Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Chagas Cardiomyopathy”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1998

Echocardiographic analysis of regional and global left ventricular shape in Chagas' cardiomyopathy.

Chagas' heart disease is a common form of cardiomyopathy in Latin America and an important cause of cardiac morbidity and mortality there. Left ventricular (LV) apical aneurysm and LV dysfunction are frequent findings in Chagas' cardiomyopathy. Because cardiac shape has important implications for LV function, we sought to characterize regional and global changes in LV geometry in Chagas' heart disease. Quantitative shape analysis was performed on 2-dimensional echocardiograms from 43 patients with Chagas' cardiomyopathy. Regional shape was quantitated by measuring endocardial curvature and global shape was evaluated by Fourier shape analysis of the endocardial contour. Data from 22 age- and sex-matched normal test subjects were used for comparison. Regional shape analysis demonstrated decreased apical curvature (consistent with blunting of normal apical shape) in the group with Chagas' disease compared with controls (apical 2-chamber view: 19 +/- 1 vs 24 +/- 1 [p = 0.0039] at end-diastole and 20 +/- 2 vs 29 +/- 3 [p = 0.0019] at end-systole). Fourier shape power index was decreased in the Chagas' group, consistent with a more spherical ventricle (apical 2-chamber view: 9 +/- 1 vs 17 +/- 2 [p <0.0001] at end-diastole and 12 +/- 1 vs 35 +/- 3 [p <0.0001] at end-systole). Shape changes among the population with Chagas' disease were further evaluated in those with end-diastolic volumes equal to or greater than the median for the group (104 ml) and those < 104 ml. Global shape did not differ between patients with dilated ventricles and those with relatively nondilated ventricles. Diastolic Fourier shape power index = 8 +/- 2 in dilated ventricles compared with 9 +/- 5 in nondilated ventricles (p = 0.53); systolic Fourier shape power index = 10 +/- 2 in dilated versus 14 +/- 2 in nondilated ventricles (p = 0.15) (apical 2-chamber view). In Chagas' cardiomyopathy, LV apical deformation results in disruption of the optimal global prolate-ellipsoid shape, even in patients with relatively preserved LV volumes.

Adult↗
PubMed2003

Clinical management of chronic Chagas cardiomyopathy.

Chagas disease is caused by a protozoan parasite, Trypanosoma cruzi, and infects over 15 million people worldwide. New cases of the disease are now uncommon, mainly due to national control programs in Latin America. However, there is a large reservoir of chronically infected patients, many of whom will develop chagasic cardiopathy. Here, the clinical diagnosis and management of Chagas cardiopathy are discussed. Particular emphasis is placed on the clinical staging of patients and the use of various diagnostic tests that may be useful in individualizing treatment of the two most relevant clinical syndromes, ie. heart failure and arrhythmias. Finally, the relevance of specific treatment is discussed, stressing the important role of parasite persistence for disease pathogenesis.

Animals↗
PubMed2006

CHARITY: Chagas cardiomyopathy bisoprolol intervention study: a randomized double-blind placebo force-titration controlled study with Bisoprolol in patients with chronic heart failure secondary to Chagas cardiomyopathy [NCT00323973].

