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 Table of Contents  
Year : 2022  |  Volume : 6  |  Issue : 1  |  Page : 80-81

Unraveling the Mystery of Young Stroke: A Rare Cardiac Manifestation of Systemic Disease

1 Department of Cardiology, All India Institute of Medical Sciences, New Delhi, India
2 Department of Cardiology, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India

Date of Submission14-May-2021
Date of Acceptance05-Jun-2021
Date of Web Publication29-Apr-2022

Correspondence Address:
Dr. A Shaheer Ahmed
Department of Cardiology, 7th Floor, Super Speciality Block, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi - 110 029
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jiae.jiae_15_21

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A 38-year-old male presented with a history of acute-onset hemiparesis 6 months back. On evaluation, he was found to have eosinophilia. Echocardiography was done which revealed a thrombus in the left atrium attached to the posterior mitral leaflet. The rest of the cardiac chambers were normal. Diagnosis of idiopathic hypereosinophilic syndrome was made after extensive evaluation. The patient was started on steroids and oral anticoagulation, following which eosinophil count and size of thrombus reduced.

Keywords: Echocardiography, hypereosinophilic syndrome, left atrial thrombus, stroke

How to cite this article:
Deepti S, Ahmed A S. Unraveling the Mystery of Young Stroke: A Rare Cardiac Manifestation of Systemic Disease. J Indian Acad Echocardiogr Cardiovasc Imaging 2022;6:80-1

How to cite this URL:
Deepti S, Ahmed A S. Unraveling the Mystery of Young Stroke: A Rare Cardiac Manifestation of Systemic Disease. J Indian Acad Echocardiogr Cardiovasc Imaging [serial online] 2022 [cited 2023 Jun 10];6:80-1. Available from: https://jiaecho.org/text.asp?2022/6/1/80/344310

  Introduction Top

Left atrial thrombus formation may be due to primary cardiac or noncardiac systemic conditions. Various etiologies for left atrial thrombus include mitral stenosis, atrial fibrillation, restrictive cardiomyopathy, hypereosinophilic syndrome, hypercoagulable states, and connective tissue disorders such as antiphospholipid antibody (APLA) syndrome. We describe the case of a young male with isolated left atrial thrombus secondary to hypereosinophilic syndrome who presented with hemiparesis.

  Case Report Top

A 38-year-old gentleman presented with the history of acute-onset left hemiparesis 6 months back. His neurological deficit recovered completely in 6 h. He was initially evaluated by a neurologist. Magnetic resonance imaging (MRI) of the brain revealed features suggestive of acute ischemic stroke. He underwent evaluation for etiology of stroke. He did not have any conventional cardiovascular risk factors. Computed tomography angiography of brain and neck vessels was normal.

Meanwhile, his blood counts and biochemistry were done, which revealed leukocytosis and mild thrombocytopenia. Subsequently, a hematology evaluation was done. Peripheral blood smear evaluation revealed a total leukocyte count of 38,000 cells/mm3 and an absolute eosinophil count of 28,000 cells/mm3. Peripheral blood smear, stool, and urine examination did not reveal any parasitic infestation. Bone marrow biopsy showed normal cellularity and no increase in blast cells. Karyotyping was normal. Platelet-derived growth factor, fibroblast growth factor, JAK mutations were not found. The patient was referred for cardiac evaluation of the source of possible embolic stroke. Electrocardiogram was normal. Echocardiography revealed a left atrial thrombus measuring 15 mm × 28 mm attached to the atrial aspect of the posterior mitral leaflet extending to the posterolateral left atrial wall, along with mild mitral regurgitation [Figure 1]. There was no thrombus in other locations and atrial fibrillation was ruled out. The submitral region and endocardial aspect of the ventricles were normal.
Figure 1: (a) Echocardiography in parasternal long-axis view showing thrombus in the left atrium attached to the base of the posterior mitral leaflet. (b) Echocardiography in tilted parasternal short-axis view showing thrombus attached to the posterolateral aspect of left atrium

