Trypanosoma cruzi
Valeria Fabre, M.D.
MICROBIOLOGY
MICROBIOLOGY
MICROBIOLOGY
- Trypanosoma cruzi, a hemoflagellate protozoan, causes American trypanosomiasis (Chagas disease).
- Transmission occurs when triatomine feces contaminate the bite site or mucosal surfaces (not via the bite itself).
- Important vectors are blood-feeding triatomine bugs, including species of Triatoma, Rhodnius, and Panstrongylus [Fig 1].
- Enzootic transmission occurs in the southern U.S., with infected triatomines and mammalian reservoirs (especially dogs and wildlife); autochthonous human cases are rare but increasingly recognized.
- Texas has the highest number of reported autochthonous human T. cruzi infections.
- Risk factors include rural residence, history of hunting or camping, and agricultural or outdoor work.
- Canines are an important domestic reservoir and sentinel species; direct contribution to human transmission is inferred but not well quantified[3].
- See the Life cycle.
CLINICAL
CLINICAL
CLINICAL
- T. cruzi infection is endemic throughout much of Mexico, Central America, and South America
- Enzootic transmission also occurs in the southern U.S. (TX, OK).
- Expert U.S. recommendations support screening individuals with ≥ 6 months residence in endemic regions[1]:
- People who were born or lived for a prolonged period (≥ 6 months) in areas of Mexico, Central or South America where CD is endemic.
- Close (first-degree) relatives of people previously diagnosed with Chagas disease
- Consider Chagas disease in people from endemic Latin American regions who have otherwise unexplained cardiac conduction abnormalities, arrhythmias, basal or apical wall-motion abnormalities, apical aneurysm, or cardiomyopathy.
- Individuals with unexplained megacolon or megaesophagus who have lived in an endemic region.
- T. cruzi can establish lifelong infection, with progressive cardiac and/or gastrointestinal complications in a minority of infected people.
- See "Sites of Infection" below.
- Most infected are asymptomatic and may take years to develop end-organ complications.
- 60–70% remain asymptomatic (indeterminate phase).
- Acute infection: Considered with a compatible exposure history, including residence or travel in an endemic region, laboratory exposure, transfusion, transplantation, or congenital transmission.
- An estimated ~300,000 chronic carriers live in the U.S.
- Chronic T. cruzi carriers can transmit the parasite to others through blood or tissue donation.
- In the U.S., transfusion-associated transmission is now rare because of blood-donor screening.
- Donor-derived infection through organ transplantation remains uncommon but well documented.
- Reactivation is common after heart transplantation and other profound immunosuppression, with rates approaching 40–50% in some series without preemptive treatment.
- Congenital Chagas disease: in the U.S., estimated at 65-315 annual cases.
- AIDS: Advanced HIV infection may permit reactivation, most often presenting as meningoencephalitis or one or more mass-like brain lesions.
- Death in chronic Chagas cardiomyopathy usually results from progressive heart failure, malignant ventricular arrhythmia/sudden cardiac death, or thromboembolic complications.
- Diagnosis:
- Acute infection: Infants and immunocompromised patients are at the highest risk for severe acute disease.
- Immunocompetent patient: parasites (trypomastigotes) seen on wet preps or Giemsa-stained (Fig. 2) blood or buffy coat; acute serology of limited utility.
- Blood smear sensitivity is variable (often <50% on a standard smear); concentration techniques improve detection.
- PCR: sensitive test, 85-100% with specificity 95-100%.
- In acute infection, PCR is generally more sensitive than conventional blood-smear examination.
- Serology may be negative or indeterminate early in infection.
- Immunocompromised: biopsy for parasites in bone marrow, lymph node, myocardium, skin, CSF, and pericardial fluid.
- Specialized reference laboratories can perform PCR.
- Blood culture and xenodiagnosis are largely restricted to specialized or research settings.
- Chronic infection: post-acute/lifelong; parasites are difficult or impossible to find, so diagnosis typically relies on indirect evidence through serology.
- Serology: T. cruzi-specific IgG; since no assay is highly sensitive or specific, at least two tests are recommended that differ in what antigens are detected (ELISA, IFA, or immunoblot).
- Several FDA-cleared IgG assays are available, but no single assay is sufficiently sensitive and specific to establish the diagnosis.
- If the initial two serologic assays are discordant, perform a third distinct serologic assay.
