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[Evaluation of the fibrinolytic system in myocardial infarction]
J A Moreno1, R Cornudella, M Gálvez
1Servicio de Hematología y Hemoterapia, Hospital Clínico Universitario de Zaragoza.
Insights
Acute myocardial infarction (AMI) is linked to impaired fibrinolysis, characterized by increased PAI-1 and fibrinogen. This hypofibrinolysis persists for at least six months post-AMI, primarily due to elevated PAI-1 levels.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Thrombosis and Hemostasis
Context:
- Acute myocardial infarction (AMI) is a critical cardiovascular event.
- The fibrinolytic system plays a crucial role in dissolving blood clots.
- Understanding fibrinolytic system alterations in AMI is vital for patient management.
Purpose:
- To evaluate key components of the fibrinolytic system in patients with AMI.
- To assess these components during the acute phase and six months post-AMI.
- To compare findings with a healthy control group.
Summary:
- Patients with AMI exhibited increased plasminogen activator inhibitor-1 (PAI-1) and fibrinogen levels during the acute phase.
- Lower levels of plasminogen and alpha 2-antiplasmin were observed compared to controls.
- Six months post-AMI, elevated PAI-1 and persistent fibrinogen increases were noted, indicating sustained hypofibrinolysis.
Impact:
- Identifies hypofibrinolysis as a significant factor in AMI patients.
- Highlights the persistent nature of fibrinolytic dysfunction post-MI.
- Suggests PAI-1 elevation as a primary driver of hypofibrinolysis in AMI, impacting therapeutic strategies.
Purpose:
To evaluate the main components of the fibrinolytic system in patients suffering of acute myocardial infarction (AMI), both in the acute phase and once this has been overcome.
Patients And Methods:
Components of the fibrinolytic system (i.e., PAI-1, t-PA, fibrinogen, plasminogen, and alpha 2-antiplasmin) were determined in 100 patients with AMI. The studies were performed at AMI and 6 months later, and the findings were compared with those of a control group of 30 people matched with regard to age and sex with the patient group. The statistical analysis of the results was made with the BMPD pack, using Student's t test for comparing quantitative variables and the matched test for paired samples.
Results:
At the acute phase the patients showed significant increase of PAI-1 (p < 0.001) and fibrinogen (p < 0.05) concentrations. Plasminogen and alpha 2-antiplasmin rates were lower than in the control group (p < 0.01 and p < 0.005, respectively). In the 6-month study after AMI, significant increase of PAI-1 was found with respect to the control group (p < 0.001). There were also significant differences in the initial PAI-1 rates and the 6-month test (p < 0.05), whereas the increased fibrinogen rates persisted (p < 0.01). Increased antigenic t-PA was found in the patient group before venous occlusion (p < 0.001). Thus, 54 patients (54%) had hypofibrinolysis, due to increased PAI-1 in 41 cases (41%), impaired t-PA release in 13 cases (13%) and both causes in 12 cases (12%).
Conclusions:
Fibrinolytic hypofunction was found in this study during the acute phase of myocardial infarction, which was still present six months later, and was due to increased PAI-1 rates in the majority of the cases.