Chagas Heart Disease Research Articles

Chagasic megacolon: First report and management in a case from the 24 de Mayo canton, Manabí province, Ecuador

Introduction: Chagas disease is a disease belonging to the group of Neglected Tropical Diseases. The vector is Trypanosoma cruzi. In this context, Chagas megacolon constitutes an underdiagnosed condition in favor of Chagas heart disease. Case report: Consequently, a clinical case is presented in an 80-year-old male patient. The set of clinical parameters such as chronic constipation, fecaloma; Megacolon imaging and serological results of specific antibodies against Trypanosoma cruzi led to the diagnosis of Chagasic megacolon, with surgical intervention on three occasions for correction and treatment. Discussion: Prevention through vector control is essential in the fight against this disease. The main strategies should focus on the construction of decent homes, free of domestic animals inside, such as chicken coops, pigeon coops, hutches, caves, nests and other shelters for animals, where the vector could proliferate.Conclusion: It is the first report of Chagas megacolon in the province of Manabí. The need to promote greater clinical, epidemiological and comprehensive psychological care is highlighted for its prevention, diagnosis and treatment.

Vitamin D treatment distinctly modulates cytokine production by peripheral blood mononuclear cells among patients with chronic cardiac and indeterminate clinical forms of Chagas disease.

Chagas disease is caused by the protozoan Trypanosoma cruzi and is clinically divided into acute and chronic phases. Chronic Chagas cardiomyopathy is the most studied manifestation of the disease. Vitamin D deficiency has been suggested as a risk factor for cardiovascular disease. No studies demonstrate the action of this hormone in the cells of patients with chronic Chagas heart disease. To evaluate the in vitro immunomodulatory effect of vitamin D on peripheral blood mononuclear cellsof patients with the different chronic clinical forms of Chagas disease. Evaluating vitamin D's in vitro effect on blood cells by producing cytokines. Thirteen patients of the undetermined form (IND), 13 of the mild cardiac form (CARD1) and 14 of the severe cardiac form (CARD2) of Chagas disease, and 12 with idiopathic heart disease (CARDid) were included. The cells obtained from peripheral blood were treated in vitro with vitamin D (1 × 10-7 M) for 24 h and cytokines were dosed in the culture supernatant. Although it was not possible to demonstrate statistically significant differences between the groups studied, our data showed that the cells treated with vitamin D modify (p < .05) the production of interferon-γ(IFN-γ) (decrease in IND), tumor necrosis factor-α (TNF-α) (decreased in CARD1 and CARDid),interleukin(IL)-6 (increased in all groups), and IL-10 (decreased in CARD1, CARD2, and CARDid) when compared to untreated cells. In vitro treatment with vitamin D distinctly modulated the production of cytokines by mononuclear cells of peripheral blood among patients with chronic and indeterminate cardiac clinical forms of Chagas disease.

Multimodality Imaging of Chagas Heart Disease: Review and Case Presentation

Multimodality Imaging of Chagas Heart Disease: Review and Case Presentation

Early detection of cardiac autonomic dysfunction using the respiratory sinus arrhythmia accentuation maneuver in patients with stage B1 of Chagas Disease

Introduction: The maneuver to accentuate respiratory sinus arrhythmia (RSA) demonstrates to be a convenient instrument to evaluate the autonomic modulation of individuals with chronic Chagas disease cardiomyopathy (CCC), even with medication influence, as T-cruzi causes an inflammatory process creating lesions in the cardiac nerve endings of patients affected by Chagas disease. Objective: To evaluate the autonomic modulation of heart rate (HR) at rest and during the respiratory sinus arrhythmia accentuation maneuver (RSA-M) in patients with CCC in stage B1. Methods: thirty-six individuals were evaluated, divided into the CCC group, composed of 18 patients with Chagas heart disease, and the control group, formed by 18 healthy individuals. Heart rate variability (HRV) was collected beat by beat using the electrocardiography system Wincardio USB, supine for 10 minutes, and during the RSA-M for 6 minutes. Results: We observed higher values of statistical significance in Control group for mean HR (p = 0.005), IRR (p = 0.007), and worse autonomic adjustments related to SD2 / SD1 (p = 0.001) concerning CCC group in a supine position. However, evaluating the RSA-M, we observed a statistical difference in the delta I-E (p = 0,039) and the E / I rate (p = 0.045) of the Control group in relation to the CCC group. Conclusion: Patients with CCC showed better cardiovascular condition and HR control compared to the group of healthy individuals at rest. However, when subjected to RSA-M, the results showed a reduction in vagal balance in the autonomic control of individuals with CCC. Keywords: respiration; heart rate; chagas cardiomyopathy; autonomic nervous system diseases.

