Rapid Reversal of Focal Left Ventricular Hypertrophy and Systolic Dysfunction Resulting From Myocardial Infiltration by Acute Lymphoblastic Leukemia
A 33-year-old male patient with no medical history presented to our emergency room for evaluation of progressive fatigue and dry cough. Chest x-ray revealed marked mediastinal and cardiac silhouette enlargement (Figure, A). Initial laboratory work was notable for a while blood cell count of 240.9 with 96% blasts. Peripheral blood smear was consistent with T-cell acute lymphoblastic leukemia. ECG revealed sinus tachycardia (heart rate, 126 bpm) with right-axis deviation and T-wave inversions throughout the precordial leads (Figure, B). Transthoracic echocardiogram demonstrated moderate focal left ventricular (LV) hypertrophy involving the mid and apical segments of the anterior and anterolateral walls with mildly reduced LV systolic function (40%–45%). LV posterior and septal wall thicknesses were 1.3 and 1.7 cm, respectively, and the mid anterolateral wall thickness was 1.9 cm. Hypokinesis was noted in the hypertrophied segments. A moderate pericardial effusion was noted (Figure, C–E and Movies I–III in the online-only Data Supplement). Cardiac magnetic resonance imaging was obtained that revealed a large superior mediastinal mass and delayed enhancement in the apical inferior and apical septal walls in the mid chamber and apex (Figure, F and G). LV mass by cardiac magnetic resonance imaging was 100 g/m2. Endomyocardial biopsy of the right ventricle with catheterization of the right side of the heart was performed, revealing increased filling pressure, with a right atrial pressure of 26 mm Hg, mean pulmonary artery pressure of 45 mm Hg, and pulmonary capillary wedge pressure of 36 mm Hg. Cardiac biopsy revealed myocardial infiltration by leukemia cells (Figure, H and I). After 1 month of systemic chemotherapy with vincristine, daunorubicin, prednisone, and asparaginase, his white blood cell count decreased to 8.2. At this time, repeat echocardiogram revealed normalization of LV thickness, regional thickening, and global systolic function. LV posterior and septal wall thicknesses were 0.9 and 1.0 cm, respectively, and the mid anterolateral wall thickness was 1.0 cm (Figure, J–L and Movies IV–IV in the online-only Data Supplement). Myocardial dysfunction caused by infiltration by acute leukemia cells is an exceedingly rare complication of acute leukemia.
The online-only Data Supplement is available with this article at http://circ.ahajournals.org/lookup/suppl/doi:10.1161/CIRCULATIONAHA.115.020035/-/DC1.
- © 2016 American Heart Association, Inc.