Circadian variation of tissue plasminogen activator and its inhibitor, von Willebrand factor antigen, and prostacyclin stimulating factor in men with ischaemic heart disease.
Open Access
- 1 February 1993
- Vol. 69 (2), 121-124
- https://doi.org/10.1136/hrt.69.2.121
Abstract
OBJECTIVES--To determine whether plasma concentrations of tissue plasminogen activator antigen, von Willebrand factor antigen, and prostacyclin stimulating factor and plasminogen activator inhibitor activity show circadian variation in men with ischaemic heart disease. DESIGN--Blood samples were obtained every four hours for 24 hours from 10 men with ischaemic heart disease. The men were ambulant from 08:10 until 00:00 when they went to bed and they remained in bed until 08:00 the following morning. PATIENTS--Ten men with positive diagnostic exercise tolerance tests with no significant past history, who were not regularly taking any medical treatment except for glyceryl trinitrate. RESULTS--There was significant circadian variation in plasminogen activator inhibitor activity (p = 0.001) (peak value 04:00 and trough value 20:00), but not in plasma concentrations of tissue plasminogen activator antigen, von Willebrand factor, or prostacyclin stimulating factor. CONCLUSION--Men with ischaemic heart disease showed a significant circadian variation in fibrinolysis. The combination of peak values of plasminogen activator inhibitor activity and failure of plasma concentrations of tissue plasminogen activator antigen to increase in the early morning must predispose to thrombosis at this time. The circadian variation in fibrinolysis may contribute to the increased incidence of myocardial infarction in the morning.Keywords
This publication has 21 references indexed in Scilit:
- Circadian variation of endothelial cell function, red blood cell deformability and dehydro-thromboxane B2 in healthy volunteersBlood Coagulation & Fibrinolysis, 1991
- Major circadian fluctuations in fibrinolytic factors and possible relevance to time of onset of myocardial infarction, sudden cardiac death and strokeThe American Journal of Cardiology, 1988
- Concurrent Morning Increase in Platelet Aggregability and the Risk of Myocardial Infarction and Sudden Cardiac DeathNew England Journal of Medicine, 1987
- Increased Plasma Levels of a Rapid Inhibitor of Tissue Plasminogen Activator in Young Survivors of Myocardial InfarctionNew England Journal of Medicine, 1985
- Circadian Variation in the Frequency of Onset of Acute Myocardial InfarctionNew England Journal of Medicine, 1985
- Plasminogen activator inhibitor in the blood of patients with coronary artery disease.BMJ, 1985
- Reduced prostacyclin production in patients with different manifestations of ischemic heart diseaseThe American Journal of Cardiology, 1982
- Prevalence of Total Coronary Occlusion during the Early Hours of Transmural Myocardial InfarctionNew England Journal of Medicine, 1980
- Familial deficiency of a plasma factor stimulating vascular prostacyclin activityThrombosis Research, 1979
- Resistance to Arteriosclerosis in Pigs with von Willebrand's DiseaseJournal of Clinical Investigation, 1978