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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
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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.
Anthony Dart, BM, BCh, DPhil
Bridget Sherrard, Bsc
Baker Medical Research Institute; Prahran, Victoria, Australia
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
•Include no more than 300 words of text, three authors, and five references
•Type with double-spacing
•Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
- Copyright ©2004 by the American College of Physicians
