Life expectancy analysis in patients with Chagas' disease: prognosis after one decade (1973–1983)

doi:10.1016/0167-5273(85)90262-1

International Journal of Cardiology

Volume 8, Issue 1, May 1985, Pages 45-56

https://doi.org/10.1016/0167-5273(85)90262-1 Get rights and content

Abstract

We studied the evolution of chronic Chagas' disease in 107 patients with a positive Guerreiro-Machado reaction and 22 non-chagasic, non-heart disease control subjects for a follow-up period of 3 to 10 years (mean follow-up of 4.9 years). After completion of invasive and non-invasive studies, chagasic patients were classified into four groups: IA (normal ECG, without heart disease; 18 patients); IB (normal ECG, early left ventricular segmental abnormalities; 13 patients); II (abnormal ECG, advanced myocardial damage, no signs of heart failure; 42 patients); and III (abnormal ECG, end-stage, congestive heart failure; 34 patients). One out of five group IA patients re-studied with invasive methods evolved to group IB (20%); 4 group IB patients evolved to group II (33%) and 6 group II patients evolved to group III (15%). The life expectancy of patients in groups IA and IB (normal ECG) was similar to that of our control group, whereas in groups II and III it was significantly decreased (P < 0.001). Nine group II patients (23%) and 28 group III patients (82%) died during the follow-up period. Main terminal events were refractory congestive heart failure, sudden death and systemic thromboembolism.

Our findings suggest that chronic Chagas' disease follows an evolutionary course from asymptomatic, normal ECG group I stage to arrhythmic (II) and congestive (III) stages. Subjects with a positive Guerreiro-Machado reaction showed a significantly lower life expectancy than our control group, but only when clinical and/or ECG abnormalities were identified.

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Cited by (96)

