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Year : 2023  |  Volume : 24  |  Issue : 2  |  Page : 109-113  

Acute lymphoblastic leukemia presenting with acute decompensated cardiac failure

Department of Adult Cardiology, Heart Hospital, Hamad Medical Corporation, Doha, Qatar

Date of Submission19-Sep-2022
Date of Acceptance16-Feb-2023
Date of Web Publication24-Mar-2023

Correspondence Address:
Dr. Mohamed Salah Abdelghani
Department of Adult Cardiology, Heart Hospital, Hamad Medical Corporation, P. O. Box 3050, Doha
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/heartviews.heartviews_85_22

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We report the case of acute lymphoblastic leukemia (ALL) in a 29-year-old male with no past medical history who presented with symptoms and signs of heart failure due to possible infiltrative cardiomyopathy as suggested by echocardiography. Workup including different imaging modalities confirmed the diagnosis of ALL. The patient completed his treatment course with a resolution of heart failure symptoms and normalization of cardiac function which was confirmed by different imaging modalities.

Keywords: Acute lymphoblastic leukemia, cardiac imaging, heart failure, restrictive cardiomyopathy

How to cite this article:
Abdelghani MS, Altermanini M, El-Hassan M, Allam AG, Patel A. Acute lymphoblastic leukemia presenting with acute decompensated cardiac failure. Heart Views 2023;24:109-13

How to cite this URL:
Abdelghani MS, Altermanini M, El-Hassan M, Allam AG, Patel A. Acute lymphoblastic leukemia presenting with acute decompensated cardiac failure. Heart Views [serial online] 2023 [cited 2023 Jun 2];24:109-13. Available from: https://www.heartviews.org/text.asp?2023/24/2/109/372462

   Introduction Top

Cardiac infiltration by hematologic neoplasms is an unusual complication reported in a few cases.[1] Heart failure as a presenting manifestation is extremely rare and very few antemortem cases have been reported. Cases with such presentation require a high level of clinical suspicion and extensive workup to reach a definitive diagnosis.

Cardiac complications in leukemia are usually secondary to chemotherapy, anemia, or infection.[2]

Our patient had clinical and echocardiographic features suggestive of cardiomyopathy subsequently confirmed by radiological imaging, namely cardiac magnetic resonance imaging (MRI). A hematological workup established a diagnosis of acute lymphoblastic leukemia (ALL). The cardiac function normalized with complete resolution of the infiltrative process upon treatment of the primary systemic disease with the appropriate chemotherapy regimen.

   Case Presentation Top

A 29-year-old Sri Lankan male with no past medical history presented with a 2-week history of progressive shortness of breath associated with a productive cough of whitish, blood-tinged sputum. There was no history of any systemic symptoms such as weight loss, night sweats, or fever. He had no recent travel history or sick contact.

Physical examination revealed a sick-looking male afebrile at 36.9°C, tachypneic with a respiratory rate of 30/min, blood pressure of 90/60 mmHg, heart rate of 110 beats/min, and oxygen saturation of 92% on 15 L of a nonrebreathing mask. Chest examination revealed decreased air entry on the right side of the chest with dull percussion on the same side up to the mid-lung zone posteriorly as well as bibasilar late inspiratory crackles. A cardiac examination revealed normal heart sounds with an S3 gallop. No murmurs were noted. Jugular venous pressure was not raised and there was no lower limb edema. Examination of other systems was unremarkable.

The main laboratory investigations at presentation were unremarkable except for an elevated serum creatinine 128 umol/L (normal 64–110 umol/L), elevated serial high sensitive troponin-T levels (290 ng/L) 300 ng/L 6 h later followed by 310 ng/L (normal 0–17 ng/L). Pro-BNP was elevated significantly at 11,300 pg/ml (normal 0–133 pg/ml). Electrocardiogram showed diffuse T-wave inversions without dynamic ischemic changes [Figure 1].
Figure 1: Electrocardiogram upon admission shows sinus rhythm with diffuse T-wave inversion

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Transthoracic echo showed severely impaired left ventricular systolic function. Left ventricular ejection fraction was calculated at 30% with a restrictive filling pattern, an increase in global wall thickness of the right ventricle, and marked thickening of the right ventricular outflow tract were noted as suggestive of infiltrative cardiomyopathy.

Chest X-ray showed bilateral pleural effusion on the right side compared to the left with increased bronchovascular markings [Figure 2].
Figure 2: Chest X-ray showed right-sided obliteration of costophrenic angle suggestive of pleural effusion

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The patient was admitted to the intensive care unit and was treated as a case of new-onset decompensated heart failure with reduced ejection fraction (HFrEF). An ultrasound-guided thoracentesis of the pleural effusion was done, culture showed no bacterial growth, and microscopy from the pleural effusion showed atypical cells consistent with lymphoblastic leukemia suggesting a lymphocytic exudative effusion. In addition, a flow cytometric analysis of pleural fluid showed approximately 52% immature cells with immunophenotype profile consistent with precursor T-cells (positive for terminal deoxynucleotidyl transferase) indicating involvement by precursor T lymphoblastic lymphoma/leukemia (medullary subtype).