Right-Sided Cardiac Thrombosis and Pulmonary Thromboembolism in Chronic Chagas Disease: A Review of Clinical Features and Post-Mortem Examination.

Pulmonary thromboembolism (PE) is a potential major complication in patients with chronic Chagas heart disease (CChD). The source of PE is the right-sided chambers instead of deep vein thrombosis. Little is known regarding risk factors, clinical picture, and the clinical course of patients with PE secondary to CChD. The aim of this review was to try to provide doctors with such data. We searched for papers related to PE in CChD patients in the PUBMED from 1955 to 2020. Twenty-six manuscripts were retrieved, of which 12 fulfilled entry criteria and were included in the study. Right-sided cardiac thrombosis or PE was confirmed on morphological or imaging studies. A total of 431 patients with PE were reported. Age varied from 30 to 85 years. About 332 patients were reported to have chronic heart failure (CHF), whereas 41 (9%) sudden cardiac death (SCD) at autopsy. Clinical manifestations reported were sudden onset dyspnea was found in 1 patient, haemoptysis in 2, worsening CHF in 2, and chest pain in 1. An X-ray chest was reported for 6 patients: abnormalities consistent with PE were found in 3. The resting electrocardiogram (ECG) was reported for 5 patients: it was abnormal in all. One study reported a mean left ventricular ejection fraction of 42.1 18.7%. The prevalence of right-sided cardiac thrombosis varied from 66% to 85% patients. PE was the cause of death in 17% of patients. The clinical diagnosis of PE in patients with Chagas cardiomyopathy (ChCM) is very difficult in the absence of a prediction score that performs well. However, in the presence of haemoptysis or worsening heart failure (HF), abnormal ECG, or chest X-ray, the diagnosis of PE should be raised, and patients promptly referred to detailed Doppler Tissue Echocardiography and computed tomography angiography, and treated in a timely manner.

Chagas Cardiomyopathy and Myocardial Sympathetic Denervation.

More than a century since its discovery, the pathogenesis of Chagas heart disease (CHD) remains incompletely understood. The role of derangements in the autonomic control of the heart in triggering malignant arrhythmia before the appearance of contractile ventricular impairment was reviewed. Although previous investigations had demonstrated the anatomical and functional consequences of parasympathetic dysautonomia upon the heart rate control, only recently, coronary microvascular disturbances and sympathetic denervation at the ventricular level have been reported in patients and experimental models of CHD, exploring with nuclear medicine methods their impact on the progression of myocardial dysfunction and cardiac arrhythmias. More important than parasympathetic impaired sinus node regulation, recent evidence indicates that myocardial sympathetic denervation associated with coronary microvascular derangements is causally related to myocardial injury and arrhythmia in CHD. Additionally, 123I-MIBG imaging is a promising tool for risk stratification of progression of ventricular dysfunction and sudden death.

Inspiratory muscle endurance is similarly reduced in the early and late stages of chronic Chagas heart disease.

Inspiratory muscle strength (IMS) appears to be reduced in subjects with chronic Chagas heart disease (CHD), especially in the presence of heart failure (HF). However, only one study about IMS and inspiratory muscle endurance (IME) in those with CHD without heart failure is available. This study aimed to compare IMS and IME in subjects with CHD in the presence and absence of HF. This is a cross-sectional study in which 30 CHD adult patients were divided into CHD-CC group (initial phase of CHD, without HF; n = 15) and CHD-HF group (advanced phase of CHD, with HF; n = 15). We assessed IMS by maximum inspiratory pressure (MIP) and IME by incremental (Pthmax) and constant load (TLim) tests. Reduced IMS and IME were considered by predicted MIP values <70% and Pthmax/MIP <75%, respectively. Inspiratory muscle weakness (IMW) was more frequent in CHD-HF than in CHD-CC (46.7% vs. 13.3%; p = 0.05), and both groups had high frequencies of reduced IME (93.3% CHD-CC vs. 100.0% CHD-HF; p = 0.95). Age-adjusted logistic regression analysis using HF as a dependent variable showed that HF was associated with an increased chance of IMW compared with the CHD-CC group (OR = 7.47; p = 0.03; 95% CI 1.20-46.19). This study suggests that, in patients with CHD, HF is associated with IMW, and that reduction of IME is already present in the initial phase, similar to the advanced phase with HF.