BACKGROUND: Chagas' disease is the major cause of disability secondary to tropical diseases in young adults from Latin America, and around 20 million people are currently infected by T. cruzi. Heart failure due to Chagas cardiomyopathy is the main clinical presentation in Colombia. Heart failure due to Chagas' disease may respond to digoxin, diuretics and vasodilator therapy. Beta-adrenoreceptor antagonism seems to protect against the increased risk of cardiac arrhythmia and sudden death due to chronic sympathetic stimulation. The aim of this study is to evaluate the effects of the selective beta-adrenergic receptor blocker Bisoprolol on cardiovascular mortality, hospital readmission due to progressive heart failure and functional status in patients with heart failure secondary to Chagas' cardiomyopathy. METHODS/DESIGN: A cohort of 500 T. cruzi seropositive patients (250 per arm) will be selected from several institutions in Colombia. During the pretreatment period an initial evaluation visit will be scheduled in which participants will sign consent forms and baseline measurements and tests will be conducted including blood pressure measurements, twelve-lead ECG and left ventricular ejection fraction assessment by 2D echocardiography. Quality of life questionnaire will be performed two weeks apart during baseline examination using the "Minnesota living with heart failure" questionnaire. A minimum of two 6 minutes corridor walk test once a week over a two-week period will be performed to measure functional class. During the treatment period patients will be randomly assigned to receive Bisoprolol or placebo, initially taking a total daily dose of 2.5 mgrs qd. The dose will be increased every two weeks to 5, 7.5 and 10 mgrs qd (maximum maintenance dose). Follow-up assessment will include clinical check-up, and blood collection for future measurements of inflammatory reactants and markers. Quality of life measurements will be obtained at six months. This study will allow us to explore the effect of beta-blockers in chagas' cardiomyopathy.

Journal Article↗
PubMed2006

Proteomic inventory of myocardial proteins from patients with chronic Chagas' cardiomyopathy.

Chronic Chagas' disease cardiomyopathy (CCC) is an often fatal outcome of Trypanosoma cruzi infection, with a poorer prognosis than other cardiomyopathies. CCC is refractory to heart failure treatments, and is the major indication of heart transplantation in Latin America. A diffuse myocarditis, plus intense myocardial hypertrophy, damage and fibrosis, in the presence of very few T. cruzi forms, are the histopathological hallmarks of CCC. To gain a better understanding of the pathophysiology of CCC, we analyzed the protein profile in the affected CCC myocardium. Homogenates from left ventricular myocardial samples of end-stage CCC hearts explanted during heart transplantation were subjected to two-dimensional electrophoresis with Coomassie blue staining; protein identification was performed by MALDI-ToF mass spectrometry and peptide mass fingerprinting. The identification of selected proteins was confirmed by immunoblotting. We demonstrated that 246 proteins matched in gels from two CCC patients. They corresponded to 112 distinct proteins. Along with structural/contractile and metabolism proteins, we also identified proteins involved in apoptosis (caspase 8, caspase 2), immune system (T cell receptor ss chain, granzyme A, HLA class I) and stress processes (heat shock proteins, superoxide dismutases, and other oxidative stress proteins). Proteins involved in cell signaling and transcriptional factors were also identified. The identification of caspases and oxidative stress proteins suggests the occurrence of active apoptosis and significant oxidative stress in CCC myocardium. These results generated an inventory of myocardial proteins in CCC that should contribute to the generation of hypothesis-driven experiments designed on the basis of the classes of proteins identified here.

Adult↗
PubMed2006

Confirmation of Chagas' cardiomyopathy following heart transplantation.

We report a case of Chagas' cardiomyopathy confirmed in a patient after heart transplantation. The patient initially presented with symptoms of congestive heart failure and was found to have positive serology for prior Trypanosoma cruzi infection. Despite optimal medical management, the patient had deterioration of his cardiac function and he underwent heart transplantation. Pathology examination of the explanted heart confirmed Chagas' cardiomyopathy. The cardiac sequelae of Chagas' disease include arrhythmias, aneurysm, thromboembolism, cardiomyopathy, and sudden death. We review the epidemiology, cardiac pathology, and evaluation of patients with Chagas' cardiac disease. We discuss the clinical features of Chagas' cardiomyopathy and available treatments including cardiac transplantation.

Animals↗
PubMed1992

Chagas cardiomyopathy and captopril.