Trypanosomiasis
2022, Greene's Infectious Diseases of the Dog and Cat, Fifth Edition
American Trypanosomiasis (Chagas disease)
- •
  First Described: Chagas disease (American trypanosomiasis) was first described in humans in 1909 by Dr. Carlos Chagas.¹ The first canine Chagas disease cases in the United States were diagnosed in the early 1970s in Texas.²
- •
  Cause: Trypanosoma cruzi, a protozoan parasite (order Kinetoplastida, family Trypanosomatidae).
- •
  Affected Hosts: Dogs, cats, humans, horses, nonhuman primates, and other domestic and wild mammalian species.
- •
  Geographic Distribution: Endemic across the Americas including South and Central America, Mexico, and the southern United States.
- •
  Mode of Transmission: Contact with infected feces from, or ingestion of, triatomine (kissing bug) vectors, primarily Triatoma species. Transmission through blood transfusion and vertical transmission can occur.
- •
  Major Clinical Signs: Infected dogs may be subclinically infected. Clinical disease manifests as lethargy, inappetence, mucosal pallor, lymphadenopathy, splenomegaly, arrhythmias, heart failure, or sudden death. Neurologic signs such as pelvic limb ataxia and exaggerated spinal reflexes may also occur.
- •
  Differential Diagnoses: The differential diagnoses for suspected Chagas myocarditis include dilated cardiomyopathy, parvoviral myocarditis in puppies, canine monocytic ehrlichiosis, babesiosis, and leishmaniosis. The primary differential diagnoses for suspected Chagas meningoencephalitis in puppies are CDV infection and neosporosis, but other infectious and inflammatory causes of meningoencephalitis should also be considered.
- •
  Human Health Significance: Chagas disease is a neglected tropical disease with as many as 8 million humans infected. Infected animals may be sentinels for human disease risk when there are infected triatomine vectors in the environment. Direct transmission from infected dog to human has not been shown. Transmission to humans has the potential to occur after needle-stick injuries; caution is advised when handling tissues or clinical specimens from dogs with suspected trypanosomiasis.
African Trypanosomiasis
- •
  First Described: Reports of African trypanosomiasis date back to Egyptian times. Trypanosomes were identified as the cause in 1895, when they were detected in cattle by a Scottish microbiologist, David Bruce (after whom Brucella was named).³
- •
  Cause: Trypanosoma brucei rhodesiense, Trypanosoma congolense, Trypanosoma evansi (protozoan parasites, family Trypanosomatidae).
- •
  Affected Hosts: Dogs and a variety of other mammalian host species. Humans are infected with Trypanosoma brucei gambiense and T. brucei rhodesiense.
- •
  Geographic Distribution: Central Africa (T. brucei, T. congolense); T. evansi is found in Africa as well as in Asia, Latin America, and the Canary Islands in Spain.
- •
  Mode of Transmission: A bite from the tsetse fly (T. brucei or T. congolense) or mechanical transmission by hematophagous flies (T. evansi).
- •
  Major Clinical Signs: Lethargy, inappetence, weight loss, pallor, peripheral edema, ascites, hematemesis, hemorrhagic diarrhea, uveitis, corneal edema, neurologic signs due to meningoencephalitis.
- •
  Differential Diagnoses: These include canine monocytic ehrlichiosis, babesiosis, leishmaniosis, and systemic immune-mediated diseases. CDV infection and neosporosis are important differential diagnoses in dogs with meningoencephalitis.
- •
  Human Health Significance: Although most Trypanosoma species that cause African trypanosomiasis in dogs do not infect humans, T. brucei rhodesiense does, so caution is advised when handling tissues or clinical specimens from dogs or cats with suspected trypanosomiasis.
Age-related anomalies of electrocardiograms in patients from areas with differential Seroprevalence of Chagas disease in Southern Bolivia
2021, Parasite Epidemiology and Control
Chagas disease currently affects some 6 million people around the world. At the chronic stage, cardiomyopathy occurs in about 20–30% of infested people. Most prevalence studies have focused on young to adult people due to the drastic consequences of acquiring the pathogen and the possibility to cure the disease at this age; the prevalence of this disease, the effect of patients' sex and the consequences to senescent people have been largely neglected. This study looks to characterize the seroprevalence of Chagas disease and its relation with occurrence of electrocardiographic anomalies associated with sex and age, and to compare rural and urban populations in Bolivia.
Seroprevalence of Chagas disease was determined in blood samples and electrocardiograms were performed on seropositive individuals.
The rural population showed higher seroprevalence than the urban population (92% and 40%, respectively). The proportion of Chagasic cardiac anomalies in seropositive persons was highest in patients of the 50–59 age group (36%) as compared with the 40–49 (8%) and the ≥60 (17%) age groups.
Higher seroprevalence in rural population was attributable to a higher probability to encounter the vector in rural areas. Increased exposure to infection and to development of the disease symptoms together with increased lethality of the disease as patients age explains the age-related Chagasic electrocardiographic anomalies. Since rural and urban populations showed different reactions under Chagas disease and the rural population was mainly of guaraní stock, the genetic and environmental determinants of the results should be further explored.
Chronic Chagas Heart Disease Management: From Etiology to Cardiomyopathy Treatment
2017, Journal of the American College of Cardiology
Trypanosoma cruzi (T. cruzi) infection is endemic in Latin America and is becoming a worldwide health burden. It may lead to heterogeneous phenotypes. Early diagnosis of T. cruzi infection is crucial. Several biomarkers have been reported in Chagas heart disease (ChHD), but most are nonspecific for T. cruzi infection. Prognosis of ChHD patients is worse compared with other etiologies, with sudden cardiac death as an important mode of death. Most ChHD patients display diffuse myocarditis with fibrosis and hypertrophy. The remodeling process seems to be associated with etiopathogenic mechanisms and neurohormonal activation. Pharmacological treatment and antiarrhythmic therapy for ChHD is mostly based on results for other etiologies. Heart transplantation is an established, valuable therapeutic option in refractory ChHD. Implantable cardioverter-defibrillators are indicated for prevention of secondary sudden cardiac death. Specific etiological treatments should be revisited and reserved for select patients. Understanding and management of ChHD need improvement, including development of randomized trials.