TNF blockers alone and associated with Benznidazole impact in vitro cytokine dynamics in chronic Chagas disease.

Studies involving the immune response in Chagas disease suggest an imbalance in the immune response of symptomatic patients, with an inflammatory profile dominating in Chagas heart disease, mainly by tumour necrosis factor (TNF). TNF is considered a key cytokine in immunopathology in chronic carriers in several processes during the immune response. Our work aimed to evaluate regulatory (interleukin [IL]-4 and IL-10) and inflammatory (TNF, interferon-gamma [IFN-γ], IL-2 and IL-6) cytokines in peripheral blood mononuclear cells culture supernatants. of affected patients with undetermined clinical forms-IND (n = 13) mild heart form-CARD1 (n = 13) and severe cardiac form-CARD2 (n = 16), treated in vitro with two TNF blockers, Adalimumab (ADA) and Etanercept (ETA) alone or in association with Benznidazole (BZ). The results indicate that ADA was more competent in blocking TNF (compared to ETA) in all groups but with much lower levels in the CARD2 group. ETA statistically decreased TNF levels only in the CARD2 group. IFN-γ increased in the CARD2 group after treatment with ETA relative to ADA. IL-4 had its levels decreased when treated by both drugs. IL-2 was detected in cells from CARD2 carriers compared to the NEG group after treatment with both drugs. The association with BZ decreased levels of IL-2/TNF and increased IL-4. These data reinforce the participation of TNF in severe Chagas heart disease and bring perspectives on using these blockers in the immunological treatment of Chagas disease since the use of BZ is extremely limited in these patients.

Molecular mimic between cardiovascular diseases and microorganism antigens

Cardiovascular diseases are the result of genetic and environmental interaction that conditions the integrity of the heart and blood vessels. Risk factors include infections. The inflammatory response against the infectious agent is a trigger of autoimmune cardiovascular diseases due to the similarity between the pathogen proteins and human antigens, since the immune response can present cross-reactivity caused by molecular mimicry. We performed a search for pathogens involved in autoimmune heart diseases and autoantigens 9 associated with these diseases in the Pubmed and Google Scholar search engines. Identity between proteins was performed through global alignments using PSI-BLAST. The 3D structures of the proteins were obtained by Uniprot or NCBI and, if not found, the structure was modeled by homology using the Swiss Model server. Epitope prediction was performed through Ellipro and the Immunological Epitope Database (IEDB). In addition, the PYMOL program was used to visualize proteins in 3D and position the epitopes in the structure. A total of ten cardiovascular proteins showed identity (30-88,24%) in their amino acid sequences with antigens from 10 pathogens. Actin proteins and heat shock protein (HSP) families had higher levels of identity with Trypanosoma Cruzi, Cryptococcus neoformans, and Chlamydia trachomatis, 71,47%, 88,24%, and 80,61%, respectively. Other pathogens, such as Streptococcus pyogenes, Bacillus sp, Magnetospirillum gryphiswaldense, Helicobacter pylori and Chlamydia pneumoniae, presented a moderate identity with a maximum value of 65,79%. Human actin and HSPs share a high degree of conservation with epitopes from various microorganisms, such as bacteria, fungi and protozoa, suggesting molecular mimicry and cross-reactivity as a mechanism for the development of atherosclerosis, heart disease rheumatic disease, myocarditis and Chagas heart disease. In vitro and in vivo work is needed to demonstrate the results obtained in the In Silico analysis.