Chagas disease is a leading cause of heart failure in Latin America. Sudden death occurs in approximately 40% of patients with heart failure due to Chagas disease. We report a single blind, cross-over trial of prolonged treatment with captopril and placebo in 18 Chagas disease patients with class IV NYHA heart failure. Ventricular dimensions, neurohormones, electrolytes and ventricular arrhythmias were analysed in 11 men and seven women receiving stable doses of digoxin and frusemide who were randomly divided into two intervention groups. Group I patients were given increasing doses of captopril up to 150 mg.day-1 maintained for 6 weeks, group II received the placebo. A 24 h Holter, 2-D echocardiogram, urinary catecholamines, plasma renin and electrolyte determinations were performed at the end of each phase. After a 2-week washout period, the two groups crossed over and another period of 6 weeks was observed. Ventricular arrhythmias were analysed by either Mann-Whitney or the Wilcoxon test. Remaining data were assessed by the Student t-test. A significant reduction in heart rate and urinary catecholamine levels, and enhanced plasma levels of renin, together with a reduction in ventricular couplets was found in the captopril-treated group. We conclude that captopril has a beneficial effect on neurohormones with a subsequently reduced heart rate and diminished incidence of ventricular arrhythmias in patients with Chagas disease. This effect might result in a reduction of mortality caused by the disease, suggesting the need for further investigations.

Adult↗
PubMed1996

Organ-specific circulating heart autoantibodies in Chagas' cardiomyopathy: exploratory study.

Chagas' disease can evolve to a chronic phase with cardiomyopathy that may include autoimmune mechanisms, among others. Recently an organ-specific anti-heart muscle antibody was detected in idiopathic cardiomyopathy, using human heart muscle as antigen. We decide to standardize an indirect immunofluorescence assay using rat organs in order to evaluate frequency of organ-specific anti-heart antibodies in chagasic cardiomyopathy. We tested 18 patients with chagasic cardiomyopathy for serum organ-specific anti-heart muscle antibodies. Nine patients were positive for organ-specific anti-heart antibodies (positive in heart muscle but negative in tongue muscle) and one was positive for non-organ-specific anti-heart muscle antibodies (positive in both heart and tongue muscle). We conclude that organ-specific anti-heart muscle antibodies can be detected using rat organs as antigens. Organ-specific anti-heart muscle antibodies are present in patients with chagasic cardiomyopathy.

Adult↗
PubMedDate not supplied

QT interval dispersion in patients with chronic heart failure secondary to Chagas' cardiomyopathy: correlation with clinical variables of prognostic significance.

BACKGROUND: QTc interval dispersion has rarely been studied in patients with chronic heart failure (CHF) secondary to Chagas' cardiomyopathy. One study has demonstrated an association between QT interval dispersion and sudden cardiac death. No data exist regarding the association of clinical variables and QT interval dispersion in patients with this condition. METHODS: Sixty three patients with CHF due to Chagas' cardiomyopathy, 34 Chagas' disease patients with no systolic dysfunction on echocardiography, and 36 individuals with no previous cardiac history, matched by sex and a 10-year age interval, were included in the investigation. The QTc interval dispersion was defined as the difference between maximum and minimum QTc. RESULTS: The mean QTc interval dispersion was 74+/-30.3 ms in surviving and 87+/-30.6 ms in nonsurviving patients (P=.13). Mean QTc dispersion was 95.20+/-28.46 ms in patients who died from pump failure, 73.33+/-29.61 ms in patients who died suddenly, and 74.46+/-30.27 in survivors (P=.07). Mean QTc dispersion value was higher in patients in the Class III or IV (P=.01).). Mean QTc interval dispersion was 67.2+/-22.7 ms in patients with and 85.5+/-33.5 ms in patients without premature ventricular contractions (P=.01), and 67.5+/-29.8 ms in patients with and 84.7+/-31.8 ms in patients without left ventricular apical aneurysm (P=.03). A correlation could be observed in QTc interval dispersion and left atrium dimension (r=.32; P=.009) Thus, QTc interval dispersion is associated to some prognostic indicators in patients with CHF secondary to Chagas' cardiomyopathy.

Chagas Cardiomyopathy↗
PubMed2005

Peculiar aspects of cardiogenic embolism in patients with Chagas' cardiomyopathy: a transthoracic and transesophageal echocardiographic study.