The role of CCR5 in Chagas disease - a systematic review
2016, Infection, Genetics and Evolution
Citation Excerpt :
This period of infection is called the indeterminate phase of chronic Chagas disease. Annually approximately 10% of patients in the indeterminate phase of chronic Chagas disease progress to chronic Chagas cardiomyopathy (CCC) (Espinosa et al., 1985). About 30% of chronically infected patients will develop CCC, and 10% digestive tract disease about 20 years after the initial infection (Taylor and Bestetti, 2009).
Chagas disease is an infection caused by the protozoan Trypanosoma cruzi. The clinical manifestations result from the chronic forms of the disease: indeterminate, cardiac, digestive or mixed. The pathogenesis of this disease is related to the genetic variability of both the parasite and the host with polymorphisms of genes involved in immune response possibly being involved in the variable clinical course. Cytokines play a key role in regulating immune response, in particular chemokines exert a crucial role in the control of leukocyte migration during the host's response to infectious processes. Furthermore, inflammatory cytokines and chemokines have been implicated in the generation of inflammatory infiltrates and tissue damage. The involvement of the CC Chemokine Receptor 5 (CCR5) in leukocyte migration to sites of inflammation has been elucidated and this receptor has been investigated in Chagas disease. Here we review the role of CCR5 in T. cruzi infection as well as its importance in the pathogenesis of the Chagas disease.
Clinical predictors of inducible sustained ventricular tachycardia during electrophysiologic study in patients with chronic Chagas' heart disease
2015, IJC Heart and Vasculature
Citation Excerpt :
Nonetheless, we have no explanation for the difference observed in our study as compared with that of Silva et al. [12]. The results of this investigation are in contrast to other studies in which several clinical and laboratorial variables were associated with SCD, a condition which can be predicted by sustained VT inducibility during EPS [11]. Such clinical characteristics are represented by electrocardiographic changes (left anterior fascicular block, QT dispersion, and premature ventricular contractions) [23] as well echocardiographic abnormalities (left ventricular diastolic diameter > 70 mm and apical aneurysm) [9], which have independently been associated with SCD in patients with Chagas' cardiomyopathy.
Clinical independent predictors of inducible sustained ventricular tachycardia (VT) during electrophysiologic study (EPS) are not known in patients with chronic Chagas' heart disease. The purpose of this investigation was to fill this gap.
The medical charts of 47 patients with a positive serology for Chagas' disease who had undergone EPS between September 2006 and July 2012 at our institution were reviewed. Reasons for the EPS were the presence of unexplained syncope, non-sustained ventricular tachycardia (NSVT) on either resting ECG or 24 h-Holter monitoring as well as a LVEF < 55% and > 35% at echocardiography. A stepwise logistic regression analysis was performed to identify noninvasive predictors of inducible sustained VT/ventricular fibrillation during EPS.
On univariate analysis, syncopal episodes (p = 0.04), amiodarone therapy (p < 0.005), diastolic blood pressure (p = 0.03), creatinine serum levels (p < 0.001), potassium serum levels (p < 0.001), and lengthening of the QRS complex (p = 0.03) were associated with inducible sustained VT during EPS. In the multivariate model, amiodarone therapy (p = 0.03; hazard ratio = 10; Wald coefficient = 4.5; 95% confidence interval 1.2 to 85.2) was the only variable retained as independent predictor of inducible sustained VT during EPS.
Amiodarone therapy was the only independent variable associated with sustained VT inducibility during EPS in patients with chronic Chagas' heart disease.
Global economic burden of Chagas disease: A computational simulation model
2013, The Lancet Infectious Diseases
As Chagas disease continues to expand beyond tropical and subtropical zones, a growing need exists to better understand its resulting economic burden to help guide stakeholders such as policy makers, funders, and product developers. We developed a Markov simulation model to estimate the global and regional health and economic burden of Chagas disease from the societal perspective.
Our Markov model structure had a 1 year cycle length and consisted of five states: acute disease, indeterminate disease, cardiomyopathy with or without congestive heart failure, megaviscera, and death. Major model parameter inputs, including the annual probabilities of transitioning from one state to another, and present case estimates for Chagas disease came from various sources, including WHO and other epidemiological and disease-surveillance-based reports. We calculated annual and lifetime health-care costs and disability-adjusted life-years (DALYs) for individuals, countries, and regions. We used a discount rate of 3% to adjust all costs and DALYs to present-day values.
On average, an infected individual incurs US$474 in health-care costs and 0·51 DALYs annually. Over his or her lifetime, an infected individual accrues an average net present value of $3456 and 3·57 DALYs. Globally, the annual burden is $627·46 million in health-care costs and 806 170 DALYs. The global net present value of currently infected individuals is $24·73 billion in health-care costs and 29 385 250 DALYs. Conversion of this burden into costs results in annual per-person costs of $4660 and lifetime per-person costs of $27 684. Global costs are $7·19 billion per year and $188·80 billion per lifetime. More than 10% of these costs emanate from the USA and Canada, where Chagas disease has not been traditionally endemic. A substantial proportion of the burden emerges from lost productivity from cardiovascular disease-induced early mortality.
The economic burden of Chagas disease is similar to or exceeds those of other prominent diseases globally (eg, rotavirus $2·0 billion, cervical cancer $4·7 billion) even in the USA (Lyme disease $2·5 billion), where Chagas disease has not been traditionally endemic, suggesting an economic argument for more attention and efforts towards control of Chagas disease.
Bill & Melinda Gates Foundation, the National Institute of General Medical Sciences Models of Infectious Disease Agent Study.