Discovery of circulating miRNAs as biomarkers of chronic Chagas heart disease via a small RNA-Seq approach

Chagas disease affects approximately 7 million people worldwide in Latin America and is a neglected tropical disease. Twenty to thirty percent of chronically infected patients develop chronic Chagas cardiomyopathy decades after acute infection. Identifying biomarkers of Chagas disease progression is necessary to develop better therapeutic and preventive strategies. Circulating microRNAs are increasingly reliable biomarkers of disease and therapeutic targets. To identify new circulating microRNAs for Chagas disease, we performed exploratory small RNA sequencing from the plasma of patients and performed de novo miRNA prediction, identifying potential new microRNAs. The levels of the new microRNAs temporarily named miR-Contig-1519 and miR-Contig-3244 and microRNAs that are biomarkers for nonchagasic cardiomyopathies, such as miR-148a-3p and miR-224-5p, were validated by quantitative reverse transcription. We found a specific circulating microRNA signature defined by low miR-Contig-3244, miR-Contig-1519, and miR-148a-3 levels but high miR-224-5p levels for patients with chronic Chagas disease. Finally, we predicted in silico that these altered circulating microRNAs could affect the expression of target genes involved in different cellular pathways and biological processes, which we will explore in the future.

Predictors of Appropriate Therapies and Death in Patients with Implantable Cardioverter-Defibrillator and Chronic Chagas Heart Disease.

There are few retrospective and prospective studies on implantable cardioverter-defibrillators (ICD) in primary and secondary prevention of sudden death in chronic Chagas heart disease (CCHD). To describe the long-term evolution of patients with CCHD and ICD and to identify and analyze predictors of mortality and appropriate device therapy in this population. This was a historical prospective study with 117 patients with ICD and CCHD. Devices were implanted from January 2003 to December 2021. Predictors of appropriate therapies and long-term mortality were identified and analyzed. The level of statistical significance was p < 0.05. Patients (n = 117) had a median follow-up of 61 months (25 to 121 months); they were predominantly male (74%), with a median age of 55 years (48 to 64 years). There were 43.6% appropriate shocks, 26.5% antitachycardia pacing (ATP), and 51% appropriate therapies. During follow-up, 46 patients (39.7%) died. Mortality was 6.2% person-years (95% confidence interval [CI]: 4.6 to 8.3), with 2 sudden deaths during follow-up. Secondary prevention (hazard ratio [HR] 2.1; 95% CI: 1.1 to 4.3; p = 0.029) and ejection fraction less than 30% (HR 1.8; 95% CI: 1.1 to 3.1; p < 0.05) were predictors of appropriate therapies. Intermediate Rassi score showed a strong association with the occurrence of ATP alone (p = 0.015). Functional class IV (p = 0.007), left ventricular ejection fraction < 30 (p = 0.010), and age above 75 years (p = 0.042) were predictors of total mortality. ICDs in CCHD showed a high incidence of appropriate activation, especially in patients with secondary prevention, low left ventricular ejection fraction, and intermediate Rassi score. Patients with congestive heart failure, elevated functional class, and age over 75 years showed elevated mortality. Survival function of patients with implantable cardioverter-defibrillators and chronic Chagas heart disease. A - According to New York Heart Association functional class; B - According to left ventricular ejection fraction; C - According to Rassi score. D - According to age. CCHD: chronic Chagas heart disease; HR: hazard ratio; ICD: implantable cardioverter-defibrillator.

Chagas Disease, A Review of the Literature

Chagas disease is a vector-borne (triatomine) infection caused by the protozoan parasite Trypanosoma cruzi. Synonyms for this disease are: American trypanosomiasis, Chagas disease and T. cruzi infection. 10, 5 The most common form of transmission of Chagas disease is through hematophagous triatomine insects (triatominae), which develop in dwellings in precarious conditions, The disease can also be transmitted by blood transfusion, organ transplantation, oral and congenital routes, and even more rarely by exceptional routes such as sexual contact and non-Triatominae vectors. American Trypanosomiasis is endemic in much of Mexico, Central and South America 1,11. it is estimated that ~6 million individuals are infected throughout Latin America, while ~300,000 are infected in the U.S.1, 10, 11,16 Chagas disease has two clearly differentiated phases. Initially, the acute phase lasts about two months after infection, they may have a skin lesion or a purplish swelling of an eyelid, they may have fever, headache, enlarged lymph nodes, pallor, muscle aches, shortness of breath, swelling, and abdominal or chest pain. During the chronic phase, the infection can cause sudden death due to cardiac arrhythmias or progressive heart failure due to destruction of the cardiac muscle and its innervations. 15 Appropriate diagnostics for acute infection, nucleic acid amplification testing (NAAT) from blood is recommended; For chronic infection, serological testing is employed. Antitrypanosomal agents, benznidazole and nifurtimox, have shown efficacy in treating T. cruzi infection, The most serious complication is chronic chagasic heart disease, since it is the main cause of death in sick patients. 16