OBJECTIVES: We sought to detect cardiac thrombi by transthoracic and transesophageal echocardiography in patients with Chagas' cardiomyopathy and to determine the relationship of these thrombi with left ventricular systolic function and with the presence of stroke. BACKGROUND: Thromboembolic events are a serious complication of Chagas' cardiomyopathy. Because most data come from autopsy studies, the prevalence of cardiac thrombi for patients who are clinically stable is unknown. METHODS: A total of 75 patients (52 men; mean age 48 +/- 13 years) with Chagas' cardiomyopathy were prospectively studied by transthoracic and transesophageal echocardiography and followed for 24 +/- 10 months. RESULTS: In all, 14 patients (19%) had a history of stroke at the time of enrollment and two had this complication at follow-up. Most patients (88%) were in New York Heart Association (NYHA) functional classes I and II and 9 (12%) were in classes III and IV. Mean ejection fraction was 40 +/- 13%. A total of 17 patients (23%) had left ventricular thrombus on transthoracic echocardiography and this finding was associated with a history of stroke ( P = .01). Apical aneurysm occurred in 35 patients (47%) and it was associated both with thrombus and stroke ( P = .04). Strokes were more frequent ( P = .04) among patients with mild systolic dysfunction (57% of patients with strokes were in NYHA I). Four patients (5%) had thrombi at the left atrial appendage, and one (1%) at the right atrial appendage. A total of 13 patients (17%) died at follow-up. CONCLUSIONS: Stroke was frequent in Chagas' cardiomyopathy and associated with mild systolic dysfunction and with intracardiac thrombi. These occurred mainly in the typical apical aneurysm of Chagas' disease.

Brazil↗
PubMed1996

[Normal maximal functional capacity in patients with congestive heart failure due to Chagas' cardiomyopathy].

PURPOSE: To compare patients with heart failure due to Chagas' cardiomyopathy and maximal oxygen consumption greater than 20mL/kg-1/min-1 to normal individuals. METHODS: We studied 104 male patients with heart failure due to Chagas' cardiomyopathy, functional classe II-IV, age 18 to 65 years (40.3 +/- 9.0), and 23 normal sedentary male individuals (GI) age 17 to 51 years (35 +/- 8.7). Maximal oxygen consumption (VO2max) was obtained using a Beckman metabolic measurement cart, and left ventricular ejection fraction (EF) by conventional transthoracic echocardiography. Comparisons between means were made with t-test. RESULTS: Thirty seven patients (35.6%) presented VO2max above 20mL/kg-1/min-1 (G2), with values ranging from 20.5 to 30 (24.5 +/- 2.9) and EF between 19 and 63% (42 +/- 11.7). GI had VO2max between 21 and 42mL/kg-1/min-1 (33.3 +/- 5.6) and EF between 70 and 82% (75.1 +/- 3.2). Ages were not significantly different for the two groups (p = 0.1136). VO2max and EF were lower in G2, and this was statistically significant (p < 0.0001). CONCLUSION: These results indicate that patients with congestive heart failure due to Chagas disease may show values of VO2max, greater than 20mL/kg-1/min-1 which does not mean that they have normal maximal functional capacity.

Adolescent↗
PubMed1978

Stress testing and working capacity in Chagas' cardiomyopathy.

The EKG response to exercise and the working capacity in a group of 70 patients with positive serology for Chagas' disease has been determined by stress testing on a bicycle-ergometer, in order to establish the usefulness of such a test in the early diagnosis of Chagas' cardiomyopathy. The exercise EKG provides information which cannot be obtained by other diagnostic procedures, since the stress test can induce or increase ventricular arrhythmia, and is particularly indicated in patients with Chagas' infection and the incipient forms of Chagas' cardiomyopathy. Measuring the working capacity is useful in order to establish the degree of functional impairment of each individual patient. After the application of oral digoxin, no significant increase of ventricular extrasystoles following exercise has been observed and the working capacity has improved in the majority of the studied cases with Chagas' cardiomyopathy.

Administration, Oral↗
PubMed1998

[Study of the factors determining an unexpected occurrecne of Chagas cardiomyopathy in Sucre, Bolivia].

