THROMBOLYTIC THERAPY OF ACUTE MYOCARDIAL-INFARCTION ALTERS COLLAGEN-METABOLISM

The objective of the study was to monitor collagen metabolism after th rombolytic therapy. Sequential measurements of serum aminoterminal typ e-III procollagen propeptide (S-PIIINP) and carboxyterminal type-I pro collagen propeptide (S-PICP) were made in 62 patients suspected of acu te myocardial infarction and receiving thrombolytic therapy. Regardles s of whether acute myocardial infarction was confirmed or not, S-PIIIN P increased (94-120%) 4 h after streptokinase therapy (p less than or equal to 0.02), and decreased during the next 20 h with median values at 24 h still above the baseline (p < 0.02). With confirmed acute myoc ardial infarction, S-PIIINP increased from 24 h towards a plateau reac hed at day 2-3 (p < 0.01), with values still elevated at 6 months. No similar biphasic pattern was found for S-PICP, but patients with acute myocardial infarction had S-PICP above baseline at 1, 2, and 6 months (p < 0.05). A less pronounced S-PIIINP increase was noted with tissue -plasminogen activator than with streptokinase. Thrombolytic therapy i nduces collagen breakdown regardless of whether acute myocardial infar ction is confirmed or not. With confirmed acute myocardial infarction collagen metabolism is altered for at least 6 months. Furthermore, fib rin-specific and nonspecific thrombolytic agents appear to affect coll agen metabolism differently.