- A confirmed diagnosis requires positive results from at least two different assays.
- PCR is not sufficiently sensitive to exclude chronic infection, as it is unreliable (20-70% sensitive) because parasitemia is intermittent and low-level.
- Providers can contact CDC with questions about CD (chagas@cdc.gov, 404–718–4745). Coordinate requests for CDC testing with the state or local health department.
- No gold standard reference exists.
- Congenital disease[7]:
- Direct visualization of parasites (trypomastigotes) in blood or body fluids
- PCR
- At birth: sensitivity ~70–90%
- 1–2 months (repeat PCR): sensitivity improves to >90–95%
- Specificity: ~100%
- A positive PCR from a specimen obtained near birth should be confirmed on a second infant specimen, as it may reflect maternal blood contamination.
- Clinical implication:
- A single negative PCR at birth does not exclude infection
- Repeat testing at 4-6 weeks is standard
- Serology: useful at age 9–12 months, after maternally derived antibody has waned.
- Blood donation screening for T. cruzi has been widespread in the U.S. since 2007.
- GI and cardiac workup as appropriate
- Screening: All patients with confirmed T. cruzi infection, including asymptomatic patients, should undergo clinical staging.
- Patients who screen positive for CD (even if asymptomatic) should undergo an evaluation to determine which stage they are at.
- At a minimum, obtain a 12-lead ECG.
- Obtain a transthoracic echocardiogram when cardiac involvement is suspected or as part of baseline staging, per local expert practice.
SITES OF INFECTION
SITES OF INFECTION
SITES OF INFECTION
- Acute disease generally begins 1–2 weeks after vector-borne infection; incubation may differ after transfusion, transplantation, oral transmission, or laboratory exposure.
- Chagoma: red, indurated lesion at the site of inoculation.
- Romaña’s sign [Fig. 3]: painless unilateral periorbital edema, often with ipsilateral regional lymphadenopathy.
- Systemic: fever, malaise, face/leg edema, general lymphadenopathy, hepatosplenomegaly.
- Cardiac: severe myocarditis may occur with acute infection; may see conduction problems or left ventricular dysfunction. Infants are at the highest risk for developing severe manifestations during the acute stage.
- Indeterminate stage: Following resolution of acute infection, patients without clinical, electrocardiographic, radiographic, or gastrointestinal evidence of disease are considered to have chronic indeterminate infection; low-level intermittent parasitemia and antibodies persist.
- Chronic disease: occurs in 30-40% of chronically infected individuals and after 10-30 years of infection. It involves the heart and GI systems, with cardiac problems far more common than GI. Involvement of the CNS only in the immunocompromised host.
- Cardiac: occurs in 15-45% of chronically infected.
- Cardiac disease includes conduction abnormalities, ventricular dysfunction, apical aneurysm, and arrhythmias (including PVCs, AV block, and atrial fibrillation).
- GI: occurs in 10-20% of chronically infected (more common in southern South America); manifestations may include megaesophagus, megacolon, dysphagia, regurgitation, constipation, and abdominal pain.
- CNS: Primary CNS infection is principally a manifestation of reactivation in severely immunocompromised patients and may cause meningoencephalitis or mass-like brain lesions.
- Cardioembolic stroke may complicate Chagas cardiomyopathy.
TREATMENT
TREATMENT
TREATMENT
General Comments
General Comments
- Antiparasitic therapy is most effective in acute, congenital, and recently acquired infections.
- It reduces parasitemia in chronic infection, but its effect on long-term clinical outcomes is less certain.
- In the BENEFIT trial, benznidazole reduced parasite detection but did not significantly reduce major clinical outcomes in patients with established Chagas cardiomyopathy.
- Benznidazole is FDA-approved for children 2–12 years of age, and nifurtimox is FDA-approved for term infants and children from birth to younger than 18 years who weigh at least 2.5 kg.
- These age-restricted indications reflect the populations studied for regulatory approval; use in adults is off-label in the United States.
- Serologic conversion occurs more frequently and more rapidly in children than in adults.
- In adults, a negative PCR after treatment indicates suppression or clearance of detectable parasitemia but is not a validated surrogate for preventing clinical progression.
Acute Chagas’ Disease
Acute Chagas’ Disease
- Treat all acute infections, including congenital and reactivated infections, with benznidazole or nifurtimox.