Importance of CD40/CD40L dyad in the course of infection with Trypanosoma cruzi: Impact of its inhibition

Chagas heart disease (CHD), caused by the protozoan parasite Trypanosoma cruzi, consists of a progressive myocarditis which may lead to congestive heart failure or sudden death. Previous work from our laboratory has demonstrated that the experimental infection of mice with T. cruzi positively modulates the expression of CD40 by myocardial cells, whose ligation potentiates IFN-γ-induced IL-6 production. Herein, we investigate the role of the CD40/CD40L interaction during T. cruzi infection using a CD40-targeted peptide and evaluating parasitological, histopathological and serological parameters. To reproduce acute and chronic phases of theT. cruzi infection, we used two experimental models: Balb/c mice infected with RA strain of T. cruzi (Balb/c-RA) and C3H/HeN mice infected with Sylvio X-10/4 parasites (C3H/HeN-Sylvio), respectively. Balb/c-RA treated with CD40-tageted peptide since day 0 post infection (pi), were unable to control the acute infection dying within 23–26 days pi with marked tissue damage. In contrast, treatment of C3H/HeN-Sylvio treated with CD40-targeted peptide starting on day 30 pi resulted in amelioration of myocardial and skeletal muscle damage. Altogether, our results indicate a dual role of CD40/CD40L dyad in the control of T.cruzi infection as well as the associated pathology, depending on the timing of treatment initiation.

Use of PET/CT to detect myocardial inflammation and the risk of malignant arrhythmia in chronic Chagas disease.

Chagas heart disease (CHD) is characterized by progressive myocardial inflammation associated with myocardial fibrosis and segmental abnormalities that may lead to malignant ventricular arrhythmia and sudden cardiac death. This arrhythmia might be related to the persistence of parasitemia or inflammation in the myocardium in late-stage CHD. Positron emission tomography/computed tomography (PET/CT) has been used to detect myocardial inflammation in non-ischemic cardiomyopathies, such as sarcoidosis, and might be useful for risk prediction in patients with CHD. Twenty-four outpatients with chronic CHD were enrolled in this prospective cross-sectional study between May 2019 and March 2022. The patients were divided into two groups: those with sustained ventricular tachycardia and/or aborted sudden cardiac death who required implantable cardioverter-defibrillators, and those with the same stages of CHD and no complex ventricular arrhythmia. Patients underwent 18F-fluorodeoxyglucose (18F-FDG) and 68Ga-DOTATOC PET/CT, and blood samples were collected for qualitative parasite assessment by polymerase chain reaction. Although similar proportions of patients with and without complex ventricular arrhythmia showed 18F-FDG and 68Ga-DOTATOC uptake, 68Ga-DOTATOC corrected SUVmax was higher in patients with complex arrhythmia (3.4 vs 1.7; P = .046), suggesting that inflammation could be associated with the presence of malignant arrhythmia in the late stages of CHD. We also detected Trypanosoma cruzi in both groups, with a nonsignificant trend of increased parasitemia in the group with malignant arrhythmia (66.7% vs 33.3%). 18F-FDG and 68Ga-DOTATOC uptake on PET/CT may be useful for the detection of myocardial inflammation in patients with Chagas cardiomyopathy, and 68Ga-DOTATOC uptake may be associated with the presence of malignant arrhythmia, with potential therapeutic implications.

Chronic Trypanosoma cruzi infection activates the TWEAK/Fn14 axis in cardiac myocytes and fibroblasts driving structural and functional changes that affect the heart.

