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LETTER
Protein S, von Willebrand Factor, and Euglobulin Lysis Time as Markers of Coronary Heart Disease
Anthony Dart, BM, BCh, DPhil;
Bridget Sherrard, BSc; and
Hatem Salem, MBBS, FRACP
1 January 1997 | Volume 126 Issue 1 | Page 89
TO THE EDITOR:
Considerable evidence has recently emerged to indicate a change in endothelial-dependent dilatation in patients with coronary disease or coronary risk factors [1]. It is less clear whether the release of endothelially derived hemostatic and fibrinolytic factors is also impaired. Endothelial cells are the major source of von Willebrand factor and protein S. The euglobulin lysis time is a global assessment of the fibrinolytic system and reflects the balance of tissue plasminogen activator and its inhibitor, plasminogen activator inhibitor I. Both proteins are exclusively synthesized by endothelial cells.
Fifty-five patients (62% men; mean age ± SE, 62.5 ± 0.6 years) with newly diagnosed angina pectoris were recruited depending on results of a chest-pain questionnaire and exercise electrocardiography (
1.5-mm ST-segment depression). Patients with coronary heart disease were studied within 5 days of diagnosis and before institution of lifestyle changes, antianginal therapy, or aspirin therapy. Fifty-five age- and sex-matched controls were selected.
Blood samples were collected from an antecubital vein before and after 10 minutes of hand-grip exercise. Platelet-poor plasma was prepared and subsequently analyzed for protein C, protein S, and von Willebrand factor [2, 3]. Euglobulin lysis was done at 37 °C according to the method of Robertson and colleagues [4].
Baseline concentrations of protein S and von Willebrand factor but not protein C significantly differed between patients who had newly diagnosed angina and controls. Euglobulin lysis time was shortened after exercise in controls but not in patients with coronary disease (Table 1).
The findings of elevated levels of von Willebrand factor and protein S with no change in protein C (which is not of endothelial origin) and the impaired decrease of the euglobulin lysis time with exercise (which can be attributed to an imbalance between tissue plasminogen activator and its inhibitor) support the concept of a generalized alteration in the synthetic function of the endothelium in patients with coronary disease.
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Author and Article Information
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Baker Medical Research Institute; Prahran, Victoria, Australia
Box Hill, Melbourne, Australia
1. Yasue H, Matsuyama K, Okumura K, Morikami Y, Ogawa H. Responses of angiographically normal human coronary arteries to intra-coronary injection of acetylcholine by age and segment. Possible role of early atherosclerosis. Circulation. 1990; 81:482-90.
2. Tsuchida A, Salem H, Thomson N, Hancock W. Tumor necrosis factor production during human renal allograft rejection is associated with depression of plasma protein C and free protein S levels and decreased intragraft thrombomodulin expression. J Exp Med. 1992; 175:81-90.
3. McFarlane DE, Stibbe J, Kirkby EP, Zucker MB, Grant RA, McPherson JA. A method for assaying von Willebrand factor (Ristocetin co-factor). Diathesis Haemorrhogica. 1975; 34:306-7.
4. Robertson BR, Pandolf M, Nilsson IM. Fibrinolytic capacity in healthy volunteers as estimated from the effect of venous occlusion of arms. Acta Chirugica. 1972; 138:429.
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