The patient underwent cardiac MRI that showed an anterior mediastinal mass, as well as patchy and nodular postgadolinium myocardial enhancement in both ventricles suggesting infiltrative myocardial disease [Figure 3]. Positron emission tomography (PET) scan showed an anterior mediastinal mass with intense hypermetabolism, and bilateral pleural left ventricular, renal, and bone uptakes which indicate active involvement by the lymphoblastic process. The biopsy from the mediastinal mass confirmed the same finding of pleural fluid.
Figure 3: Before chemotherapy. (a) Anteroposterior chest radiograph (chest X-ray) shows evidence of bilateral pleural effusion and bilateral paratracheal opacity. (b) Cardiac MRI-right ventricular outflow tract images showing biventricular myocardial hypertrophy markedly encroached upon the right ventricular outflow tract causing partial obstruction, bilateral pleural effusion, and pericardial effusion are also seen. (c) Cardiac MRI 4-chambers. (d) Cardiac MRI show patchy, nodular, and linear mid-wall myocardial enhancement. (e) Cardiac MRI late postgadolinium contrast enhancing in 4-chambers. (f) Positron emission tomography-computed tomography study shows increased uptake in the left ventricle mainly the apical region. MRI: Magnetic resonance imaging

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Following a multidisciplinary team recommendation, he was immediately treated with high-dose dexamethasone to relieve his symptoms. He was thereafter transferred to the hematology service and started on the UKALL 14 chemotherapy protocol (dexamethasone, vincristine, cyclophosphamide, intrathecal methotrexate, then, daunorubicin, polyethylene glycol-asparaginase, vincristine, methotrexate, dexamethasone, and then, cyclophosphamide, cytarabine, mercaptopurine, rituximab, and dexamethasone).

A follow-up cardiac MRI was done after 5 months which showed complete normalization of systolic function and normal wall thickness of both the right and left ventricles with complete resolution of the previously described infiltrative process [Figure 4]. Repeated echocardiogram showed normal global systolic left ventricular function with an ejection fraction of 61% and normal right ventricular function with a resolution of the infiltrative picture which was noted at the initial echocardiogram at the time of presentation and repeated PET scan showed resolution of the initially seen intense hypermetabolism with no new lesion.
Figure 4: Postchemotherapy. (a) Follow-up chest X-ray showing resolution of bilateral pleural effusion and normal cardiac shadow. (b) Follow-up cardiac MRI after 3 months of chemotherapy (RVOT image showing the significant reduction. of hypertrophy and resolution of RVOT obstruction. (c) Follow-up cardiac MRI 4 chambers. (d and e) Follow-up 3 months late postgadolinium contrast enhancing cardiac MRI showing significant reduction in RV and septal hypertrophy as well as moderate resolution of the patchy enhancing lesions. (f) Follow-up positron emission tomography-computed tomography study after 6 months showing significant reduction of the uptake. MRI: Magnetic resonance imaging, RVOT: Right ventricular outflow tract, RV: Right ventricular

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   Discussion Top

Leukemic cardiac involvement is nonspecific and can present differently according to the involved part. It may be associated with heart failure, pericardial effusion, and rarely, constrictive pericarditis making the diagnostic process extremely challenging. However, cases that present with cardiac failure at initial presentation are exceedingly rare, necessitating a high level of suspicion and extensive workup to establish the diagnosis.[3]

In our case described above, the patient was initially admitted to the cardiology service as a case of newly diagnosed HFrEF. Cardiac MRI is used in cardiomyopathy cases to identify the etiology based on characteristics found which are suggestive of ischemic or nonischemic cardiomyopathy.[4],[5]

Infiltrative diseases such as cardiac amyloidosis and hemochromatosis were considered in the differential diagnosis, but MRI findings were not consistent with any of them as well as having a normal iron profile. In patients with heart failure, pleural effusion might have to be considered part of generalized fluid overload related to heart failure and may have been treated empirically with diuretics. However, a diagnostic tap of the pleural fluid led us to the diagnosis of such hematological malignancy. A PET scan was done to assess the extent of the disease which also confirmed the myocardial involvement.

   Conclusion Top

Lymphoblastic leukemia with cardiac involvement is rarely reported in the literature.[1],[6] Furthermore, it may result in cardiac dysfunction and a poor prognosis. Newly diagnosed infiltrative cardiomyopathy in young patients necessitates an extensive workup with comprehensive imaging. In addition, newly diagnosed pleural effusion is recommended to be investigated even if explained in the clinical setting of heart failure, a simple bedside test such as pleurocentesis can reveal a diagnosis of a serious systemic illness which could be the primary cause of heart failure as in our case.

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 his identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

   References Top

Barbaric D, Holley D, Lau KC, McCowage G. It is ALL in the heart: A patient with acute lymphoblastic leukemia and cardiac infiltration at time of diagnosis. Leuk Lymphoma 2002;43:2417-9.  Back to cited text no. 1
Lam KY, Dickens P, Chan AC. Tumors of the heart. A 20-year experience with a review of 12,485 consecutive autopsies. Arch Pathol Lab Med 1993;117:1027-31.  Back to cited text no. 2
Butany J, Nair V, Naseemuddin A, Nair GM, Catton C, Yau T. Cardiac tumours: Diagnosis and management. Lancet Oncol 2005;6:219-28.  Back to cited text no. 3
Mahrholdt H, Wagner A, Judd RM, Sechtem U, Kim RJ. Delayed enhancement cardiovascular magnetic resonance assessment of non-ischaemic cardiomyopathies. Eur Heart J 2005;26:1461-74.  Back to cited text no. 4
Mohty D, Damy T, Cosnay P, Echahidi N, Casset-Senon D, Virot P, et al. Cardiac amyloidosis: Updates in diagnosis and management. Arch Cardiovasc Dis 2013;106:528-40.  Back to cited text no. 5
Hori T, Suzuki N, Mizue N, Hatakeyama N, Takamuro M, Tsutsumi H. Relapse of T-cell all after stem cell transplant presenting as hypertrophic cardiomyopathy: The value of non-invasive diagnostic imaging in detecting cardiac leukemia. Pediatr Blood Cancer 2006;46:108-11.  Back to cited text no. 6


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]


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