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In young post-myocardial infarction male patients elevated plasminogen activator inhibitor-1 correlates with insulin
1Department of Vascular Disease, University Clinical Centre, Zaloška 2, 1000, Ljubljana, Slovenia, erzen_b@yahoo.com.
Insights
Increased plasminogen activator inhibitor (PAI-1) and insulin resistance are linked to myocardial infarction (MI) in young men. Impaired fibrinolysis with elevated PAI-1 may be a key nonclassical risk factor for MI in this population.
Area of Science:
- Cardiovascular Medicine
- Endocrinology
- Hematology
Background:
- Myocardial infarction (MI) in young patients involves both classical and nonclassical risk factors.
- Insulin resistance and impaired fibrinolysis are potential nonclassical contributors to MI.
- Plasminogen activator inhibitor-1 (PAI-1) plays a crucial role in the fibrinolytic system.
Purpose of the Study:
- To investigate the presence of insulin resistance and impaired fibrinolysis (elevated PAI-1) in young male post-MI patients.
- To examine the relationship between these factors and cardiovascular risk markers like endothelial dysfunction (ED) and intima-media thickness (IMT).
- To explore the link between PAI-1, insulin resistance, obesity, and MI in young males.
Main Methods:
- Study included 41 young male post-MI patients and 25 healthy male controls.
- Measurements included Body Mass Index (BMI), waist-to-hip ratio, insulin resistance, coagulation/fibrinolytic parameters, and inflammation markers.
- Endothelial dysfunction (ED) assessed via flow-mediated dilatation (FMD) and intima-media thickness (IMT) measured on the carotid artery.
Main Results:
- Post-MI patients exhibited increased BMI compared to controls.
- Significantly elevated PAI-1 antigen, PAI-1 activity, and fibrinogen were observed in post-MI patients.
- Increased PAI-1 (antigen and activity) positively correlated with insulin resistance and negatively with FMD in patients.
Conclusions:
- Impaired fibrinolysis, indicated by elevated PAI-1, is present in young male post-MI patients.
- Elevated PAI-1 is significantly associated with insulin resistance and endothelial dysfunction in this cohort.
- PAI-1 may serve as a crucial link between obesity, insulin resistance, and myocardial infarction in young males.
Abstract:
Classical and nonclassical risk factors contribute to the development of myocardial infarction (MI) in young patients. The aim of the present study was to find out whether insulin resistance and impaired fibrinolysis, with increased plasminogen activator inhibitor (PAI-1), are present in young male post-MI patients, and their relation to additional markers of cardiovascular risk such as endothelial dysfunction (ED) and intima-media thickness (IMT). Forty-one male patients (on average 44 years old) in the stable phase after MI were recruited, with 25 healthy males who did not differ from patients regarding age as controls. Body mass index (BMI) and waist-to-hip ratio were measured and insulin resistance was calculated. Several coagulation/fibrinolytic parameters and inflammation markers were measured. ED was estimated by ultrasound measurement of the flow-mediated dilatation (FMD) of the brachial artery, and IMT was measured on the common carotid artery. BMI was increased in post-MI patients in comparison with healthy controls. Compared with the control group, in post-MI patients PAI-1 antigen (13.8 ± 10.6 vs 9.1 ± 7.6 ng/ml, P = 0.042), PAI-1 activity (14.8 ± 10.8 vs 9.0 ± 8.0 IU/ml, P = 0.015), and fibrinogen were significantly elevated. In patients increased PAI-1, antigen and activity were both significantly positively related to insulin resistance. We found an important negative relation between PAI-1 antigen and FMD (r = -0.32, P = 0.04) and between PAI-1 activity and FMD (r = -0.39, P = 0.01). Our results suggest that PAI-1 can be a link between obesity, insulin resistance, and MI in young patients. It is thus concluded that impaired fibrinolysis with increased PAI-1 may be an important nonclassical risk factor for MI, particularly in young males with increased BMI and insulin resistance.
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