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Fibrinolytic variables in postmenopausal women with unstable coronary artery disease
N E Nielsen1, E Logander, E Swahn
1Department of Cardiology, University Hospital, S-581 85 Linköping, Sweden. Niels-Erik.Nielsen@lio.se
Insights
Women with unstable coronary artery disease (CAD) and normal coronary angiograms do not show an activated fibrinolytic system. This suggests thrombosis is unlikely to cause their chest pain, contrary to those with coronary atherosclerosis.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Thrombosis Research
Background:
- Many women experience anginal chest pain despite normal coronary angiograms.
- The underlying cause of chest pain in these patients remains unclear.
- Altered fibrinolytic function, potentially enhancing thrombosis, is a suspected mechanism.
Purpose of the Study:
- To evaluate tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) in women with unstable coronary artery disease (CAD).
- To investigate the role of fibrinolytic system components in chest pain pathogenesis in women with normal coronary angiograms.
Main Methods:
- Examined 158 patients with unstable CAD and 101 controls.
- Assessed plasma concentrations of t-PA antigen (t-PA-ag) and PAI-1 activity (PAI-1-act).
- Compared fibrinolytic markers between patients with normal coronary vessels and those with coronary atherosclerosis.
Main Results:
- Patients with unstable CAD and coronary atherosclerosis had higher t-PA-ag and PAI-1-act levels than controls.
- Patients with normal coronary vessels showed lower PAI-1-act levels than controls.
- Differences in t-PA-ag and PAI-1-act largely disappeared after adjusting for covariates.
Conclusions:
- An activated fibrinolytic system was observed in postmenopausal women with unstable CAD and coronary atherosclerosis.
- This activation was not present in women with unstable CAD but normal coronary vessels.
- Findings argue against reduced fibrinolytic capacity and thrombosis as causes of chest pain in women with normal coronary angiograms.
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), p=n.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.