BACKGROUND: There is evidence based on experimental models studies in infections by Trypanosoma cruzi, as well as histopathologic studies in individuals with Chagas heart disease, suggesting that ischemia plays a role in the pathogenesis of myocardial lesions in the chronic phase of the disease. These ischemic disorders are caused by microcirculatory dysregulation. Atypical angina is a common symptom in patients in the chronic phase of Chagas heart disease. In a large number of patients, despite the absence of significant angiographic coronary obstructions, the occurrence of perfusion abnormalities is documented by myocardial scintigraphy during stress, which is reversible after rest. METHODS: This is a single center, prospective, single cohort study, with a therapeutic intervention, followed by a late quantitative reevaluation of the myocardial perfusion defects, initially detected in patients with Chagas heart disease and angiographically normal coronary arteries. Myocardial perfusion single-photon emission computed tomography (SPECT) will be performed before and 90 days after the therapeutic intervention, using sestamibi-Tc99m as a radiotracer and physical exercise or vasodilation stimulation with dipyridamole as stressors. Therapeutic intervention will consist of acetylsalicylic acid (single daily dose of 100 mg) associated to verapamil (80 mg bid and a total daily dose of 160 mg). The primary endpoint of the study is a reduction > 50% of the area of ischemic myocardium calculated by the polar scintigraphic map. CONCLUSIONS: This is the first study of a therapeutic approach to attenuate or revert ischemic myocardial perfusion abnormalities of microvascular origin in patients with chronic Chagas heart disease.
Chagas disease; Myocardial ischemia; Microvascular angina; Acetylsalicylic acid; Verapamil