The purpose of this case-control study carried out between February 1, 1994 and December 22, 1994 at the "Instituto de Gastroenterologia Boliviano-Japonés" in Sucre, Bolivia was to determine risk factors for chronic Chagas cardiomyopathy in adult patients with positive serological tests for Trypanosoma cruzi. A total of 196 subjects were included. Inclusion criteria were positive serological tests for Trypanosoma cruzi, residence in the city of Sucre, Bolivia for at least 3 months, and age over 14 years. There were 62 cases presenting electrocardiographic findings consistent with Chagas cardiomyopathy and 134 controls presenting normal electrocardiographic findings. Both cases and controls underwent a standardized protocol including physical examination and laboratory tests. Interviews were set up to evaluate personal and familial history of Chagas disease, socioeconomic status, and presence of Triatoma infestans in the home. Bivariate analysis of data indicated that Chagas cardiomyopathy was associated with the following risk factors: heart rate (p < 0.05), fecaloma (p < 0.05), occupation requiring strenuous physical exertion (p < 0.001), proximity with domestic animals (p < 0.005), especially pigs (p < 0.005), dwelling features including outbuildings, more than 2 bedrooms, and inside ceilings (p < 0.001). Multivariate analysis revealed the following risk factors: occupation requiring strenuous physical exertion (p < 0.005), a yard around the house (p < 0.05), and inside ceilings (p < 0.05). The results of this study show that prevention of chronic Chagas cardiomyopathy in Sucre, Bolivia will depend on improvement of living conditions.

Adolescent↗
PubMed1995

Heart transplantation for Chagas' cardiomyopathy.

We present 2 patients who underwent orthotopic heart transplantation for end-stage Chagas' cardiomyopathy. Despite immunosuppressive therapy, postoperative prophylaxis with nifurtimox appeared to prevent Trypanosoma cruzi reactivation. Neither patient has shown signs of Chagas' myocarditis, and both are clinically well 12 and 72 months after transplantation. The successful outcome of our patients suggests that heart transplantation is a reasonable therapeutic option in patients with end-stage Chagas' cardiomyopathy.

Adult↗
PubMed2000

Relation of regional sympathetic denervation and myocardial perfusion disturbance to wall motion impairment in Chagas' cardiomyopathy.

Impairment of sinus node autonomic control and myocardial perfusion disturbances have been described in patients with chronic Chagas' cardiomyopathy. However, it is not clear how these conditions contribute to myocardial damage. In this investigation, iodine-123 (I-123) meta-iodobenzylguanidine (MIBG) and thallium-201 myocardium segmental uptake were studied in correlation with the severity of left ventricular (LV) dysfunction detected in various phases of Chagas' heart disease. Group I consisted of 12 subjects (43 +/- 4 years, 7 men) with no symptoms and no cardiac involvement on electrocardiogram (ECG) or echocardiography; group II consisted of 13 patients (48 +/- 3 years, 9 men) with abnormal resting ECG and/or echocardiographic segmental abnormalities, and LV ejection fraction of > or = 0.5; group III was comprised of 12 patients (59 +/- 3 years, 10 men) with more severe heart disease, LV dilation, and LV ejection fraction of < 0.5. Eighteen control volunteers (38 +/- 3 years, 9 men) were also included in the study. I-123 MIBG single-photon emission computed tomographic (SPECT) segmental uptake defects were observed in group I (33%), group II (77%), and group III (92%). Quantitative analysis showed mean areas of reduced LV I-123-MIBG uptake: group I was 3.7 +/- 2.1%; group II was 8.3 +/- 2.3%; and group III was 19.0 +/- 3.3%. The differences between group I and both groups II and III were statistically significant (p < 0.001, analysis of variance test). Myocardial perfusion defects (reversible, fixed, and paradox) were observed in group I (83%), group II (69%), and group III (83%). A marked topographic association between perfusion, innervation, and wall motion abnormalities (assessed by gated-SPECT perfusion studies) was observed in all the groups. Defects predominated in the inferior, posterior lateral, and apical LV regions. Thus, extensive impairment of cardiac sympathetic function at the ventricular level occured early in the course of Chagas' cardiomyopathy and was related to regional myocardial perfusion disturbances, before wall motion abnormalities. Both conditions are associated with progression of ventricular dysfunction.

