Acute Ventricular Wall Thickening: Sepsis, Thrombotic Microangiopathy, or Myocarditis?
Background. Acute myocardial oedema has been documented in experimental models of ischemia-reperfusion injury or sepsis and is usually investigated by magnetic resonance imaging. Purpose. We describe a case of acute ventricular wall thickening documented by echocardiography in a patient developing s...
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| Format: | Article |
| Language: | English |
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Wiley
2015-01-01
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| Series: | Case Reports in Cardiology |
| Online Access: | http://dx.doi.org/10.1155/2015/275825 |
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| author | Nicolas De Schryver Delphine Hoton Diego Castanares-Zapatero Philippe Hantson |
| author_facet | Nicolas De Schryver Delphine Hoton Diego Castanares-Zapatero Philippe Hantson |
| author_sort | Nicolas De Schryver |
| collection | DOAJ |
| description | Background. Acute myocardial oedema has been documented in experimental models of ischemia-reperfusion injury or sepsis and is usually investigated by magnetic resonance imaging. Purpose. We describe a case of acute ventricular wall thickening documented by echocardiography in a patient developing sepsis and thrombotic microangiopathy. Case Description. A 40-year-old woman, with a history of mixed connective tissue disease, was admitted with laryngeal oedema and fever. She developed Streptococcus pneumoniae septicaemia and subsequent laboratory abnormalities were consistent with a thrombotic microangiopathy. Echocardiography revealed an impressive diffuse thickening of the whole myocardium (interventricular septum 18 mm; posterior wall 16 mm) with diffuse hypokinesia and markedly reduced left ventricular ejection fraction (31%). There was also a moderate pericardial effusion. Echocardiography was normal two months before. The patient died from acute heart failure. Macroscopic and microscopic examination of the heart suggested that the ventricular wall thickening was induced by oedematous changes, together with an excess of inflammatory cells. Conclusion. Acute ventricular wall thickening that corresponded to myocardial oedema as a first hypothesis was observed at echocardiography during the course of septicaemia complicated by thrombotic microangiopathy. |
| format | Article |
| id | doaj-art-9412a877c5654eadbf1d507496e1ec98 |
| institution | Kabale University |
| issn | 2090-6404 2090-6412 |
| language | English |
| publishDate | 2015-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Case Reports in Cardiology |
| spelling | doaj-art-9412a877c5654eadbf1d507496e1ec982025-02-03T01:02:35ZengWileyCase Reports in Cardiology2090-64042090-64122015-01-01201510.1155/2015/275825275825Acute Ventricular Wall Thickening: Sepsis, Thrombotic Microangiopathy, or Myocarditis?Nicolas De Schryver0Delphine Hoton1Diego Castanares-Zapatero2Philippe Hantson3Department of Intensive Care, Cliniques Universitaires Saint-Luc, Université Catholique de Louvain, 1200 Brussels, BelgiumDepartment of Pathology, Cliniques Universitaires Saint-Luc, Université Catholique de Louvain, 1200 Brussels, BelgiumDepartment of Intensive Care, Cliniques Universitaires Saint-Luc, Université Catholique de Louvain, 1200 Brussels, BelgiumDepartment of Intensive Care, Cliniques Universitaires Saint-Luc, Université Catholique de Louvain, 1200 Brussels, BelgiumBackground. Acute myocardial oedema has been documented in experimental models of ischemia-reperfusion injury or sepsis and is usually investigated by magnetic resonance imaging. Purpose. We describe a case of acute ventricular wall thickening documented by echocardiography in a patient developing sepsis and thrombotic microangiopathy. Case Description. A 40-year-old woman, with a history of mixed connective tissue disease, was admitted with laryngeal oedema and fever. She developed Streptococcus pneumoniae septicaemia and subsequent laboratory abnormalities were consistent with a thrombotic microangiopathy. Echocardiography revealed an impressive diffuse thickening of the whole myocardium (interventricular septum 18 mm; posterior wall 16 mm) with diffuse hypokinesia and markedly reduced left ventricular ejection fraction (31%). There was also a moderate pericardial effusion. Echocardiography was normal two months before. The patient died from acute heart failure. Macroscopic and microscopic examination of the heart suggested that the ventricular wall thickening was induced by oedematous changes, together with an excess of inflammatory cells. Conclusion. Acute ventricular wall thickening that corresponded to myocardial oedema as a first hypothesis was observed at echocardiography during the course of septicaemia complicated by thrombotic microangiopathy.http://dx.doi.org/10.1155/2015/275825 |
| spellingShingle | Nicolas De Schryver Delphine Hoton Diego Castanares-Zapatero Philippe Hantson Acute Ventricular Wall Thickening: Sepsis, Thrombotic Microangiopathy, or Myocarditis? Case Reports in Cardiology |
| title | Acute Ventricular Wall Thickening: Sepsis, Thrombotic Microangiopathy, or Myocarditis? |
| title_full | Acute Ventricular Wall Thickening: Sepsis, Thrombotic Microangiopathy, or Myocarditis? |
| title_fullStr | Acute Ventricular Wall Thickening: Sepsis, Thrombotic Microangiopathy, or Myocarditis? |
| title_full_unstemmed | Acute Ventricular Wall Thickening: Sepsis, Thrombotic Microangiopathy, or Myocarditis? |
| title_short | Acute Ventricular Wall Thickening: Sepsis, Thrombotic Microangiopathy, or Myocarditis? |
| title_sort | acute ventricular wall thickening sepsis thrombotic microangiopathy or myocarditis |
| url | http://dx.doi.org/10.1155/2015/275825 |
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