Blood DNA methylation marks discriminate Chagas cardiomyopathy disease clinical forms.

Chagas disease is a parasitic disease from South America, affecting around 7 million people worldwide. Decades after the infection, 30% of people develop chronic forms, including Chronic Chagas Cardiomyopathy (CCC), for which no treatment exists. Two stages characterized this form: the moderate form, characterized by a heart ejection fraction (EF) ≥ 0.

Epigenetic regulation of transcription factor binding motifs promotes Th1 response in Chagas disease cardiomyopathy.

Chagas disease, caused by the protozoan , is an endemic parasitic disease of Latin America, affecting 7 million people. Although most patients are asymptomatic, 30% develop complications, including the often-fatal Chronic Chagasic Cardiomyopathy (CCC). Although previous studies have demonstrated some genetic deregulations associated with CCCs, the causes of their deregulations remain poorly described.

Rare Pathogenic Variants in Mitochondrial and Inflammation-Associated Genes May Lead to Inflammatory Cardiomyopathy in Chagas Disease.

Unlabelled: Cardiomyopathies are an important cause of heart failure and sudden cardiac death. Little is known about the role of rare genetic variants in inflammatory cardiomyopathy. Chronic Chagas disease cardiomyopathy (CCC) is an inflammatory cardiomyopathy prevalent in Latin America, developing in 30% of the 6 million patients chronically infected by the protozoan Trypanosoma cruzi, while 60% remain free of heart disease (asymptomatic (ASY)).

Corrigendum: Polymorphisms in Genes Affecting Interferon-γ Production and Th1 T Cell Differentiation Are Associated With Progression to Chagas Disease Cardiomyopathy.

[This corrects the article DOI: 10.3389/fimmu.2020.

Polymorphisms in Genes Affecting Interferon-γ Production and Th1 T Cell Differentiation Are Associated With Progression to Chagas Disease Cardiomyopathy.

Chagas disease, caused by the protozoan , is endemic in Latin America. Thirty percent of infected individuals develop chronic Chagas cardiomyopathy (CCC), an inflammatory dilated cardiomyopathy that is the most important clinical consequence of infection, while the others remain asymptomatic (ASY). IFN-γ and IFN-γ-producing Th1-type T cells are increased in peripheral blood and CCC myocardium as compared to ASY patients, while the Th1-antagonizing cytokine IL-10 is more expressed in ASY patients.

Dysregulation of insulin levels in Chagas heart disease is associated with altered adipocytokine levels.

Metabolic, inflammatory, and autonomic nervous system (ANS) dysfunction are present in patients with heart failure. However, whether these changes are due to left ventricular dysfunction or heart failure etiology is unknown. We evaluated metabolism and inflammatory activity in patients with idiopathic dilated cardiomyopathy (IDC) and Chagas cardiomyopathy (CHG) and their correlation with the ANS.

Archaea Symbiont of Infection May Explain Heart Failure in Chagas Disease.

Archaeal genes present in may represent symbionts that would explain development of heart failure in 30% of Chagas disease patients. Extracellular vesicles in peripheral blood, called exosomes (< 0.1 μm) or microvesicles (>0.

Left Atrial Function in Patients with Chronic Chagasic Cardiomyopathy.

Background: Chagas disease is a cause of dilated cardiomyopathy, and information about left atrial (LA) function in this disease still lacks.

Objective: To assess the different LA functions (reservoir, conduit and pump functions) and their correlation with the echocardiographic parameters of left ventricular (LV) systolic and diastolic functions.

Methods: 10 control subjects (CG), and patients with Chagas disease as follows: 26 with the indeterminate form (GI); 30 with ECG alterations (GII); and 19 with LV dysfunction (GIII).

Functional IL18 polymorphism and susceptibility to Chronic Chagas Disease.

Background: Chronic Chagas Disease cardiomyopathy (CCC), a life-threatening inflammatory dilated cardiomyopathy, affects 30% of the approximately 8 million patients infected by Trypanosoma cruzi, the rest of the infected subjects remaining asymptomatic (ASY). The Th1 T cell-rich myocarditis plays a pivotal role in CCC pathogenesis. Local expression of IL-18 in CCC myocardial tissue has recently been described.

Polymorphism in the alpha cardiac muscle actin 1 gene is associated to susceptibility to chronic inflammatory cardiomyopathy.

