IMPORTANCE OF THROMBOSIS AND THROMBOLYSIS IN SILENT ISCHEMIA - COMPARISON OF PATIENTS WITH ACUTE MYOCARDIAL-INFARCTION AND UNSTABLE ANGINA

Objective-To investigate whether plaque rupture and thrombosis have a role in silent ischaemia as well as in unstable angina. Design-Prospec tive analysis of the results of haemostatic diagnostic tests at the mo ment of developing silent ischaemia at rest. Setting-Coronary care uni t. Patients-22 patients with acute myocardial infarction, 12 patients with symptomatic angina (unstable angina), and 10 normal volunteers (c ontrol group). Interventions-Continuous cardiac monitoring detected 15 asymptomatic episodes (silent ischaemia) in 6 patients with unstable angina. Blood samples were obtained at admission and when an asymptoma tic alteration was detected and 10 minutes later. Main outcome measure s-Comparisons of concentrations of tissue plasminogen activator, uroki nase type plasminogen activator, tissue plasminogen activator inhibito r-1, cross-linked fibrin degradation products, von Willebrand factor, and thrombin-antithrombin III complexes in patients and controls at ad mission; same comparisons in patients with silent ischaemia at the sta rt of an episode and 10 minutes later. Results-Tissue plasminogen acti vator concentrations were raised at admission in patients with acute m yocardial infarction (mean (SD) 14.2 (6) ng/ml) and in patients with u nstable angina (10.1 (2.5) ng/ml) in comparison with controls (5.1 (2. 7) ng/ml, p < 0.01 and < 0.05 respectively). There was no differences between the two groups of patients, however. Similar results were obse rved at the start of a silent ischaemic episode (9.8 (1.9) ng/ml) and 10 minutes later (10.5 (2.9) ng/ml) compared with controls (p < 0.05). Tissue plasminogen activator inhibitor-1 concentrations were raised i n patients with acute myocardial infarction (45.1 (15) ng/ml) compared with volunteers (20.6 (16) ng/ml, p < 0.01). In patients with silent ischaemia tissue plasminogen activator inhibitor-1 concentrations were slightly but not significantly increased. Concentrations of cross-lin ked fibrin degradation products (D dimer) increased during unstable an gina (2150 (350) ng/ml) and silent ischaemia (2270 (450) ng/ml) compar ed with the concentrations in volunteers (340 (80) ng/ml) and patients with acute myocardial infarction (310 (120) ng/ml; p < 0.01). Conclus ions-The results suggest that thrombosis mediates the pathophysiologic al mechanisms of silent ischaemia and unstable angina.