Sustained interaction between the cytokine tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its functional receptor, fibroblast growth factor-inducible 14 (Fn14), has been linked to cardiovascular disorders. Chagas cardiomyopathy, elicited by Trypanosoma cruzi infection, is associated with chronic inflammation, fibrosis and hypertrophy. This study aimed to explore the involvement of the TWEAK/Fn 14 axis in development of Chagas heart disease. Parasite infection in vitro triggered Fn14 overexpression in atrial HL-1 myocytes and cardiac MCF fibroblasts. Fn14 levels were also increased in heart tissue from C57BL/6 mice at 130 days post-infection, particularly in myocytes and fibroblasts. Concurrently, TWEAK expression in circulating monocytes from this group was higher than that determined in uninfected controls. TWEAK/Fn14 interaction was functional in myocytes and fibroblasts isolated from infected hearts, leading to TNF receptor-associated factor 2 (TRAF2)-mediated activation of nuclear factor kappa B (NFκB) signaling. Ex vivo stimulation of both cell types with recombinant TWEAK for 24h boosted the NFκB-regulated production of proinflammatory/profibrotic mediators (IL-1β, IL-6, TNF-α, IL-8, CCL2, CCL5, MMP-2, MMP-9, ICAM-1, E-selectin) involved in chronic T. cruzi cardiomyopathy. We further evaluated the therapeutic potential of the soluble decoy receptor Fn14-Fc to interfere with TWEAK/Fn14-dependent pathogenic activity. Fn14-Fc treatment of chronically infected mice was effective in neutralizing the ligand and reverting electrocardiographic abnormalities, maladaptive inflammation, adverse remodeling and hypertrophy in myocardium. Altogether, these findings suggest that sustained TWEAK/Fn14 induction by persistent T. cruzi infection is implicated in cardiopathogenesis and make TWEAK/Fn14 axis a promising target for the treatment of chronic Chagas heart disease.

Plasma Levels of Matrix Metalloproteinases 2 and 9 in Patients with Chronic Chagas Heart Disease and Systemic Arterial Hypertension: Correlation with TGF-Beta Plasma Levels.

Chronic Chagas heart disease (CCHD) and systemic arterial hypertension (SAH) frequently coexists in areas where Chagas disease is endemic. The effects of the association of both conditions (CCHD-SAH) on the extracellular matrix (ECM) remodeling are unknown. Matrix metalloproteinases (MMP) 2 and 9 are involved in ECM remodeling. The aim of this study was to evaluate MMP 2 and MMP9 in CCHD-SAH patients and to correlate their levels with those of the profibrogenic cytokine TGF-beta. We included 19 patients with CCHD-SAH, 14 patients with CCHD alone, and 19 controls matched by sex and age. MMP-2 and MMP-9 plasma levels were studied by gel zymography and showed as optical densities (OD). TGF-beta plasma levels were measured by double-ligand ELISA and expressed as pg/mL. Median (5th, 95th) MMP-2 plasma levels were 1224.7 OD (1160, 1433.5) in patients with CCHD alone, 1424.1 OD (1267.5, 1561) in patients with CCHD-SAH, and 940 OD (898.1, 1000.8) in controls (p=0.001). MMP-9 plasma levels were 1870 OD (1740, 1904.1) in patients with CCHD alone, 1754.6 OD (1650, 2049) in those with CCHD-SAH and 89.7 OD (80, 96) in controls (p=0.0003). MMP-9 plasma levels were higher than those of MMP 2 in patients with CCHD-SAH (p=0.01). No correlation was found between TGF-beta plasma levels with MMP-2 serum levels (r = 0.12; p=0.7), but a moderate negative correlation (r = -0.46; p=0.048) was observed between TGF-beta and MMP-9 plasma levels. MMP-2 and especially MMP-9 may play a role in the ECM remodeling process in patients with CCHD-SAH. TGF-Beta may counteract the MMP effect on the ECM remodeling process in patients with CCHD-SAH.

Prevalencia de alteraciones digestivas asociadas a Chagas importado (estudio PADChI): un estudio observacional

BackgroundChagas disease (CD) is a parasitic disease caused by Trypanosoma cruzi in which up to 10% to 20% of those affected may experience digestive disorders. Multiple studies have been carried out on CD in non-endemic countries, mainly related to cardiological involvement. However, digestive disorders have not been analyzed in such depth. The objective of the study was to determine the prevalence of digestive disorders in imported CD at the time of first care. MethodsAn observational, cross-sectional, descriptive analysis of imported CD was performed. Chagasic structural damage and infectious digestive comorbidity were evaluated. The association between Chagasic structural damage and heart disease in Chagas patients was also investigated. ResultsAfter reviewing a total of 1,216 medical records, those of 464 patients were selected for analysis. Globally, the prevalence of digestive disorders in imported Chagas was 57.76% (95%CI: 53.25-62.27). The prevalence of infectious disease comorbidity was 40.73% (95%CI: 36.25-45.22). Colonic abnormalities were found in 84 of 378 barium enema patients. CD-related esophageal abnormalities were present in 63 of 380 patients studied by means of an esophagram. ConclusionsThe prevalence of digestive disorders associated with CD is high. Therefore, the presence of infectious diseases (mainly parasitic diseases and Helicobacter pylori infection) should be ruled out. It is important to rule out structural involvement in all symptomatic patients and asymptomatic patients should also be considered and offered the option of doing so.

