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Reduced synthesis of tissue plasminogen activator by vascular endothelium during acute myocardial infarction
Authors:R. M. Norris  P. A. Ockelford  D. B. Cross  J. T. Rivers  J. M. Smith  M. Takayama  H. D. White
Affiliation:Cardiologist, Coronary-Care Unit, Green Lane Hospital, Auckland, New Zealand.;Haematologist. Auckland Hospital, New Zealand;Research Fellow, Gran Lane Hospital, New Zealand.;Reserch Fellow, Green Lane Hospital, New Zealand.;Research Technician, Department of Haematology, Auckland Hospital, New Zealand.;Research Fellow, Green Lane Hospital, New Zealand.;Specialist in Cardiovascular Research, Green Lane Hospital, New Zealand.
Abstract:We management levels of tissue plasminogen activator (t-PA) antigen in 100 patients within six hours of the onset of acute myocardial infarction, in 34 patients with chronic angina but no recent infarction, and in 36 normal subjects. We also assayed von Willebrand factor in the acute patients and in the normal subjects. Measurements were repeated in 40 acute patients at three weeks after myocardial infarction. Although resting levels of t-PA antigen were not significantly different from normal during myocardial infarction, the capacity of the vascular endothelium to release t-PA after five minutes of venous occlusion was impaired ( P <0.01). The acute phase vessel wall release of von Willebrand factor was increased during acute iafarction ( p <0.01). We conclude that impairment of t-PA production is associated with acute coronary thrombosis although it is not possible to differentiate between a causative role or a secondary response due to exhaustion of the t-PA producing mechanism.
Keywords:Tissue plasminogen activator,    coronary thrombosis,    von Willebrand factor.
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