Blood viscosity during thrombolytic therapy with anistreplase in acute myocardial infarction.
It has been postulated that a reduction in blood viscosity due to degradation of plasma fibrinogen may be of benefit to patients with acute myocardial infarction (AMI), who are treated with thrombolytic agents. The aims of this study were to investigate the time course of rheologic parameters, to identify the principal factors determining blood viscosity, and to find possible correlations between viscosity and cardiac function during thrombolytic therapy with anistreplase. Therefore, the viscosity of whole blood and plasma and the hematocrit were measured before and at 10 time points after thrombolysis in 10 patients with AMI. In addition, plasma fibrinogen and fibrin(ogen) degradation products were determined. Immediately after the start of thrombolysis, the viscosity of blood (both at high and low shear rate) and plasma decreased significantly and continued to do so for 24 hours. The mean hematocrit also decreased markedly, and even after correction for these hematocrit changes, the reduction in blood viscosity remained significant: it decreased to 72% of pretreatment (measured at low shear rate), whereas the high-shear viscosity decreased to 95% of baseline. The viscosity of plasma significantly decreased from 1.39 +/- 0.13 mPa.s (mean +/- SD) before thrombolysis to 1.22 +/- 0.08 mPa.s after 2 hours. There was a rapid, nearly complete depletion in fibrinogen, followed by a striking rebound after the second day. The decrease in blood viscosity lasted for 2 days after anistreplase and was mainly accounted for by the reduction in hematocrit. The contribution of fibrinogen to blood viscosity appeared less prominent. Despite these rheologic changes, no improvement in cardiac output was noticed in the patients.
Hoffmann
J J
JJ
Department of Clinical Laboratories (Hemostasis division), Catharina Hospital, Eindhoven, The Netherlands.
Bonnier
J J
JJ
Melman
P G
PG
Bartholomeus
I
I
D000368:Aged; D016255:Anistreplase / Q000627:therapeutic use*; D001779:Blood Coagulation Factors / Q000032:analysis; D001809:Blood Viscosity; D002302:Cardiac Output / Q000502:physiology; D003331:Coronary Vessels / Q000473:pathology; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005340:Fibrinogen / Q000032:analysis; D006400:Hematocrit; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D010949:Plasma; D012044:Regression Analysis; D012212:Rheology; D015912:Thrombolytic Therapy; D014654:Vascular Patency
D001779:Blood Coagulation Factors; D005338:Fibrin Fibrinogen Degradation Products; D016255:Anistreplase; D005340:Fibrinogen