Aims: Chagas disease, caused by the protozoan Trypanosoma cruzi is endemic in Latin America, and may lead to a life-threatening inflammatory dilated, chronic Chagas cardiomyopathy (CCC). One third of T. cruzi-infected individuals progress to CCC while the others remain asymptomatic (ASY).

Genetic susceptibility to Chagas disease cardiomyopathy: involvement of several genes of the innate immunity and chemokine-dependent migration pathways.

Background: Chagas disease, caused by the protozoan Trypanosoma cruzi is endemic in Latin America. Thirty percent of infected individuals develop chronic Chagas cardiomyopathy (CCC), an inflammatory dilated cardiomyopathy that is, by far, the most important clinical consequence of T. cruzi infection.

Myocardial chemokine expression and intensity of myocarditis in Chagas cardiomyopathy are controlled by polymorphisms in CXCL9 and CXCL10.

Background: Chronic Chagas cardiomyopathy (CCC), a life-threatening inflammatory dilated cardiomyopathy, affects 30% of the approximately 8 million patients infected by Trypanosoma cruzi. Even though the Th1 T cell-rich myocarditis plays a pivotal role in CCC pathogenesis, little is known about the factors controlling inflammatory cell migration to CCC myocardium.

Methods And Results: Using confocal immunofluorescence and quantitative PCR, we studied cell surface staining and gene expression of the CXCR3, CCR4, CCR5, CCR7, CCR8 receptors and their chemokine ligands in myocardial samples from end-stage CCC patients.

Plasma pro-B-type natriuretic peptide testing as a screening method for hypertrophic cardiomyopathy.

Background: Clinical multistage risk assessment associated with electrocardiogram (ECG) and NT-proBNP may be a feasible strategy to screen hypertrophic cardiomyopathy (HCM). We investigated the effectiveness of a screening based on ECG and NT-proBNP in first-degree relatives of patients with HCM.

Methods And Results: A total of 106 first-degree relatives were included.

Evidence for T Cell Help in the IgG Response against Tandemly Repetitive Trypanosoma cruzi B13 Protein in Chronic Chagas Disease Patients.

The tandemly repetitive Trypanosoma cruzi B13 protein is an immunodominant antigen among Chagas disease patients. Such repetitive domains may behave as T-independent antigens. However, T cells can recognize B13 epitopes in an HLA class II-restricted fashion and could potentially provide cognate T cell help and boost antibody titers.

Serum NT pro-BNP: relation to systolic and diastolic function in cardiomyopathies and pericardiopathies.

Background: NT pro-BNP is a marker of systolic and diastolic dysfunction.

Objective: To determine NT pro-BNP levels in patients with chagasic, hypertrophic, and restrictive heart diseases, as well as with pericardial diseases, and their relation to echocardiographic measurements of systolic and diastolic dysfunction.

Methods: A total of 145 patients were divided into the following groups: 1) Chagas' heart disease (CHD)--14 patients; 2) hypertrophic cardiomyopathy (HCM)--71 patients; 3) endomyocardial fibrosis (EMF)--26 patients; 4) pericardial effusion (PE)--18 patients; and 5) constrictive pericarditis (CP)--16 patients.

Coronary flow reserve in sickle cell anemia.

Background: Patients with sickle cell anemia (SCA) frequently present with episodes of chest pain, alterations in the resting electrocardiogram, and changes in cardiac structure and functions.

Objective: To evaluate the effect of recurrent episodes of vaso-occlusion on the coronary microcirculation.

Methods: Coronary flow velocity and coronary flow reserve (CFR) of stable patients with SCA (n=10, 5 females, 24.

Lack of association of tumor necrosis factor-alpha polymorphisms with Chagas disease in Brazilian patients.

One third of Trypanosoma cruzi-infected individuals develop chronic Chagas disease cardiomyopathy (CCC) while the majority remains asymptomatic (ASY). About 30% of CCC patients develop heart failure due to end-stage inflammatory dilated cardiomyopathy. Increased production of tumor necrosis factor (TNF)-alpha has been described in all clinical forms of Chagas disease, and the highest levels are detected in CCC patients with severe ventricular dysfunction.

Relationship between outflow obstruction and left ventricular functional impairment in hypertrophic cardiomyopathy: a Doppler echocardiographic study.

