Case Presentation: This abstract highlights Chagas Cardiomyopathy (CCM) and aims to elucidate key features and improve understanding and patient outcomes.A 49-year-old Honduran male with a two-year history of HFrEF (EF 25-30%) secondary to non-ischemic cardiomyopathy of unknown etiology and prior embolic stroke presented with nine days of worsening dyspnea, palpitations, and RUQ pain despite GDMT and diet adherence. He denied recent illness, stressors, or travel. Examination revealed irregular pulse, tender hepatomegaly, and volume overload. EKG showed atrial fibrillation, RBBB, and left anterior fascicular block (LAFB). Echocardiography demonstrated EF decline (10-15%), severe biatrial/LV dilation, inferolateral/apical akinesia, and Grade 4 MR with tethered mitral valve leaflets.A diagnosis of acute decompensated heart failure consistent with dilated cardiomyopathy (DCM) was made and treated with IV diuresis and GDMT. Persistent hypotension and end organ damage prompted transfer to CCU for cardiogenic shock management with milrinone. Right heart catheterization confirmed low output state (cardiac output 2.29 L/min; cardiac index 1.3 L/min/m²). Cardiac MRI revealed extensive late gadolinium enhancement with a meso-cardial pattern consistent with myocardial fibrosis and DCM. Chagas serologies, prompted by his Honduran descent, returned positive, confirming chronic CCM. Anti-trypanosomal therapy was deferred due to a high RASSI score (15).Heart transplant consideration was precluded by socioeconomic barriers and prior substance abuse. INTERMACS-3 dependence on milrinone persisted during a month long hospital stay. Mitraclip placement led to clinical improvement, enabling milrinone discontinuation despite sustained severe MR. He was discharged on GDMT with plans for AICD placement due to high sudden cardiac death risk.
Discussion: Cardiac imaging’s integration in diagnosis and risk stratification enhances patient management and underscores the importance of tailored approaches in combating Chagas cardiomyopathy; as its recognition extends beyond solely understanding a patient’s medical history.Conduction abnormalities, contractile dysfunction and thromboembolism represent clinical and EKG manifestations; commonly linked to causes of mortality. EKG features suggestive of CCM with which the patient presented included RBBB with LAFB and atrial fibrillation due to conduction abnormalities. Additionally, increased thromboembolism risk in CCM led to prior unexplained embolic stroke. Echocardiography’s pivotal role in detecting segmental LV wall motion abnormalities, particularly inferolateral and apical hypokinesia/akinesia, and features of dilated cardiomyopathy highlights the disease’s multifaceted impact on cardiac function; all features noted in our patient. Cardiac MRI further elucidated myocardial fibrosis by showcasing transmural late gadolinium enhancement, a hallmark feature of CCM.The RASSI score, a risk stratifier used to assess the severity and prognosis of chronic CCM, was used to guide management. Score > 7 indicated poor prognosis not warranting use of anti-trypanosomal therapy. Patients are thus treated using GDMT for heart failure +/- advanced heart therapy based on disease severity.
Conclusions: With over 68 million U.S. Latin-Americans [2024], understanding Chagas disease’s demographics and at risk populations is essential for early identification. Cardiac imaging is integral in the diagnosis and management of CCM.