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Fibrinolytic Variables in Postmenopausal Women with Unstable Coronary Artery Disease
Linköping University, Department of Medicine and Care, Cardiology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Centre, Department of Cardiology UHL.
Linköping University, Department of Medicine and Care, Cardiology. Linköping University, Faculty of Health Sciences.
Linköping University, Department of Medicine and Care, Cardiology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Centre, Department of Cardiology UHL.ORCID iD: 0000-0002-2608-2062
2001 (English)In: Journal of Thrombosis and Thrombolysis, ISSN 0929-5305, E-ISSN 1573-742X, Vol. 12, no 3, 217-223 p.Article in journal (Refereed) Published
Abstract [en]

Objectives: Many women with typical anginal chest pain have normal coronary angiograms. The pathogenetic mechanisms behind the chest pain in these patients is unknown but may be due to altered fibrinolytic function enhancing thrombosis formation. We evaluated the two key components of the fibrinolytic system, tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) in women with clinical signs of unstable coronary artery disease (CAD).

Methods and results: 158 patients with unstable CAD and 101 controls were examined. Of the patients 16% had normal vessels and 84% coronary atherosclerosis at coronary angiography. Mean plasma concentration of t-PA-ag, but not of PAI-1-act was higher in patients than in controls (t-PA-ag: 2.12 (2.05;2.19) vs. 1.98 (1.89;2.07), p<0.05; PAI-1-act: 1.55 (1.35;1.74) vs. 1.49 (1.24;1.73), p¼n.s.). Patients with coronary atherosclerosis had significantly higher mean plasma levels of both t-PA-ag and PAI-1-act than patients with normal coronary vessels (t-PA-ag: 2.16 (2.08;2.33) vs. 1.94 (1.78;2.10), p<0.05; PAI-1-act: 1.68 (1.47;1.90) vs. 0.82 (0.43;1.21), p<0.01), and these differences were seen whether markers of myocardial damage were elevated or not. Mean plasma levels of PAI-1-act in patients with normal coronary vessels were even lower than in the control group (p<0.05). Almost all significant differences in mean plasma t-PA-ag and PAI-1-act disappeared after adjustments for known covariates.

Conclusion: Our results indicate, regardless of myocardial marker elevation or not, an activated fibrinolytic system in postmenopausal women with unstable CAD and coronary atherosclerosis, but not in the same group of patients with normal coronary vessels. This argues against reduced fibrinolytic capacity in the latter patients and therefore against thrombosis formation as the cause of chest pain in these women. However, we cannot exclude that the differences can be an effect of inequality among some common risk factors between the groups.

Place, publisher, year, edition, pages
2001. Vol. 12, no 3, 217-223 p.
Keyword [en]
tissue plasminogen activator, plasminogen activator inhibitor, unstable coronary artery disease, women
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-79488DOI: 10.1023/A:1015270907430OAI: oai:DiVA.org:liu-79488DiVA: diva2:542973
Available from: 2012-08-06 Created: 2012-08-06 Last updated: 2017-12-07Bibliographically approved
In thesis
1. Clinical and Laboratory Investigations in Postmenopusal Women with Unstable Coronary Artery Disease
Open this publication in new window or tab >>Clinical and Laboratory Investigations in Postmenopusal Women with Unstable Coronary Artery Disease
2000 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Coronary artery disease (CAD) is the major cause of death in both sexes in the western world. In men with chest pain the diagnostic methods are more useful than in women. An exercise test is considered less reliable in women, mostly due to a high percentage offalse positive tests. Furthermore, 20-40% of women with typical angina have normal vessels at coronary angiography. The mechanisms behind the chest pain in these patients are unknown, but could be due to disturbances in endothelial, thrombogenetic and/or fibrinolytic function.

In a prospective multicentre trial we examined 200 postmenopausal women with unstable CAD and 101 healthy controls. At coronary angiography 15% had normal vessels, 14% had non-significant atherosclerosis and 71% had at least one significant stenosis.

The diagnostic information from basic clinical parameters, ECG and an early exercise test were evaluated. The prevalence of coronary atherosclerosis was high, 85%, and the early exercise test was just as valuable as in men for identifying patients with significant CAD.

Endothelial markers, cyclic GMP (cGMP) and immunoreactive endothelin (irET), were analysed regarding presence or not of coronary atherosclerosis. Patients with normal vessels had low levels of ir-Ef, indicating different mechanisms for ischemia/angina in these patients compared with patients with atherosclerosis. No differences were found regarding cGMP, unless the patient had long-term nitroglycerin treatment, which increased plasma cGMP. Patients with exerciseinduced ischemia had higher cGMP plasma levels compared to those without. This may reflect a general compensatory mechanism.

New lipid variables, apolipoproteins and lipoprotein particles, were no better than the routine lipid examination in separating women with and without coronary atherosclerosis, and the measurement of apolipoproteins and lipoprotein particles on the basis of diagnostic accuracy alone is not justified. Also, elevated triglycerides was most pronounced in women with unstable CAD and coronary atherosclerosis.

Plasma total homocysteine (tHey) is considered a risk factor for CAD, but the relationship between tHey and well-defined CAD in women is still unclear. Mild hyperhomocysteinemia was not related to the risk of unstable CAD in postmenopausal women. Our study stresses the importance of adjusting tHey for the covariates, i.e. age and serum values of folate, vitamin Bl2 and creatinine.

Fibrinolytic and coagulation variables did neither reveal signs of disturbed fibrinolysis nor were in favour of a hypercoagulable/hyperthrombotic state in patients with unstable CAD and normal vessels.

In summary, the prevalence of coronary atherosclerosis in postmenopausal women with signs and symptoms of unstable CAD is high. An early exercise test together with basic clinical parameters is a valuable diagnostic tool. Although there were differences in biochemical markers between patients with and without coronary atherosclerosis, the overlapping between the groups was high. No clinically useful test to separate these two groups was found. Patients with normal vessels were much alike the control group and it is still unclear whether these patients have CAD without atherosclerosis or another mechanism for their chest pain.

Place, publisher, year, edition, pages
Linköping: Linköpings universitet, 2000. 105 p.
Series
Linköping University Medical Dissertations, ISSN 0345-0082 ; 615
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-27526 (URN)12182 (Local ID)91-7219-572-X (ISBN)12182 (Archive number)12182 (OAI)
Public defence
2000-02-04, Berzeliussalen, Universitetssjukhuset, Linköping, 09:00 (Swedish)
Opponent
Available from: 2009-10-08 Created: 2009-10-08 Last updated: 2012-08-06Bibliographically approved

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Nielsen, Niels ErikSwahn, Eva

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