- Treatment shortens the duration of parasitemia and is most likely to achieve parasitologic cure when initiated early.
- Cure rates can range up to 85% during the acute phase.
- Benznidazole:
- 5-8 mg/kg PO daily in two divided doses
- Duration: 60 days
- Management:
- Obtain a baseline CBC and hepatic and renal chemistries; monitor periodically during treatment.
- Assess promptly for rash, gastrointestinal intolerance, cytopenias, hepatotoxicity, and peripheral neuropathy.
- Nifurtimox:
- Adults:
- 8–10 mg/kg PO per day, divided into three doses with food.
- Older references have used 10–15 mg/kg/day in adults, but current U.S. expert practice commonly uses 8–10 mg/kg/day in three divided doses.
- Children (birth to < 18 years of age and weighing at least 2.5 kg):
- < 40 kg: 10-20 mg/kg/day in 3 divided doses
- ≥ 40 kg: 8-10 mg/kg/day in 3 divided doses
- Duration: 60 days
- Management: monitor LFTs, CBC, and chemistries at baseline, weeks 4-6, and end of therapy. Observe for signs of peripheral neuropathy. May cause depression and dizziness/vertigo[8].
- Exclude pregnancy before treatment. Avoid nifurtimox during pregnancy and advise effective contraception because of potential fetal harm.
- After a high-risk laboratory exposure, consider benznidazole 5–8 mg/kg per day or nifurtimox 8–10 mg/kg per day for 10–14 days.
- Donor-derived infection:
- Perform serial whole-blood PCR and microscopic monitoring after transplantation. Promptly initiate benznidazole or nifurtimox if parasitemia or clinical infection is detected.
- Benznidazole 5–8 mg/kg per day or nifurtimox 8–10 mg/kg per day for 60 days.
- Routine prophylaxis solely because the donor is seropositive is generally not recommended; management should be coordinated with transplant-infectious-disease and Chagas experts.
Indeterminate Stage Chagas’ Disease
Indeterminate Stage Chagas’ Disease
Indeterminate Stage Chagas’ Disease
- Treatment is recommended for children with chronic indeterminate infection because parasitologic and serologic responses are highest at younger ages.
- Treatment is also generally recommended for adults ≤50 years without advanced cardiomyopathy, although evidence that it prevents long-term clinical complications is less certain.
Chronic Chagas’ Disease
Chronic Chagas’ Disease
- .Treatment is strongly recommended for adults ≤50 years with chronic infection who do not have advanced cardiomyopathy.
- For adults >50 years old, decisions should be individualized based on age, clinical status, comorbidities, and treatment risks.
- Patients with severe cardiomyopathy and uncompensated CHF: Antiparasitic treatment is unlikely to alter outcomes in advanced Chagas cardiomyopathy and is generally not recommended solely to reverse established cardiac disease.
- Treatment is generally recommended for younger patients without advanced cardiomyopathy; in older adults, decisions require individualized risk assessment.
- Offer antiparasitic treatment to women of reproductive age before pregnancy because treatment reduces the risk of subsequent congenital transmission.
- Benznidazole and nifurtimox should not be given during pregnancy.
- Medications. Both benznidazole and nifurtimox are commercially available in the U.S. with FDA pediatric approval; adult use has historically been off-label.
- Benznidazole: preferred due to better tolerability profile.
- 5- 8mg/kg daily in 2 divided doses
- Duration: 60 days
- Management: Check baseline CBC and chemistries before treatment.
- Follow CBC q 2 wks. Observe for rashes, GI sx, and peripheral neuropathy.
- Nifurtimox: divide the drug dose into 3 doses per day with food. Adverse effects are common and may limit completion, particularly with nifurtimox.
- Adults: 8-10 mg/kg/day (obtain a pregnancy test in women before prescribing nifurtimox and advise on contraception due to fetal harm associated with the drug).
- Children (birth to < 18 years of age, term and weighing at least 2.5 kg):
- < 40kg: 10-20 mg/kg/day in 3 divided doses
- ≥ 40kg: 8-10 mg/kg/day in 3 divided doses
- Duration: 60 days.
- Management: monitor LFTs, CBC, and chemistries at baseline, weeks 4-6, and end of therapy. Observe for signs of peripheral neuropathy.
