title: Markers of activated hemostasis and fibrinolysis in patients with pulmonary malignancies: comparison of plasma levels in central venous and pulmonary venous blood.
abstract: Malignancy frequently is accompanied by activated coagulation and fibrinolysis indicating a hypercoagulable state. The purpose of our study was to estimate the contribution of local tumor-induced mechanisms to the activation of hemostasis and fibrinolysis. In a prospective study, we compared the plasma levels of thrombin-antithrombin complexes, prothrombin fragment 1+2, and D-dimers in blood samples that simultaneously were drawn from the superior vena cava and the pulmonary vein of a tumor-bearing pulmonary lobe. Samples from the superior vena cava were drawn before operation and served as controls. After thoracotomy, a second group of samples was simultaneously taken from the pulmonary veins of the tumor-bearing lobe and the superior vena cava. Forty-five patients with pulmonary malignancies were included (25 adenocarcinomas and 20 squamous cell carcinomas). There were no significant differences of thrombin-antithrombin complexes, prothrombin fragment 1+2, and D-dimers levels in patients suffering from adenocarcinoma and from squamous cell carcinoma. Intraoperatively, prothrombin fragment 1+2 and D-dimers levels were markedly increased when compared with the preoperative values (p<0.0001). There was no increase of thrombin-antithrombin complexes levels due to the operative traumatization. Prothrombin fragment 1+2, thrombin-antithrombin complexes, and D-dimers plasma levels were significantly higher in the pulmonary venous blood than in the blood simultaneously drawn from the superior vena cava (p<0.0001). Our findings indicate that malignant lung tumors directly contribute to the activation of hemostasis and fibrinolysis in these clinical settings.
authors.affiliation: Department of Cardio-Thoracic Surgery, Heinrich Heine University, Düsseldorf, Germany.
authors.forename: G A
authors.initials: GA
authors.lastname: Kalweit
authors.forename: P
authors.initials: P
authors.lastname: Feindt
authors.forename: M
authors.initials: M
authors.lastname: Micek
authors.forename: E
authors.initials: E
authors.lastname: Gams
authors.forename: P
authors.initials: P
authors.lastname: Hellstern
mesh_terms: D000368:Aged; D000933:Antifibrinolytic Agents / Q000097:blood; D000990:Antithrombin III / Q000032:analysis; D015415:Biomarkers / Q000097:blood; D001777:Blood Coagulation; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005342:Fibrinolysis / Q000502:physiology*; D006487:Hemostasis / Q000502:physiology*; D006801:Humans; D008175:Lung Neoplasms / Q000097:blood* / Q000401:mortality; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000032:analysis; D010447:Peptide Hydrolases / Q000032:analysis; D011013:Pneumonectomy; D011498:Protein Precursors / Q000032:analysis; D011516:Prothrombin / Q000032:analysis; D011667:Pulmonary Veins / Q000737:chemistry / Q000502:physiology; D015996:Survival Rate; D019851:Thrombophilia; D014683:Vena Cava, Superior / Q000737:chemistry
chemical_list: D000933:Antifibrinolytic Agents; D015415:Biomarkers; D005338:Fibrin Fibrinogen Degradation Products; D010446:Peptide Fragments; D011498:Protein Precursors; C046193:antithrombin III-protease complex; C036309:fibrin fragment D; C029733:prothrombin fragment 1; C044183:prothrombin fragment 2; D000990:Antithrombin III; D011516:Prothrombin; D010447:Peptide Hydrolases