cardiovascular-agents and Chagas-Disease

Chagas cardiomyopathy is an emerging form of non-ischemic cardiomyopathy in the USA. This review aims to summarize current concepts in pathophysiology, disease transmission, medical therapy, and heart transplantation for patients with chronic Chagas cardiomyopathy.. The incidence of Chagas cardiomyopathy is increasing in the USA, driven mainly by immigration from countries where Chagas disease is endemic. Chagas cardiomyopathy is a chronic, progressive myocarditis, with hallmark features of biventricular dysfunction, ventricular arrhythmias, thromboembolic complications, and a high risk of mortality. Currently, there is no effective treatment for chronic Chagas cardiomyopathy. Heart transplantation is the only treatment for patients with end-stage Chagas cardiomyopathy, but is associated with unique challenges including risk of reactivation. As the prevalence of Chagas cardiomyopathy increases in the USA, practitioners must be aware of the unique challenges in diagnosis and management that Chagas cardiomyopathy presents.

Topics: Cardiovascular Agents; Chagas Cardiomyopathy; Chagas Disease; Heart Transplantation; Humans; Myocarditis; Risk Factors; Treatment Outcome; Trypanocidal Agents; Trypanosoma cruzi; United States

Chagas' disease or American trypanosomiasis, is a potentially lethal parasitic zoonosis prevalent and endemic only in Latin America, caused by the flagellate protozoa Trypanosoma cruzi. It has 3 different stages, acute, indeterminate and chronic phase, with the chance of an etiological approach in the first stage and pharmacological and non-pharmacological treatment in the chronic phase. There are five main clinical forms of chronic chagasic cardiomyopathy: indeterminate, arrhythmogenic (predominantly dromotropic and extrasystolic), with ventricular dysfunction, thromboembolic and mixed forms. There are several diagnostic tests at the different stages, however, the ECG is the method of choice in longitudinal population studies in endemic areas because it is simple, with a low cost and a good sensitivity. Microscopic examination or parasitological diagnosis in the acute phase or immunodiagnostic tests are used to confirm the disease. The antiarrhythmic drug amiodarone, the most frequently prescribed agent for symptomatic ventricular arrhythmia treatment of Chagas' disease patients, has also recently been shown to have antifungal activity. Cardiac device implantation is very common, and chronic Chagas disease patients require pacemaker implantation at a younger age in contrast with patients with other cardiac pathologies. In summary, Chagas disease is a social disease, endemic in Latin America and shows different prevalence rates in Latin American countries.

Topics: Cardiac Pacing, Artificial; Cardiovascular Agents; Chagas Disease; Diagnostic Techniques, Cardiovascular; Humans; Quality Assurance, Health Care

The SHIFT trial showed that ivabradine reduced heart rate (HR) and the risk of cardiovascular outcomes. Concerns remain over the efficacy and safety of ivabradine on heart failure (HF) due to Chagas disease (ChD). We therefore conducted a post hoc analysis of the SHIFT trial to investigate the effect of ivabradine in these patients.. SHIFT was a randomized, double-blind, placebo-controlled trial in symptomatic systolic stable HF, HR ≥ 70 b.p.m., and in sinus rhythm. The ChD HF subgroup included 38 patients, 20 on ivabradine, and 18 on placebo. The ChD HF subgroup showed high prevalence of bundle branch right block and, compared with the overall SHIFT population, lower systolic blood pressure; higher use of diuretics, cardiac glycosides, and antialdosterone agents; and lower use of angiotensin-converting enzyme inhibitor/angiotensin II receptor blocker or target daily dose of beta-blocker. ChD HF presented a poor prognosis (all-cause mortality at 2 years was ~60%). The mean twice-daily dose of ivabradine was 6.26 ± 1.15 mg and placebo 6.43 ± 1.55 mg. Ivabradine reduced HR from 77.9 ± 3.8 to 62.3 ± 10.1 b.p.m. (P = 0.005) and improved functional class (P = 0.02). A trend towards reduction in all-cause death was observed in ivabradine arm vs. placebo (P = 0.07). Ivabradine was not associated with serious bradycardia, atrioventricular block, hypotension, or syncope.. ChD HF is an advanced form of HF with poor prognosis. Ivabradine was effective in reducing HR in these patients and improving functional class. Although our results are based on a very limited sample and should be interpreted with caution, they suggest that ivabradine may have a favourable benefit-risk profile in ChD HF patients.

Topics: Argentina; Brazil; Cardiovascular Agents; Chagas Disease; Dose-Response Relationship, Drug; Double-Blind Method; Drug Administration Schedule; Female; Follow-Up Studies; Heart Failure, Systolic; Heart Rate; Humans; Ivabradine; Male; Middle Aged; Stroke Volume; Survival Rate; Treatment Outcome; Ventricular Function, Left

In addition to the long-established role in erythropoiesis, erythropoietin (Epo) has protective functions in a variety of tissues, including the heart. This is the most affected organ in chronic Chagas disease, caused by the protozoan Trypanosoma cruzi. Despite seven million people being infected with T. cruzi worldwide, there is no effective treatment preventing the disease progression to the chronic phase when the pathological involvement of the heart is often observed. Chronic chagasic cardiomyopathy has a wide variety of manifestations, like left ventricular systolic dysfunction, dilated cardiomyopathy, and heart failure. Since Epo may help maintain cardiac function by reducing myocardial necrosis, inflammation, and fibrosis, this study aimed to evaluate whether the Epo has positive effects on experimental Chagas disease. For that, we assessed the earlier (acute phase) and also the later (chronic phase) use of Epo in infected C57BL/6 mice. Blood cell count, biochemical parameters, parasitic load, and echocardiography data were evaluated. In addition, histopathological analysis was carried out. Our data showed that Epo had no trypanocide effect nor did it modify the production of anti-T. cruzi antibodies. Epo-treated groups exhibited parasitic burden much lower in the heart compared to blood. No pattern of hematological changes was observed combining infection with treatment with Epo. Chronic Epo administration reduced CK-MB serum activity from d0 to d180, irrespectively of T. cruzi infection. Likewise, echocardiography and histological results indicate that Epo treatment is more effective in the chronic phase of experimental Chagas disease. Since treatment is one of the greatest challenges of Chagas disease, alternative therapies should be investigated, including Epo combined with benznidazole.

Topics: Animals; Cardiovascular Agents; Chagas Cardiomyopathy; Chagas Disease; Disease Models, Animal; Erythropoietin; Humans; Mice; Mice, Inbred C57BL; Parasite Load; Trypanosoma cruzi

Topics: Brazil; Cardiac Surgical Procedures; Cardiovascular Agents; Chagas Disease; Heart Failure; Humans; Marketing; Placebos; Rheumatic Diseases