- Cardiac:
- Manage cardiomyopathy according to standard heart-failure and arrhythmia principles, including guideline-directed heart-failure therapy, anticoagulation when indicated, pacemaker or implantable cardioverter-defibrillator placement, and evaluation for transplantation in advanced disease.
- GI: Antiparasitic therapy does not reverse established megaesophagus or megacolon.
- Treat gastrointestinal complications symptomatically and procedurally.
- Eligibility for antiparasitic treatment should otherwise be determined by age, disease stage, and cardiac status.
- Megaesophagus: treat for idiopathic achalasia, i.e., balloon dilation of the lower esophageal sphincter, botulinum toxin, or surgery.
- Megacolon/colonic dysfunction: symptomatic; high-fiber diet, manual disimpaction, surgical intervention for toxic megacolon, volvulus, or decompression.
- Consider antiparasitic treatment before planned immunosuppression or transplantation in selected chronically infected patients, with expert consultation.
- After transplantation, use serial PCR monitoring to detect reactivation and treat promptly.
- Post-transplant reactivation: Benznidazole 5–8 mg/kg per day for 60 days or nifurtimox 8–10 mg/kg per day for 60- 90 days.
- HIV-associated reactivation, including CNS disease:
- Secondary prophylaxis has been used after treatment of reactivation in patients with persistent severe immunosuppression, but the optimal regimen and duration are not established.
- One reported approach is benznidazole 5 mg/kg/day three times weekly or 200 mg daily until sustained virologic suppression and a CD4 count >200–250 cells/µL for at least 6 months.
Selected Drug Comments
Selected Drug Comments
Drug | Recommendation |
Nifurtimox | Preferred alternative to benznidazole for acute, congenital, or reactivated infection, including donor-derived infection or post-transplant reactivation. High incidence of GI side effects. May have disulfiram-like effects; avoid alcohol. |
Benznidazole | Generally preferred over nifurtimox because of better tolerability. Most effective for acute, congenital, and reactivated infection, and in children or recently infected patients. In established Chagas cardiomyopathy, it reduces detectable parasitemia but has not improved major clinical outcomes. Common adverse effects include dermatitis, photosensitivity, gastrointestinal intolerance, and peripheral neuropathy; discontinue if neuropathy develops. Rare severe dermatitis, cytopenias, and hepatotoxicity may occur. Avoid during pregnancy and avoid alcohol because of a possible disulfiram-like reaction. |
Posaconazole | Although the drug has anti-trypanosomal activity in a murine model of Chagas, an RCT showed that the posaconazole arm had more treatment failures than benznidazole. The drug cannot be recommended currently for the treatment of chronic Chagas[10]. |
OTHER INFORMATION
OTHER INFORMATION
OTHER INFORMATION
- Estimates suggest that ~7 million are infected globally, most in Latin America, and that ~280,00 to 300,000 are believed to be infected and reside in the U.S. after immigrating.
- In the U.S., consultations can be facilitated through the CDC Parasitic Diseases Public Inquiries Line (www.cdc.gov/parasites/chagas) at 404-718-4745 for routine treatment questions and 770-488-7100 for emergencies.
- Many people experience no symptoms or only a transient fever with acute infection.
- Acute phase problems last 4-8 weeks; acute phase case fatality ~0.25-0.5%.
- Serologic tests commonly remain positive for years after treatment and cannot by themselves distinguish persistent infection from successfully treated infection.
Basis for recommendation
Basis for recommendation
Basis for recommendation
- Forsyth CJ, Manne-Goehler J, Bern C, et al. Recommendations for Screening and Diagnosis of Chagas Disease in the United States. J Infect Dis. 2022;225(9):1601-1610. [PMID:34623435]
Comment: A group of Chagas disease experts in the United States provides recommendations using the GRADE system.
- Viotti JB, Morris MI, Simkins J, et al. Screening and Reactivation of Chagas Disease Among Solid Organ Transplant Candidates and Recipients: A 10-Year Single Center Experience in Florida. Transpl Infect Dis. 2026;28(4):e70207. [PMID:41934437]
Comment: Retrospective single center experience. 1898 candidates (31%) were screened, and 21 (1.1%) tested positive for T. cruzi, of whom 10 were SOT recipients. All seropositive recipients were born in historically endemic areas. Seven patients developed Chagas disease reactivation (CDR) diagnosed by serum PCR; all were asymptomatic. Median time from transplantation to reactivation was 48 days (range 22-426). Treatment with benznidazole for 60 days cleared the parasitemia in all patients. At 2 years, 80% (8/10) had graft survival, one patient died unrelated to CDR.
