Evidence for Trypanosoma cruzi in adipose tissue in human chronic Chagas disease.

Trypanosoma cruzi the cause of Chagas disease persists in tissues of infected experimental animals and humans. Here we demonstrate the persistence of the parasite in adipose tissue from of three of 10 elderly seropositive patients with chronic chagasic heart disease. Nine control patients had no parasites in the fat. We also demonstrate that T. cruzi parasitizes primary adipocytes in vitro. Thus, in humans as in mice the parasite may persist in adipose tissue for decades and become a reservoir of infection.

Complete atrioventricular block associated with toxoplasma myocarditis.

Myocarditis has been described during and after a wide variety of infectious agents: viral, rickettsial, bacterial, protozoal, and metazoal diseases may cause cardiac inflammation. We report a case of toxoplasma myocarditis in a young healthy man.

Trypanosoma cruzi myocardial infection reactivation presenting as complete atrioventricular block in a Chagas' heart transplant recipient.

A 56-year-old man underwent orthotopic heart transplantation because of end-stage Chagas' cardiomyopathy. One hundred and ten days following heart transplantation, an electrocardiogram tracing showed complete atrioventricular block, which was treated with temporary transvenous pacemaker insertion. An underlying endomyocardial biopsy was graded 3A. The patient was treated with pulse steroid therapy. One week later, the patient died of multiorgan failure secondary to septicemia. A careful review of the endomyocardial biopsy showed nests of parasites in the myocardial tissue accompanied by mononuclear cell infiltrate similar to that found in acute graft rejection. Thus, complete atrioventricular block may be another clinical manifestation of Trypanosoma cruzi infection reactivation in Chagas' heart transplant recipients.

Risk progression to chronic Chagas cardiomyopathy: influence of male sex and of parasitaemia detected by polymerase chain reaction.

BACKGROUND: Polymerase chain reaction (PCR) allows detection of Trypanosoma cruzi in blood throughout the course of Chagas' disease. OBJECTIVE: To determine whether T cruzi DNA detected by PCR is associated with progression to chronic Chagas cardiomyopathy. DESIGN: Prospective cohort study. SETTING: A tertiary care centre in Argentina. PATIENTS: 56 consecutive patients with chronic T cruzi infection. METHODS: Clinical examination, ECG, and Doppler echocardiography were carried out at baseline and at the end of the follow up. Detection of T cruzi DNA by PCR amplifying a nuclear sequence was undertaken in all patients at baseline. MAIN OUTCOME MEASURES: Progression was defined as death from chronic cardiomyopathy or the presence of a new ECG or left ventricular echocardiographic abnormality at the end of follow up. RESULTS: The 56 patients (21 male, 35 female; mean (SD) age, 56.0 (11.3) years) were followed for a mean 936.3 (244.39) days. Progression to cardiomyopathy was detected in 12 patients (21.4%). Three of these patients died after baseline evaluation. Univariate analysis showed that a positive PCR (relative risk 4.09, 95% confidence interval (CI) 1.60 to 9.85) and male sex (5.00, 95% CI 1.65 to 15.73) were associated with progression. Multivariable logistic regression indicated that both sex and PCR were independent variables affecting the outcome. CONCLUSIONS: In a cohort of seropositive individuals, patients with T cruzi DNA detected by PCR and male patients were at higher risk of progression. These results highlight the importance of T cruzi in the pathophysiology of chronic cardiomyopathy.

Sera from chronic chagasic patients with complex cardiac arrhythmias depress electrogenesis and conduction in isolated rabbit hearts.

BACKGROUND: Immune dysfunction has long been proposed as a mechanism for the etiopathogenesis of the chronic phase of Chagas' disease. Antibodies of chagasic patients have been shown to interfere with electric and mechanical activity of embryonic myocardial cells in culture. Here, we demonstrate that antibodies derived from a group of chronic chagasic patients are able to induce disturbances in the electrogenesis and conduction in isolated adult rabbit hearts. METHODS AND RESULTS: Sera from chronic chagasic patients with complex cardiac arrhythmias (ChA+) decreased heart rate (from 131+/-26 to 98+/-37 bpm [mean+/-SD]; n=6; P<.05) in isolated rabbit hearts when perfused at a dilution of 1:100 (vol:vol) by the Langendorff method. Sera from another experimental group of four chronic chagasic patients without complex arrhythmias (ChA-) and two control groups composed of five Wolff-Parkinson-White (WPW) syndrome patients and five orthopedic surgery patients did not affect heart rate when tested under similar conditions. In addition, sera from five of six ChA+ patients and from one WPW patient induced AV conduction blockade. Effects of the sera from ChA+ patients are due to their IgG fractions. Both serum and IgG effects are blocked by atropine (10 micromol/L). CONCLUSIONS: Antibodies of ChA+ patients decrease heart rate and induce AV conduction block in isolated adult rabbit hearts through activation of muscarinic receptors.