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Myocardial necrosis in patients with thrombotic thrombocytopenic purpura: pathophysiology and rationale for specific therapy
Author(s) -
Sane David C.,
Streer Nathan P.,
Owen John
Publication year - 2009
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1111/j.1600-0609.2008.01172.x
Subject(s) - medicine , thrombotic thrombocytopenic purpura , von willebrand factor , immunosuppression , pathophysiology , plasmapheresis , purpura (gastropod) , intensive care medicine , vasospasm , immunology , platelet , subarachnoid hemorrhage , antibody , ecology , biology
Myocardial necrosis is now recognized as a common feature of thrombotic thrombocytopenic purpura (TTP), usually due to platelet plugging in the microvasculature. Despite reports that TTP patients with myocardial damage have higher morbidity and mortality, there are no established guidelines for managing these high‐risk patients. The universal occurrence of thrombocytopenia and variable findings including renal dysfunction present unique challenges in this setting. Established therapies including plasma exchange and immunosuppression are the mainstay of therapy for all TTP patients. For the subset of patients with myocardial damage, therapy with more potent antiplatelet drugs, agents that enhance NO availability and alleviate vasospasm and drugs that suppress von Willebrand factor levels may have additional benefit. However, clinical trials are needed to optimize therapy for this subset of TTP patients.

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