The Treatment of Chronic Heart Failure Secondary to Chagas Cardiomyopathy in the Contemporary Era

Chronic Heart Failure affects about half patients with Chagas cardiomyopathy. Poor outcomes of CHF secondary to Chagas cardiomyopathy are relentless with an annual mortality approaching 20%, which is higher than that observed in non-Chagas disease heart failure. The pathophysiology of Chagas disease is similar to that found in non-Chagas disease heart failure with a marked activation of the neurohormonal system. No randomized trial has been conducted in patients with Chagas cardiomyopathy with CHF to assess the effect of a drug on mortality of such patients. Therefore, the treatment of CHF secondary to Chagas cardiomyopathy relies on drugs prescribed to patients with non-Chagas disease heart failure. Patients with Chagas disease heart failure have been classified into stages A to D according to the American College of Cardiology/American Heart Association. Little can be done to patients in the stage A of CHF, except for treatment of comorbidities. In patients in the stage B of CHF, aldosterone receptor antagonist, angiotensin converting enzyme inhibitors (ACEI), and Betablockers (BB) are indicated. In patients in the stage C of CHF, the same drugs are of value. In addition, diuretics, digoxin, angiotensin receptor blockers to patients intolerant to ACEI have also been used. Cardiac Resynchronization Therapy and Implantable Cardioverter Defibrillator may have indications similar to that of non-Chagas disease patients. In stage D of CHF, heart transplantation is a valid option for patients with this condition

Carlos Chagas Discoveries as a Drop Back to Scientific Construction of Chronic Chagas Heart Disease

Abstract The scientific construction of chronic Chagas heart disease (CCHD) started in 1910 when Carlos Chagas highlighted the presence of cardiac arrhythmia during physical examination of patients with chronic Chagas disease, and described a case of heart failure associated with myocardial inflammation and nests of parasites at autopsy. He described sudden cardiac death associated with arrhythmias in 1911, and its association with complete AV block detected by Jacquet's polygraph as Chagas reported in 1912. Chagas showed the presence of myocardial fibrosis underlying the clinical picture of CCHD in 1916, he presented a full characterization of the clinical aspects of CCHD in 1922. In 1928, Chagas detected fibrosis of the conductive system, and pointed out the presence of marked cardiomegaly at the chest X-Ray associated with minimal symptomatology. The use of serological reaction to diagnose CCHD was put into clinical practice in 1936, after Chagas' death, which along with the 12-lead ECG, revealed the epidemiological importance of CCHD in 1945. In 1953, the long period between initial infection and appearance of CCHD was established, whereas the annual incidence of CCHD from patients with the indeterminate form of the disease was established in 1956. The use of heart catheterization in 1965, exercise stress testing in 1973, Holter monitoring in 1975, Electrophysiologic testing in 1973, echocardiography in 1975, endomyocardial biopsy in 1981, and Magnetic Resonance Imaging in 1995, added to the fundamental clinical aspects of CCHD as described by Carlos Chagas

Comprometimento parassimpático no estágio pré-clínico da doença de chagas crônica

Universidade Federal de São Paulo (UNIFESP)UNIFESPSciEL