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^☆: Supported by grant N^o M-226 from the “Consejo de Desarrollo Científico y Humanistico de la Universidad de Los Andes”, Mérida, Venezuela.

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Original studyLife expectancy analysis in patients with Chagas' disease: prognosis after one decade (1973–1983)☆

Abstract

Prog Cardiovasc Dis

Am Heart J

Int J Cardiol

Am J Cardiol

Am J Cardiol

Am Heart J

Lancet

Am J Cardiol

Am Heart J

Nova entidad morbida do homen: resumo general dos estudos etiologicos e clinocos

Mem Inst Oswaldo Cruz

Chagas' disease. A clinical, epidemiologic and pathologic study

Circulation

Mortality in Chagas' disease: life-table for the period 1949–1967 in an unselected population

Rev Inst Méd Trop São Paulo

Cuatro años de estudio longitudinal de una comunidad rural con endemicidad chagásica

Bol Of Sanit Panam

La dinámica epidemiológica de la enfermedad de Chagas en El Valle de los Naranjos. Estado Carabobo-Venezuela

Arch Ven Med Trop Parasitol Med

Contribución al estudio de la patología de la miocarditis chagásica en Venezuela

Arch Hosp Vargas

Aspectos clínicos de la enfermedad de Chagas: diagnóstico de daño miocardico

Interciencia

Diagnóstico por métodos no invasivos de daño ventricular izquierdo incipiente en pacientes chagásicos. Utilidad de la ecocardiografía y la fonomecanocardiografía

Arch Inst Cardiol Mex

La prueba de esfuerzo en la miocardiopatía chagásica crónica. Su valor en el diagnóstico precoz

Arq Bras Cardiol

Estudio de la función del nodo sinusal y de la conducción atrioventricular en pacientes con enfermedad de Chagas

Arch Inst Cardiol Mex

Original study
Life expectancy analysis in patients with Chagas' disease: prognosis after one decade (1973–1983)☆