References
References
References
- Beatty NL, Hamer GL, Moreno-Peniche B, et al. Chagas Disease, an Endemic Disease in the United States. Emerg Infect Dis. 2025;31(9):1691-1697. [PMID:40866797]
Comment: Review of the epidemiology of T. cruzi in the United States. There is evidence that wildlife, captive animals, and especially dogs are commonly infected with T. cruzi parasites in the southern United States, serving as reservoirs. Autochthonous human cases have been reported in 8 states, most notably in Texas.
Rating: Important
- Teixeira SM, Burle-Caldas GA, Castro JT, et al. The time has come for a vaccine against Chagas disease. Lancet Reg Health Am. 2025;45:101059. [PMID:40206818]
Comment: Narrative review of recent advances towards the development of a Chagas disease vaccine.
Rating: Important
- Altcheh J, Grossmann U, Stass H, et al. Redefining the treatment of Chagas disease: a review of recent clinical and pharmacological data for a novel formulation of nifurtimox. PLoS Negl Trop Dis. 2025;19(2):e0012849. [PMID:39999088]
Comment: Summarizes: Benznidazole vs. nifurtimox efficacy/toxicity; age-dependent treatment benefit (strongest in children, less certain in older adults); emerging therapies (azole failures, pipeline agents).
- Bosch-Nicolau P, Fernández ML, Sulleiro E, et al. Efficacy of three benznidazole dosing strategies for adults living with chronic Chagas disease (MULTIBENZ): an international, randomised, double-blind, phase 2b trial. Lancet Infect Dis. 2024;24(4):386-394. [PMID:38218195]
Comment: Randomized, double-blind, phase 2b trial performed in Argentina, Brazil, Colombia, and Spain. Included participants aged 18 years and older diagnosed with Chagas disease. Advanced cardiomyopathy cases were excluded. Participants were randomized to receive benznidazole at one of three doses: 300 mg/day for 60 days (control group), 150 mg/day for 60 days (low-dose group), or 400 mg/day for 15 days (short-treatment group). Discontinuations were less frequent in the short treatment group compared with the control group (2 [2%] vs 11 [14%]; OR 0·20, 95% CI 0·04–0·95; p=0·044), while both groups had similar parasitological responses.
Rating: Important
- Chancey RJ, Edwards MS, Montgomery SP. Congenital Chagas Disease. Pediatr Rev. 2023;44(4):213-221. [PMID:37002357]
Comment: Strong U.S.-relevant congenital review covers: screening of at-risk mothers, timing/interpretation of infant PCR vs serology and treatment outcomes in infants (high cure rates).
- Abbott A, Montgomery SP, Chancey RJ. Characteristics and Adverse Events of Patients for Whom Nifurtimox Was Released Through CDC-Sponsored Investigational New Drug Program for Treatment of Chagas Disease - United States, 2001-2021. MMWR Morb Mortal Wkly Rep. 2022;71(10):371-374. [PMID:35271563]
Comment: CDC investigational-use data demonstrate frequent adverse events with nifurtimox. Most were mild, but approximately 25% were moderate and 10% severe; reported events included peripheral neuropathy, dizziness or vertigo, and depression.
Rating: Important
- Morillo CA, Marin-Neto JA, Avezum A, et al. Randomized Trial of Benznidazole for Chronic Chagas' Cardiomyopathy. N Engl J Med. 2015;373(14):1295-306. [PMID:26323937]
Comment: In patients with established Chagas cardiomyopathy, benznidazole significantly reduced detectable parasitemia but did not reduce the composite clinical outcome over a mean follow-up of 5.4 years.
- Molina I, Gómez i Prat J, Salvador F, et al. Randomized trial of posaconazole and benznidazole for chronic Chagas' disease. N Engl J Med. 2014;370(20):1899-908. [PMID:24827034]
Comment: Disappointing RCT that did not show efficacy for posaconazole in patients with chronic infection. The drug did appear to suppress T. cruzi DNA, but more treatment failures were witnessed than in the benznidazole arm. Therefore, benznidazole remains the standard of care.
