Section: Chronic Chagas Cardiomyopathy (Ccc)mentioning

confidence: 99%

Section: Chronic Chagas Cardiomyopathy (Ccc)mentioning

confidence: 99%

See 3 more Smart Citations

Efficacy and Safety of Chagas Disease Drug Therapy and Treatment Perspectives

Kawaguchi¹,

Cerqueira²,

MillanFachi³

et al. 2018

Chagas Disease - Basic Investigations and Challenges

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Association between myocardial mechanical dispersion and ventricular arrhythmogenicity in chagas cardiomyopathy

Azevedo

Barros

Klaboe

et al. 2021

Int J Cardiovasc Imaging

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Endemic Chagas diseaseis a major health concernin LatinAmerica. Ventricular arrhythmias (VA) is a hallmark of Chagas cardiomyopathy (ChC) associated with worse prognosis. To verify if there is an association between myocardial mechanical dispersion and ventricular arrhythmogenicity in CCM. This is a cross-sectional study involving 77 patients with CCM. Global longitudinal strain (GLS) and MD were evaluated by echocardiogram, derived from the speckle tracking technique. Myocardial MD was measured from the onset of the Q / R wave on electrocardiogram to the peak longitudinal strain in 16 segments of the left ventricle. Frequency and complexity of ventricular extrasystoles (VES) were assessed by dynamic electrocardiography. The density and complexity of VES and the presence of non-sustained ventricular tachycardias (NSVTs) increase as MD increases. In logistic regression, MD was the only variable associated with the presence of VES in pairs and bigeminy. In the univariate analysis, both MD and GLS were associated with the presence of NSVT (both, p < 0.01), and MD was independently associated with NSVT (OR 1.04, 95% CI: 1.004-1.201, p = 0.031). In Chagas cardiomyopathy, MD is associated with a higher density and complexity of ventricular extrasystoles, including NSVT.

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Trypanosoma cruzi Infection Promotes Vascular Remodeling and Coexpression of α-Smooth Muscle Actin and Macrophage Markers in Cells of the Aorta

et al. 2022

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Chagas disease is an emerging global health problem; however, it remains neglected. Increased aortic stiffness (IAS), a predictor of cardiovascular events, has recently been reported in asymptomatic chronic Chagas patients. After vascular injury, smooth muscle cells (SMCs) can undergo alterations associated with phenotypic switch and transdifferentiation, promoting vascular remodeling and IAS. By studying different mouse aortic segments, we tested the hypothesis that Trypanosoma cruzi infection promotes vascular remodeling. Interestingly, the thoracic aorta was the most affected by the infection. Decreased expression of SMC markers and increased expression of proliferative markers were observed in the arteries of acutely infected mice. In acutely and chronically infected mice, we observed cells coexpressing SMC and macrophage (Mo) markers in the media and adventitia layers of the aorta, indicating that T. cruzi might induce cellular processes associated with SMC transdifferentiation into Mo-like cells or vice versa. In the adventitia, the Mo cell functional polarization was associated with an M2-like CD206+arginase-1+ phenotype despite the T. cruzi presence in the tissue. Only Mo-like cells in inflammatory foci were CD206+iNOS+. In addition to the disorganization of elastic fibers, we found thickening of the aortic layers during the acute and chronic phases of the disease. Our findings indicate that T. cruzi infection induces a vascular remodeling with SMC dedifferentiation and increased cell populations coexpressing α-SMA and Mo markers that could be associated with IAS promotion. These data highlight the importance of studying large vessel homeostasis in Chagas disease.

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Chagas Heart Failure in Patients from Latin America

Cited by 11 publications

References 60 publications

Efficacy and Safety of Chagas Disease Drug Therapy and Treatment Perspectives

Efficacy and Safety of Chagas Disease Drug Therapy and Treatment Perspectives

Association between myocardial mechanical dispersion and ventricular arrhythmogenicity in chagas cardiomyopathy

Trypanosoma cruzi Infection Promotes Vascular Remodeling and Coexpression of α-Smooth Muscle Actin and Macrophage Markers in Cells of the Aorta

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