Prevalence of digestive disorders associated with imported Chagas disease (PADChI study): an observational study

BackgroundChagas disease (CD) is a parasitic disease caused by Trypanosoma cruzi, in which up to 10–20% of those affected may suffer digestive disorders. Multiple studies have been carried out on CD in non-endemic countries, mainly related to cardiological involvement. However, digestive disorders have not been analyzed in such depth. The objective of the study was to determine the prevalence of digestive disorders in imported CD at the time of first care. MethodsAn observational cross-sectional descriptive analysis of imported CD was performed. Chagasic structural damage and infectious digestive comorbidity were evaluated. The association between Chagasic structural damage and heart disease in Chagas patients was also investigated. ResultsAfter reviewing a total of 1,216 medical records, those of 464 patients were selected for analysis. Globally, the prevalence of digestive disorders in imported Chagas was 57.76%, 95% CI (53.25–62.27). The prevalence of comorbidity of infectious diseases was 40.73% CI 95% (36.25–45.22). Colonic abnormalities were found in 84 of 378 barium enema patients. CD-related esophageal abnormalities were present in 63 of 380 patients studied with esophagogram. ConclusionsThe prevalence of digestive disorders associated with CD is high, so the presence of infectious diseases (mainly parasitic and H. pylori infection) should be ruled out. It is important to exclude structural involvement in all symptomatic patients, and asymptomatic patients should also be considered and offered.

Cytokine Networks as Targets for Preventing and Controlling Chagas Heart Disease

Chagas disease, a neglected disease caused by the protozoan Trypanosoma cruzi, is endemic in 21 Latin American countries, affecting 6-8 million people. Increasing numbers of Chagas disease cases have also been reported in non-endemic countries due to migration, contamination via blood transfusions or organ transplantation, characterizing Chagas as an emerging disease in such regions. While most individuals in the chronic phase of Chagas disease remain in an asymptomatic clinical form named indeterminate, approximately 30% of the patients develop a cardiomyopathy that is amongst the deadliest cardiopathies known. The clinical distinctions between the indeterminate and the cardiac clinical forms are associated with different immune responses mediated by innate and adaptive cells. In this review, we present a collection of studies focusing on the human disease, discussing several aspects that demonstrate the association between chemokines, cytokines, and cytotoxic molecules with the distinct clinical outcomes of human infection with Trypanosoma cruzi. In addition, we discuss the role of gene polymorphisms in the transcriptional control of these immunoregulatory molecules. Finally, we discuss the potential application of cytokine expression and gene polymorphisms as markers of susceptibility to developing the severe form of Chagas disease, and as targets for disease control.

Sudden cardiac death multiparametric classification system for Chagas heart disease's patients based on clinical data and 24-hours ECG monitoring.

About 6.5 million people are infected with Chagas disease (CD) globally, and WHO estimates that $ > million people worldwide suffer from ChHD. Sudden cardiac death (SCD) represents one of the leading causes of death worldwide and affects approximately 65% of ChHD patients at a rate of 24 per 1000 patient-years, much greater than the SCD rate in the general population. Its occurrence in the specific context of ChHD needs to be better exploited. This paper provides the first evidence supporting the use of machine learning (ML) methods within non-invasive tests: patients' clinical data and cardiac restitution metrics (CRM) features extracted from ECG-Holter recordings as an adjunct in the SCD risk assessment in ChHD. The feature selection (FS) flows evaluated 5 different groups of attributes formed from patients' clinical and physiological data to identify relevant attributes among 57 features reported by 315 patients at HUCFF-UFRJ. The FS flow with FS techniques (variance, ANOVA, and recursive feature elimination) and Naive Bayes (NB) model achieved the best classification performance with 90.63% recall (sensitivity) and 80.55% AUC. The initial feature set is reduced to a subset of 13 features (4 Classification; 1 Treatment; 1 CRM; and 7 Heart Tests). The proposed method represents an intelligent diagnostic support system that predicts the high risk of SCD in ChHD patients and highlights the clinical and CRM data that most strongly impact the final outcome.