- Kransdorf EP, Czer LS, Luthringer DJ, et al. Heart transplantation for Chagas cardiomyopathy in the United States. Am J Transplant. 2013;13(12):3262-8. [PMID:24165397]
Comment: Small case series of 11 patients who underwent heart transplant due to Chagas cardiomyopathy at a single center in the United States. In agreement with previous reports, their observed T. cruzi reactivation rate post-transplantation was high. The study also highlights some of the challenges associated with the diagnosis of Chagas Disease in a non-endemic country.
- Bern C. Antitrypanosomal therapy for chronic Chagas' disease. N Engl J Med. 2011;364(26):2527-34. [PMID:21714649]
Comment:
The author cites the increasingly common practice of offering anti-trypanosomal treatment, based on observations that treated patients (children and adults) appear to have less progression to cardiomyopathy. A number of health authorities, including the WHO and the Brazilian Health, now recommend treatment for acute, congenital, and reactivated infection, as well as children up to age 18 with chronic infection. Adults with chronic infection are often treated, but there is less evidence to support this approach.
Rating: Important
- Cordova E, Boschi A, Ambrosioni J, et al. Reactivation of Chagas disease with central nervous system involvement in HIV-infected patients in Argentina, 1992-2007. Int J Infect Dis. 2008;12(6):587-92. [PMID:18337139]
Comment: Meningoencephalitis or brain lesion presentations occur in patients with mean CD4 64 cells/ml. Most had positive serology, and 11/13 had parasites seen on CSF exam. Mortality was 79% despite treatment with benznidazole.
- Karp CL, Auwaerter PG. Coinfection with HIV and tropical infectious diseases. I. Protozoal pathogens. Clin Infect Dis. 2007;45(9):1208-13. [PMID:17918086]
Comment: Authors review considerations regarding HIV and trypanosomal infections.
- Rassi A, Rassi A, Rassi SG. Predictors of mortality in chronic Chagas disease: a systematic review of observational studies. Circulation. 2007;115(9):1101-8. [PMID:17339568]
Comment: Important prognostic features of poor outcome are impaired left ventricular function, New York Heart Association class III/IV, cardiomegaly, and nonsustained ventricular tachycardia.
- Centers for Disease Control and Prevention (CDC). Chagas disease after organ transplantation--Los Angeles, California, 2006. MMWR Morb Mortal Wkly Rep. 2006;55(29):798-800. [PMID:16874295]
Comment: Two more cases of organ transplantation-associated transmission of Chagas Disease, this time in the Los Angeles area. In one patient who had received a heart transplant, nifurtimox resulted in clearance of parasitemia; three other patients who had received organs from the same donor had no evidence of infection on the basis of serology and PCR testing. Another patient who also had received a heart transplant had parasitemia and rash resolve after nifurtimox treatment, but later died from heart failure, not thought to be due to Chagas’ disease, but an autopsy was not performed. Three other patients who had received organs from the same donor had no evidence of infection on the basis of serology and PCR testing.
Rating: Important
- Schijman AG, Altcheh J, Burgos JM, et al. Aetiological treatment of congenital Chagas' disease diagnosed and monitored by the polymerase chain reaction. J Antimicrob Chemother. 2003;52(3):441-9. [PMID:12917253]
Comment: This prospective study focused on the evaluation of anti-parasitic therapy in congenital Chagas' disease, diagnosed and monitored by PCR and conventional diagnosis. Benznidazole and nifurtimox were used for therapy. The gold standard for determining cure was the titer of anti-T. cruzi antibodies becoming negative. PCR was useful for sensitive diagnosis and therapy monitoring, allowing early detection of refractory cases.
- Centers for Disease Control and Prevention (CDC). Chagas disease after organ transplantation--United States, 2001. MMWR Morb Mortal Wkly Rep. 2002;51(10):210-2. [PMID:11922190]
Comment: This is the first report of Chagas' Disease associated with organ transplantation in the United States. The donor reportedly was from Central America. Two of three patients died, one from untreatable Chagas, the other from sepsis apparently unrelated to Chagas.
- Rosa RF, Neto AS, Franken RA. Chagas' disease and the use of implantable cardioverter-defibrillators in Brazil. Am J Geriatr Cardiol. 2006;15(6):372-6. [PMID:17086031]
Comment: Discussion of the use of implantable cardioverter/defibrillators in Brazil. Some patients, selected by electrophysiological studies may benefit.
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