Acute myocardial infarction as the presenting symptom of acute myeloblastic leukemia with extreme hyperleukocytosis

被引:43
作者
Cohen, Y
Amir, G
Da'as, N
Gillis, S
Rund, D
Polliack, A [1 ]
机构
[1] Hadassah Univ Hosp, Dept Hematol, Head Lymphoma Leukemia Unit, IL-91120 Jerusalem, Israel
[2] Hadassah Univ Hosp, Dept Pathol, IL-91120 Jerusalem, Israel
关键词
encephalopathy; myocardial infarction; acute myeloblastic leukemia; leukostasis; hyperleukocytosis;
D O I
10.1002/ajh.10155
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
This case report deals with an unusual leukostatic complication in a 56-year-old woman with acute myeloblastic leukemia (AML) and extreme hyperleukocytosis (316 x 10(9)/L) who presented with acute myocardial infarction (MI). After leukopheresis the patient achieved hemodynamic stabilization and rapid neurologic recovery of encephalopathy that had also developed after the infarction. Considering the central role of WBC in the remodeling of post MI myocardial tissue, it was obvious that administration of chemotherapy with its subsequent inevitable pancytopenia could impose an increased risk for further cardiac complications including myocardial rupture. Nevertheless, cytarabine-based induction chemotherapy was initiated 3 days after admission, and she achieved prolonged complete remission. Coronary angiography disclosed segmental atherosclerosis, but the only significant obstruction was in the right coronary artery. The patient died with relapsed leukemia 7 years later without recurrence of any cardiac symptoms or signs. Autopsy disclosed segmental coronary atherosclerosis involving the LAD (60% obstruction), suggesting that atherosclerosis was a predisposing risk factor. Additional compromise to blood perfusion due to leukostasis had led to this unusual complication of AML involving a major vessel. This is the first documented case of leukostasis causing coronary artery occlusion as well as the first report of successful induction chemotherapy for AML during a myocardial infarction. (C) 2002 Wiley-Liss, Inc.
引用
收藏
页码:47 / 49
页数:3
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