Unstable angina is classified into new-onset, progressive, and angina at rest. Though hemostasis plays a crucial role in the pathogenesis of coronary artery disease, including unstable angina, limited data exist regarding peculiarities of fibrinolytic parameters in the above-mentioned types of unstable angina. Our study aims to investigate if there is a difference in the fibrinolytic state between the groups of patients with new-onset, progressive unstable angina in comparison with stable angina patients depending on medical history data, electrocardiographic and hemodynamic features.
In our cross-sectional study, we recruited 93 coronary artery disease patients (mean age 62.32 (6.94) years, 41 males (44.1%)). They were divided into 3 groups: stable angina patients (n=22) (control), new-onset unstable angina patients (n=21), and progressive unstable angina patients (n=50). The groups were comparable by baseline characteristics. Blood samples were obtained before treatment onset. The concentrations of tissue plasminogen activator and inhibitor of plasminogen activator (type 1) were measured by the ELISA method. We registered 14 points at the admission department, particularly age, sex, body mass index, smoking, presence of the family history of cardiovascular disorders, ST-segment depression, T-wave variability, arrhythmias, left bundle branch blockage, heart rate, systolic and diastolic blood pressure, Sokolov-Lyon voltage criteria, and unstable angina type (new-onset or progressive). After comparison of fibrinolytic parameters’ concentrations among groups under investigation, we defined the main independent predictors among observed 14 parameters to create optimal regression models for assessment of fibrinolytic parameters concentrations.
The groups under investigation differ significantly in concentration of tissue plasminogen activator (P<0.001) and inhibitor of plasminogen activator (type 1) (P<0.001). The tissue plasminogen activator concentration correlated significantly with ST depression (r=0.344, P=0.001), T wave variability (r=-0.233, P=0.02), systolic blood pressure (r=-0.675, P<0.001), diastolic blood pressure (r=-0.655, P<0.001), heart rate (r=-0.568, P<0.001) and clinical unstable angina subgroups (r=-0.706, P<0.001) as well as plasminogen activator inhibitor (type 1) concentration associated with age (r=-0.560, P<0.001), body mass index (r=-0.249, P=0.049), ST-segment depression (r=0.542, P<0.001), arrhythmia (r=0.210, P=0.03), systolic blood pressure (r=0.310, P=0.04), and clinical unstable angina subgroups (r=-0.406, P<0.001). An optimal regression models for tissue plasminogen activator and its inhibitor assessment included systolic blood pressure, heart rate, unstable angina subgroup (R2adj. = 65.0%, P<0.001) and systolic blood pressure, unstable angina subgroup (R2adj. = 42.7%, P<0.001), respectively. Thus, fibrinolytic state among unstable angina clinical types differs significantly independently on observed baseline clinical, electrocardiographic and hemodynamic parameters. This finding confirms the utility of Braunwald unstable angina classification.