ABSTRACT
Pulmonary embolism (PE) is usually caused by thrombosis or tumor. We report the long-term survival of a patient with PE due to a leiomyosarcoma in the deep vein. A 71-year-old woman complained of dyspnea and swelling of the left lower limb. Computed tomography revealed filling defects in the pulmonary arteries and deep vein. She was diagnosed with PE caused by venous thrombosis and treated with anticoagulant therapy. Her symptoms were prolonged, and D-dimer tests remained negative. Biopsy of the substance in the deep vein revealed leiomyosarcoma. The possibility of PE caused by extravascular or intravascular tumors should be considered when a patient is negative for D-dimer.
Subject(s)
Leiomyosarcoma/complications , Lower Extremity/blood supply , Pulmonary Embolism/diagnostic imaging , Pulmonary Embolism/etiology , Vascular Neoplasms/complications , Venous Thrombosis/complications , Aged , Anticoagulants/therapeutic use , Biopsy , Female , Fibrin Fibrinogen Degradation Products/analysis , Humans , Pulmonary Embolism/drug therapy , Tomography, X-Ray Computed , Venous Thrombosis/diagnostic imaging , Venous Thrombosis/drug therapyABSTRACT
OBJECTIVES: We investigated whether a higher serum erythropoietin (EPO) level in patients with acute myocardial infarction (MI) subjected to successful primary percutaneous coronary intervention (PCI) can predict a smaller infarct size determined by creatine kinase (CK) release. BACKGROUND: Erythropoietin has been shown to protect cardiomyocytes from ischemia-reperfusion injury in rodents. METHODS: We prospectively studied 101 patients with first MI who received successful primary PCI within 12 h from the onset of MI. Blood samples were collected to examine the serum EPO level after the primary PCI and within 24 h from the onset of MI. RESULTS: The peak CK level and cumulative CK release were significantly lower in the above-median EPO group than in the below-median EPO group. Thrombolysis In Myocardial Infarction (TIMI) grades and collateral grades before PCI, infarct-related coronary arteries, time to the successful reperfusion from the onset of MI, and serum creatinine levels were similar in the two EPO groups. A stepwise multiple regression analysis revealed that the absolute serum EPO level (mU/ml) as well as TIMI grades after PCI and preinfarction angina was an independent predictor for the cumulative CK release. CONCLUSIONS: These data suggest that a high endogenous EPO level can predict a smaller infarct size in patients with acute MI subjected to successful primary PCI. This might be attributed to the potentially protective effect of endogenous EPO against ischemia-reperfusion injury in humans.