Left ventricular outflow tract (LVOT) obstruction is predictive of a worse outcome in hypertrophic cardiomyopathy (HCM). In a detailed Doppler echocardiographic study of 178 selected HCM patients, the group of patients (n = 73) with the obstructive form (resting peak gradient > or = 30 mmHg) presented more hypertrophy and poorer systolic and diastolic left ventricular (LV) functions than the HCM group (n = 105) without obstruction. LVOT peak gradient was positively correlated with hypertrophy (P < 0.

[NT pro-BNP levels in pericardial diseases and how they are used as complementary evaluation method of diastolic restriction. Initial experience: 25 cases].

Objective: To determine whether NT pro-BNP levels are high in patients reporting pericardial diseases, as well as to investigate how they relate to diastolic dysfunction echocardiographic measures.

Methods: Twenty-five patients were split into two groups: 1) pericardial effusion (PE): 15 patients; 2) constrictive pericarditis (CP): 10 patients. A control group was made up with 30 individuals reporting no heart disease.

TNF gene polymorphisms are associated with reduced survival in severe Chagas' disease cardiomyopathy patients.

Chronic Chagas' disease cardiomyopathy (CCC) is the most important clinical outcome of infection by the parasite Trypanosoma cruzi, affecting 18 million individuals in Latin America. One-third of CCC patients develop heart failure due to end-stage dilated cardiomyopathy, and their survival is reduced by 50% compared to patients with other cardiomyopathies. Genetic susceptibility may play a role in the differential survival of severe CCC patients.

Plasma amino-terminal pro-B-type natriuretic peptide quantification in hypertrophic cardiomyopathy.

Background: Plasma B-type natriuretic peptide (BNP) is a sensitive functional marker in heart disease including hypertrophic cardiomyopathy (HCM). The utility of plasma amino-terminal pro-BNP (NT-proBNP) quantification in heart disease has been investigated, but there are no published data regarding this test in HCM.

Methods: Plasma NT-proBNP was assessed in 71 patients with HCM and in 40 healthy subjects.

Effect of Losartan on left ventricular diastolic function in patients with nonobstructive hypertrophic cardiomyopathy.

In hypertrophic cardiomyopathy (HC), diastolic dysfunction of the left ventricle is a prominent feature caused by myocardial hypertrophy and fibrosis. Angiotensin II has trophic and profibrotic effects on the heart, and the blockade of angiotensin II receptors reverses hypertrophy and fibrosis in human cardiac diseases and in animal HC. This study investigated the short-term (6 months) effects of losartan 100 mg/day in 20 patients with nonobstructive HC, with an emphasis on left ventricular (LV) diastolic dysfunction, compared with 10 patients with HC who were not treated.

Relationships among exercise capacity, hypertrophy, and left ventricular diastolic function in nonobstructive hypertrophic cardiomyopathy.

Aim: The aim of this study was to analyze the relationships among exercise capacity (EC), hypertrophy, and diastolic function in nonobstructive hypertrophic cardiomyopathy (NOHCM).

Methods And Results: Twenty-seven patients with NOHCM were studied. Left ventricular hypertrophy (LVH) was determined by appropriate echocardiographic indexes.

[Research of markers for the genes of the heavy chain of cardiac beta-myosin and myosin binding protein C in relatives of patients with hypertrophic cardiomyopathy].

Objective: To study the molecular markers for the genes of the heavy chain of cardiac beta-myosin and the myosin binding protein C in relatives of carriers of hypertrophic cardiomyopathy.

Methods: Twelve families who had anamnesis, physical exam, electrocardiogram, echocardiogram and blood collection for the genetic study through the chain reaction of polymerase.

Results: From the 227 relatives, 25% were ill-taken, with 51% men, with an average age of 35+/-19 (2 to 95) years old.

Assessment of the ventricular function of patients with advanced chronic obstructive pulmonary disease by using magnetic resonance imaging.

Objective: To assess the mechanisms that may be involved in the evolution of right and left ventricular dysfunction in patients with chronic obstructive pulmonary disease (COPD).

Methods: Magnetic resonance imaging was used in 11 control patients (group C) and 27 patients with COPD, who were divided into 2 groups, COPDc and COPDs, according to the presence or absence of right ventricular dysfunction, respectively. Doppler echocardiography was used for assessing the degree of pulmonary hypertension.