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Left ventricular end-diastolic and end-systolic dimensions (53 mm and 36 mm, respectively) and left atrial diameter (30 mm) were normal. Left ventricular systolic and diastolic functions were normal. A final diagnosis of lymphocytic variant eosinophilia was made by the hematology team. The patient was started on oral steroid (prednisolone 60 mg daily) and warfarin. On follow-up at 3 months, the total leukocyte count had reduced to 11,200 with an absolute eosinophil count of 1050 cells/mm3. Furthermore, there was a near-complete resolution of thrombus on echocardiography done at 3 months. Steroid was gradually tapered to 10 mg per day over a period of 4 months. In an ideal situation, additional imaging techniques such as cardiac MRI would have shown inflammation in the atrial wall and confirmed the presence of thrombus. However, due to financial constraints, MRI could not be done. The differential diagnosis for such an atrial mass includes thrombus, vegetation, benign and metastatic tumors, and mediastinal tumors invading the left atrium through pulmonary veins. The left atrial mass in this patient was very likely to be thrombus, given the overall clinical presentation and rapid resolution with the treatment.

  Discussion Top

Hypereosinophilic syndrome is defined by the presence of persistent eosinophilia of more than 1500 cells/mm3 along with eosinophil-mediated end-organ damage, in the absence of any identifiable etiology.[1] Cardiovascular involvement is seen in around 40%–50% of the cases with hypereosinophilic syndrome. Although dyspnea is the most common symptom in cardiac involvement, 40% of the patients may be asymptomatic.[2] Embolic manifestations are seen in around 7%–16% of cases.[3] Cardiac involvement of hypereosinophilic syndrome is characterized by three stages: necrotic, thrombotic, and fibrotic stages. The necrotic phase is due to the eosinophilic infiltration of the myocardium leading to myonecrosis. Subsequently, thrombus forms over the denuded endothelium.[4] Cardiac thrombus is frequent in the ventricles, ventricular outflow, and subvalvular region. The most common site of thrombus formation is the left ventricle, followed by right ventricle, and subvalvular region of the posterior mitral leaflet.[3],[5] Atrial thrombus was not found in any case in various case series of cardiac hypereosinophilic syndrome.[5] The etiology for eosinophilia should be extensively evaluated. Management includes steroids and anticoagulation. Our case is unique as isolated left atrial involvement in hypereosinophilia presenting with stroke in the absence of any cardiac symptoms is uncommon. This case highlights that thrombus formation in eosinophilia is not strictly limited to the ventricles.

  Conclusion Top

Although cardiac involvement in hypereosinophilic syndrome typically manifests with thrombus in the apical portion of the left or right ventricle, atypical presentation with isolated left atrial thrombus is also possible. In patients presenting with clot in the cardiac chambers, evaluation of systemic disease after ruling out structural heart disease is of paramount importance.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Ogbogu PU, Rosing DR, Horne MK 3rd. Cardiovascular manifestations of hypereosinophilic syndromes. Immunol Allergy Clin North Am 2007;27:457-75.  Back to cited text no. 1
Parrillo JE, Borer JS, Henry WL, Wolff SM, Fauci AS. The cardiovascular manifestations of the hypereosinophilic syndrome. Prospective study of 26 patients, with review of the literature. Am J Med 1979;67:572-82.  Back to cited text no. 2
Ommen SR, Seward JB, Tajik AJ. Clinical and echocardiographic features of hypereosinophilic syndromes. Am J Cardiol 2000;86:110-3.  Back to cited text no. 3
Lorenzoni R, Cortigiani L, Melosi A. Cardiac involvement in idiopathic hypereosinophilic syndrome. Heart 2002;87:553.  Back to cited text no. 4
Waller BF, Grider L, Rohr TM, McLaughlin T, Taliercio CP, Fetters J. Intracardiac thrombi: Frequency, location, etiology, and complications: A morphologic review--Part I. Clin Cardiol 1995;18:477-9.  Back to cited text no. 5


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