3-Iodobenzylguanidine↗
PubMed1996

Autoimmunity in Chagas' disease. Identification of cardiac myosin-B13 Trypanosoma cruzi protein crossreactive T cell clones in heart lesions of a chronic Chagas' cardiomyopathy patient.

Heart tissue destruction in chronic Chagas' disease cardiomyopathy (CCC) may be caused by autoimmune recognition of heart tissue by a mononuclear cell infiltrate decades after Trypanosoma cruzi infection. Indirect evidence suggests there is molecular mimicry between T. cruzi and heart tissue. In murine models of CCC, antibodies and CD4+ T cells recognize myosin, the major heart protein. We recently identified a heart-specific epitope of cardiac myosin heavy chain (residues 1442-1447, AAALDK) that is crossreactive with a homologous sequence (AAAGDK) of the immunodominant T. cruzi antigen B13. Furthermore, cardiac myosin-B13 crossreactive antibodies are present in 100% CCC patients vs 14% asymptomatic T. cruzi-seropositive individuals (P = 2.3 x 10(-6)), suggesting a role for molecular mimicry between cardiac myosin and B13 in CCC pathogenesis. In this paper, we obtained heart-infiltrating T cell clones from CCC patients to assess whether molecular mimicry between cardiac myosin and B13 is directly involved in the genesis of heart lesions. We identified T cell clones derived from CCC heart lesions simultaneously responsive to cardiac myosin heavy chain (but not skeletal myosin heavy chain) and B13 T. cruzi protein, but could not find T cell clones primarily reactive to any T. cruzi antigen. Together with the association of myosin-B13 crossreactive antibodies with CCC, the present data strongly suggest the relevance of molecular mimicry between cardiac myosin and the T. cruzi protein B13 in the pathogenesis of heart lesions in chronic Chagas' disease cardiomyopathy.

Adult↗
PubMed2006

BAT1, a putative anti-inflammatory gene, is associated with chronic Chagas cardiomyopathy.

BACKGROUND: It is not understood why only a subset of individuals infected with Trypanosoma cruzi develop chronic Chagas cardiomyopathy (CCC). Patients with CCC display high levels of circulating proinflammatory cytokines. Heart-infiltrating lymphocytes from patients with CCC also express proinflammatory cytokines (tumor necrosis factor- alpha and interferon- gamma ) that are detectable in biopsy samples and surgical heart-tissue samples. BAT1, a putative anti-inflammatory gene, presents functional polymorphisms in its promoter region that influence its transcriptional level. METHODS: We assessed, by polymerase chain reaction restriction fragment-length polymorphism analysis, BAT1 variants in the promoter region at positions -22C/G and -348C/T in 154 patients with CCC and in 76 T. cruzi-infected but asymptomatic (ASY) patients. RESULTS: Of the patients with CCC, 16% were homozygous for the -22C allele, compared with 4% of the ASY patients (P=.004; odds ratio [OR], 4.7 [95% confidence interval {CI}, 1.4-16]). A similar trend was observed for the -348C homozygotes (P=.01; OR, 1.9 [95% CI, 1.0-3.5]). Susceptibility to CCC was conferred by the C variants at nt -22 (P=.003; OR, 1.8 [95% CI, 1.2-2.8]) and at nt -348 (P=.02; OR, 1.7 [95% CI, 1.0-2.8]). CONCLUSIONS: BAT1 variants previously associated with reduced expression of HLA-B-associated transcript 1 are predictive of the development of CCC. These variants may be less efficient in down-regulating inflammatory responses and may contribute to the elevated production of proinflammatory cytokines in patients with CCC.

Brazil↗