In young post-myocardial infarction male patients elevated plasminogen activator inhibitor-1 correlates with insulin resistance and endothelial dysfunction.

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.