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. 2006 Sep 5:6:4.
doi: 10.1186/1471-2326-6-4.

Extensive myocardial infiltration by hemopoietic precursors in a patient with myelodysplastic syndrome

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Extensive myocardial infiltration by hemopoietic precursors in a patient with myelodysplastic syndrome

Farrah J Mateen et al. BMC Blood Disord. .

Abstract

Background: Although myocardial infiltration with leukemic blasts is a known finding in patients with acute leukemia, this phenomenon in myelodysplasia is not reported in the literature. Cardiac symptoms in patients with myelodysplasia are often due to anemia and may be due to iron overload and side effects of therapy.

Case presentation: Herein we report the first case of neoplastic infiltration of the heart with associated myocardial necrosis in a patient with myelodysplasia. It was associated with unicellular and multifocal geographic areas of necrosis in the left ventricle and the interventricular septum. It is likely that cardiac compromise in our patient was due to a combination of restrictive cardiomyopathy due to leukemic infiltration, concomitant anemia, cardiac dilatation, conduction blocks and myocardial necrosis. Myocardial necrosis was most likely due to a combination of ischemic damage secondary to anemia and prolonged hypotension and extensive leukemic infiltration. Markedly rapid decrease in ejection fraction from 66% to 33% also suggests the role of ischemia, since leukemic infiltration is not expected to cause this degree of systolic dysfunction over a 24-hour period. The diagnosis was not suspected during life due to concomitant signs and symptoms of anemia, pulmonary infections, and pericardial and pleural effusions. The patient succumbed to cardiac failure.

Conclusion: Hemopoietic cell infiltration was not considered in the differential diagnosis and contributed to this patient's morbidity and mortality. This case highlights the clinical importance of considering myocardial infiltration in patients with myelodysplasia and cardiac symptoms.

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Figures

Figure 1
Figure 1
Plain radiographs of the chest (PA views) at admission (a) and four days later (b) with noticeable increase in the cardiac silhouette.
Figure 2
Figure 2
Peripheral blood smear with a circulating blast and a pseudo Pelger-Huet cell, (Giemsa × 500).
Figure 3
Figure 3
Bone marrow aspirate with marked erythroid dysplasia (Giemsa × 500).
Figure 4
Figure 4
Bone marrow core biopsy with megakaryocytic and erythroid dysplasia (H&E × 300).
Figure 5
Figure 5
Bone marrow core biopsy with abnormal localization of immature precursors (H&E × 300).
Figure 6
Figure 6
Epicardial involvement by hemopoietic precursors with fibrinous pericarditis (H&E × 50).
Figure 7
Figure 7
Extensive septal and intercellular myocardial infiltration with vascular wall andmyocardial necrosis (H&E × 50).
Figure 8
Figure 8
Cardiac infiltration by hemopoietic precursors; dysplastic megakaryocyte andmyeloid precursors; arrows point to blasts (H&E × 300).
Figure 9
Figure 9
Cardiac infiltration by hemopoietic precursors; Myeloperoxidase positive myeloidprecursors (Immunoperoxidase × 300).

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