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Multiple cerebral infarcts in Chagas cardiomyopathy with Left Ventricular reduced Ejection Fraction : A Case report.

Session Poster Session 4

Speaker Eduardo Julian Jose Chuquiure

Event : Heart Failure 2019

  • Topic : heart failure
  • Sub-topic : Chronic Heart Failure - Clinical
  • Session type : Poster Session

Authors : EJJ Chuquiure (Mexico City,MX), L Medina-Paz (Mexico City,MX), C Anaya-Morales (Mexico City,MX), D Garcia-Romero (Mexico City,MX), M Balbuena-Madera (Mexico City,MX), C Silva-Ruz (Mexico City,MX), E Tapia-Lopez (Mexico City,MX), O Fiscal-Lopez (Mexico City,MX)

EJJ Chuquiure1 , L Medina-Paz2 , C Anaya-Morales1 , D Garcia-Romero2 , M Balbuena-Madera2 , C Silva-Ruz2 , E Tapia-Lopez2 , O Fiscal-Lopez2 , 1Instituto Nacional de Cardiologia "Ignacio chavez" - Mexico City - Mexico , 2Instituto Nacional de Cardiologia Ignacio Chavez, Centro en Insuficiencia Cardiaca - Mexico City - Mexico ,


Background: Chagas disease (CD) is a vector-borne illness caused by the Trypanosoma cruzi parasite that primarily affects heart and/or digestive system. It is the third most common parasitic infection worldwide. The 40% of these patients develop a chronic form of the disease, that usually generate cardiomyopathy, cardiac arrhythmias and mural thrombus. Ischemic Stroke (IS) has been linked to CD, especially in the chronic form. Stroke recurrence has been estimated at 20% of patients, and secondary prevention measures include chronic anticoagulation in cardioembolic chagasic stroke. Deaths related to these complications have been described in 31-52% of cases. No evidence exists about the use of trypanocidal drugs in patients with chagasic stroke.

Case Summary: A previously healthy male with no vascular risk factors, presented a first cerebral vascular event at 57 years old, confirmed with MRI established in right middle cerebral artery territory. Echocardiography, carotid USG, 24h Holter monitoring and hematology and rheumatology labs were performed with no abnormalities; during his evolution he had significant recovery of the symptoms; however, at 60 and 63 years old, two other episodes of IS were documented, again with undefined etiology. It remained asymptomatic until 67 years old, when he presented a fourth IS with language alterations and left hemiparesis.

When he arrived at our Institute  a new approach was performed.  Basic lab studies were normal, except for dyslipidemia with LDL 118 mg/dL despite of high-intensity statin therapy. EKG showed left ventricular axis deviation, 24h Holter monitoring appeared normal, Transthoracic Echo showed left ventricle dilated and inferior wall hypokinesia, LVEF was 35%. NT-proBNP was 500 pg/mL. Coronary angiography appeared normal. MRI showed extensive fibrosis with mixed pattern with LVEF 34% and RVEF 40%, increase in lateral trabeculation with third apical half predominance. T. cruzi antibodies were ordered, with positive results, two positive confirmatory ELISA against T. cruzi (4.45 and 12.04). After revealing the IS etiology, we initiated optimal medical treatment for heart failure, non-Vitamin K antagonist oral anticoagulant (NOAC) and antichagasic drug, Nifurtimox, with an incredible clinical and functional improvement.


Ischemic stroke can be a rare manifestation of chagasic cardiomyopathy, which is why we strongly suggest that patients from endemic regions of Chagas disease should be screened for anti-T. cruzi antibodies when there is no other explanation for cerebral thromboembolism. Although we present a case where functional and clinical improvement was achieved with medical therapy, additional future studies are needed to assess if anti chagasic treatment is beneficial on these patients to guidelines recommendations.

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