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Extensive myocardial infiltration by hemopoietic precursors in a patient with myelodysplastic syndrome
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...
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2006
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1569821/ https://www.ncbi.nlm.nih.gov/pubmed/16953890 http://dx.doi.org/10.1186/1471-2326-6-4 |
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author | Mateen, Farrah J Harding, Sheila R Saxena, Anurag |
author_facet | Mateen, Farrah J Harding, Sheila R Saxena, Anurag |
author_sort | Mateen, Farrah J |
collection | PubMed |
description | 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. |
format | Text |
id | pubmed-1569821 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2006 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-15698212006-09-16 Extensive myocardial infiltration by hemopoietic precursors in a patient with myelodysplastic syndrome Mateen, Farrah J Harding, Sheila R Saxena, Anurag BMC Blood Disord Case Report 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. BioMed Central 2006-09-05 /pmc/articles/PMC1569821/ /pubmed/16953890 http://dx.doi.org/10.1186/1471-2326-6-4 Text en Copyright © 2006 Mateen et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Case Report Mateen, Farrah J Harding, Sheila R Saxena, Anurag Extensive myocardial infiltration by hemopoietic precursors in a patient with myelodysplastic syndrome |
title | Extensive myocardial infiltration by hemopoietic precursors in a patient with myelodysplastic syndrome |
title_full | Extensive myocardial infiltration by hemopoietic precursors in a patient with myelodysplastic syndrome |
title_fullStr | Extensive myocardial infiltration by hemopoietic precursors in a patient with myelodysplastic syndrome |
title_full_unstemmed | Extensive myocardial infiltration by hemopoietic precursors in a patient with myelodysplastic syndrome |
title_short | Extensive myocardial infiltration by hemopoietic precursors in a patient with myelodysplastic syndrome |
title_sort | extensive myocardial infiltration by hemopoietic precursors in a patient with myelodysplastic syndrome |
topic | Case Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1569821/ https://www.ncbi.nlm.nih.gov/pubmed/16953890 http://dx.doi.org/10.1186/1471-2326-6-4 |
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