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Effect of low dose aspirin on augmented plasminogen activator inhibitor type 1 activity in patients with permanent
H Abe1, K Takahara, Y Nakashima
1Second Department of Internal Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
Insights
Patients with permanent pacemakers show elevated plasminogen activator inhibitor type-1 (PAI-1) activity. Low-dose aspirin reduces platelet aggregation but does not affect PAI-1 levels in these patients.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Biochemistry
Background:
- Coagulation and fibrinolysis are critical hemostatic processes.
- Permanent pacemakers are widely used to manage cardiac rhythm disorders.
- The impact of permanent pacemakers on hemostatic activity requires further investigation.
Purpose of the Study:
- To evaluate the activity of coagulation and fibrinolysis in patients with permanent pacemakers.
- To assess the effects of low-dose aspirin on hemostatic parameters in these patients.
Main Methods:
- Studied 29 patients with permanent pacemakers (single vs. double lead) and 7 age-matched controls.
- Measured prothrombin time, activated partial thromboplastin time, fibrinogen, antithrombin III, tissue-type plasminogen activator (tPA) activity, plasminogen activator inhibitor type-1 (PAI-1) activity, and platelet aggregation.
- Assessed the effects of low-dose aspirin (81 mg/day) on these parameters in 21 patients.
Main Results:
- PAI-1 activity was significantly higher in pacemaker patients (single and double lead groups) compared to controls.
- Platelet aggregation induced by collagen was slightly elevated in pacemaker patients.
- Low-dose aspirin significantly suppressed collagen-induced platelet aggregation but did not affect PAI-1 activity.
- tPA activity increased significantly following low-dose aspirin administration.
Conclusions:
- Patients with permanent pacemakers exhibit elevated PAI-1 activity.
- Low-dose aspirin effectively reduces platelet aggregation in these patients.
- PAI-1 activity in pacemaker patients is not suppressed by low-dose aspirin.
Abstract:
To clarify the activity states of coagulation and fibrinolysis in patients with a permanent pacemaker, we studied 29 patients more than 4 months after operation. They were divided into a single pacemaker lead group (S, n = 14) and a double lead group (D, n = 15). Prothrombin time, activated partial thromboplastin time, fibrinogen, antithrombin III, tissue-type plasminogen activator (tPA) activity, plasminogen activator inhibitor type-1 (PAI-1) activity, and platelet aggregation were measured and compared to those in an age-matched control group (C, n = 7). The effects of low dose aspirin (81 mg/day) in the patients (n = 21) were also studied 2 weeks after administration. PAI-1 activity in groups S and D was significantly higher than that in the group C (53.5 +/- 36.5, 86.8 +/- 59.2 ng/mL vs 19.4 +/- 7.2 ng/mL; P < 0.01 and P < 0.005). Platelet aggregation induced by collagen was slightly higher in groups S and D than group C. Other parameters were not significantly different. In the patients, low dose aspirin significantly suppressed collagen induced platelet aggregation (71.8 +/- 20.3% vs 41.7 +/- 28.3%; P < 0.005), but not PAI-1 activity. tPA activity was increased significantly by the low dose aspirin administration (3.94 +/- 1.85 ng/mL vs 2.48 +/- 1.19 ng/mL; P < 0.005). Thus, PAI-1 activity in patients with a permanent pacemaker is elevated, and the activity is not suppressed by low dose aspirin unlike the platelet aggregation.