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Quantitative measurement of carotid atherosclerosis in relation to levels of von Willebrand factor and fibrinolytic variables in plasma - a 2-year follow-up study

Nilsson, TK; Spence, JD; Nilsson, Peter LU ; Eliasson, M; Jansson, JH and Boman, K (2002) In Journal of Cardiovascular Risk 9(4). p.215-221
Abstract
Background It has been proposed that the mechanism of action of the new risk factors for myocardial infarction and stroke, von Willebrand factor (vWF), tissue plasminogen activator (tPA) and tissue plasminogen activator inhibitor-1 (PAI-1) could possibly be mediated via a primary effect on atherogenesis but there is little data to substantiate this. Design A prospective single-centre cohort study of progression of atherosclerosis. Methods Carotid plaque area was quantitated by two-dimensional (2D) ultrasound in 258 subjects at entry and after 1 and 2 years. Plasma and serum samples were drawn at baseline and serum lipids and plasma levels of haemostatic factors were measured. Results The traditional risk factors, smoking, total... (More)
Background It has been proposed that the mechanism of action of the new risk factors for myocardial infarction and stroke, von Willebrand factor (vWF), tissue plasminogen activator (tPA) and tissue plasminogen activator inhibitor-1 (PAI-1) could possibly be mediated via a primary effect on atherogenesis but there is little data to substantiate this. Design A prospective single-centre cohort study of progression of atherosclerosis. Methods Carotid plaque area was quantitated by two-dimensional (2D) ultrasound in 258 subjects at entry and after 1 and 2 years. Plasma and serum samples were drawn at baseline and serum lipids and plasma levels of haemostatic factors were measured. Results The traditional risk factors, smoking, total cholesterol, hypertension and male gender explained 51% of the variance in plaque area at baseline and 48% at 1-year followup. There were small positive associations of plaque area with vWF, tPA and tPA/PAI-1 complex and a tendency to negative associations with PAI-1 levels, independent from the traditional risk factors. The additional explanatory power of the haemostatic factors did not exceed 3%. Conclusion The data accord with a marginal role in atherogenesis of vWF and tPA, and underline the major impact of smoking, hypertension and cholesterol on carotid plaque area progression. (C) 2002 Lippincott Williams Wilkins. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
fibrinolysis, plasminogen activators, atherosclerosis, von Willebrand factor, plaque area
in
Journal of Cardiovascular Risk
volume
9
issue
4
pages
215 - 221
publisher
Lippincott Williams & Wilkins
external identifiers
  • wos:000179082600006
  • pmid:12394330
  • scopus:0036702251
ISSN
1350-6277
language
English
LU publication?
yes
id
ed3c32d8-cc23-46d0-9884-26821fa55fbd (old id 892469)
alternative location
http://www.ejcpr.com/pt/re/ejcpr/abstract.00043798-200208000-00006.htm
date added to LUP
2008-01-23 22:00:54
date last changed
2017-01-01 04:41:58
@article{ed3c32d8-cc23-46d0-9884-26821fa55fbd,
  abstract     = {Background It has been proposed that the mechanism of action of the new risk factors for myocardial infarction and stroke, von Willebrand factor (vWF), tissue plasminogen activator (tPA) and tissue plasminogen activator inhibitor-1 (PAI-1) could possibly be mediated via a primary effect on atherogenesis but there is little data to substantiate this. Design A prospective single-centre cohort study of progression of atherosclerosis. Methods Carotid plaque area was quantitated by two-dimensional (2D) ultrasound in 258 subjects at entry and after 1 and 2 years. Plasma and serum samples were drawn at baseline and serum lipids and plasma levels of haemostatic factors were measured. Results The traditional risk factors, smoking, total cholesterol, hypertension and male gender explained 51% of the variance in plaque area at baseline and 48% at 1-year followup. There were small positive associations of plaque area with vWF, tPA and tPA/PAI-1 complex and a tendency to negative associations with PAI-1 levels, independent from the traditional risk factors. The additional explanatory power of the haemostatic factors did not exceed 3%. Conclusion The data accord with a marginal role in atherogenesis of vWF and tPA, and underline the major impact of smoking, hypertension and cholesterol on carotid plaque area progression. (C) 2002 Lippincott Williams Wilkins.},
  author       = {Nilsson, TK and Spence, JD and Nilsson, Peter and Eliasson, M and Jansson, JH and Boman, K},
  issn         = {1350-6277},
  keyword      = {fibrinolysis,plasminogen activators,atherosclerosis,von Willebrand factor,plaque area},
  language     = {eng},
  number       = {4},
  pages        = {215--221},
  publisher    = {Lippincott Williams & Wilkins},
  series       = {Journal of Cardiovascular Risk},
  title        = {Quantitative measurement of carotid atherosclerosis in relation to levels of von Willebrand factor and fibrinolytic variables in plasma - a 2-year follow-up study},
  volume       = {9},
  year         = {2002},
}