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- Nielsen, Niels Erik, et al.
(författare)
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Fibrinolytic Variables in Postmenopausal Women with Unstable Coronary Artery Disease
- 2001
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Ingår i: Journal of Thrombosis and Thrombolysis. - 0929-5305 .- 1573-742X. ; 12:3, s. 217-223
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Tidskriftsartikel (refereegranskat)abstract
- 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.
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- Nordquist, J, et al.
(författare)
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Does ultrasound influence experimentally induced thrombus formation in the central artery of the rabbit ear?
- 2000
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Ingår i: Journal of Thrombosis and Thrombolysis. - 1573-742X. ; 9:3, s. 243-249
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Thrombosis is one of the most important causes of morbidity in the medical field. Several independent in vitro studies have shown that the fibrinolytic process may be enhanced by ultrasound, but the effect of ultrasound on thrombus formation in vivo is unexplored. The present study was designed to investigate this matter. METHODS: In a blind randomized study, standardized arteriotomies and intimectomies were performed on the central arteries of the ears of 25 rabbits. The rabbits were allocated to two groups, an untreated control group and a group treated with ultrasound (10 pulses of frequency 1 MHz and intensity 1 W/cm(2) per millisecond giving an averaged intensity of 0.01 W/cm(2)). Immediately after reperfusion, patency was confirmed by a manual empty/refill test, after which blood-flow was monitored using ultrasonic flow-probes twice a minute for two hours. At two hours, patency was rechecked. RESULTS: All vessels were patent at reperfusion, but only seven vessels (three control, four treated) were patent when flow-rate measurements started. At 2 h, patency-frequencies were 12/23 in the control group and 11/22 in the treated group. Flow-rate curves in patent vessels in both groups were similar. Microscopic investigation at one week showed no difference in thrombus accumulation. CONCLUSIONS: Ultrasound with the above characteristics does not significantly improve patency in vivo.
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