Myocardial Fibrosis Secondary to Advanced Chagas Disease: A Case Presentation and Review of Literature

Case Report

Austin J Clin Cardiolog. 2021; 7(1): 1075.

Myocardial Fibrosis Secondary to Advanced Chagas Disease: A Case Presentation and Review of Literature

Younes A¹, Yalamanchili S¹, Ali H¹, Onyekwelu C² and Movahed A²*

¹Department of Internal Medicine, East Carolina University, USA

²Department of Cardiovascular Sciences, East Carolina University, USA

*Corresponding author: Assad Movahed, East Carolina Heart Institute, 115 Heart Drive, Greenville, NC 27834-4354, USA

Received: March 11, 2021; Accepted: April 01, 2021; Published: April 08, 2021


Chagas disease is a systemic infection due to Trypanosoma cruzi, a parasitic protozoan. Trypanosoma cruzi is endemic in Latin America; however, the prevalence has been increasing in the United States. The infection is mostly vector-borne secondary to triatomine or “kissing” bug bites. However, the infection can also spread via organ transplantation, blood transfusion, or transplacentally resulting in congenital manifestations. Chronic Chagas disease can cause cardiac or gastrointestinal complications that may be irreversible if left untreated. Major cardiac complications include dilated cardiomyopathy, arrhythmias, sudden cardiac death, and thromboembolism.

Keywords: Chagas disease; Trypanosoma Cruzi; Heart failure; Myocardial fibrosis; Heart failure with reduced Ejection Fraction (HFrEF); Cardiac MRI (CMRI)


HFrEF: Heart Failure with Reduced Ejection Fraction; EKG: Electrocardiogram; LVEF: Left Ventricular Ejection Fraction; ARB: Angiotensin Receptor Blocker; CC: Chagas Cardiomyopathy; SCD: Sudden Cardiac Death; ACEIs: Angiotensin Enzyme Inhibitors; VT: Ventricular Tachycardia; ICD: Implantable Cardioverter- Defibrillator

Case Presentation

A 57-year-old Hispanic male with a past medical history of Chagas disease, Heart Failure with reduced Ejection Fraction (HFrEF), and ischemic stroke. The patient presented with dyspnea on exertion for a few days. He described multiple episodes of shortness of breath and chest tightness that last about 30 minutes and improve with rest. He also endorsed bilateral lower extremity nocturnal cramps but denied lower extremity edema, paroxysmal nocturnal dyspnea, cough, nausea, vomiting, abdominal pain, or exertional chest pain.

At the time of presentation, the patient was vitally stable. Cardiac examination revealed the presence of S3 and S4, grade 2-3/6 long systolic murmur best heard over third right and left sternal borders. He had clear breath sounds bilaterally without rhonchi or crackles. Neuro exam was positive for weakness on the left side (which is residual from a previous ischemic stroke).

Pertinent labs: Brain natriuretic peptide was 883pg/ml, D-dimer was 13,185ng/ml. Complete blood count and comprehensive metabolic panel were within normal limits. His lipid panel showed mildly increased LDL and decreased HDL. Troponins were negative.

Five years before this presentation, the patient was admitted due to a right middle cerebral artery ischemic stroke with left-sided hemiparesis. As a part of the work-up, echocardiogram at that time showed dilated cardiomyopathy with an ejection fraction of 40%, and a small apical aneurysm. The patient also gave a history of Chagas disease and reported living in an endemic area. Serology was positive for Trypanosoma cruzi. The patient was thought to be an appropriate candidate for antiparasitic treatment. However, he only showed for one hospital follow-up after this admission and he stopped taking all of his medications.

At the time of the most recent admission, the patient had an x-ray that showed cardiomegaly and bilateral pleural effusions. Electrocardiogram (EKG) showed right bundle branch block and prolonged P-R interval (Figure 1). The patient had a CTA of the chest in the light of a high D-dimer with shortness of breath but it was negative for pulmonary embolism (Figure 2). An echocardiogram on admission showed severely dilated left ventricle, severe global hypokinesis with akinetic to dyskinetic apex, Left Ventricular Ejection Fraction (LVEF) of 15-20 %, and apical linear structure that was suspected to be an LV thrombus (Figure 3).