Changes in interstitial collagen metabolism during acute myocardial infarction treated with streptokinase or tissue plasminogen activator.
Collagen plays a specific role in the maintenance of vascular integrity and in the thrombosis and scar formation processes. Therefore we found it interesting to study the changes in interstitial collagen metabolism during acute myocardial infarction treated with thrombolytic agents. Changes in collagen synthesis were evaluated by obtaining assays of the serum concentrations of the carboxyterminal propeptide of type I procollagen. Except fibrin plasmin is capable of degrading extracellular matrix components including collagen, and this capability was evaluated by monitoring the serum concentrations of the aminoterminal propeptide of type III procollagen. Twenty-four patients with suspected acute myocardial infarction and indications for thrombolytic therapy were randomized to receive either streptokinase (n = 11) or tissue plasminogen activator (n = 13). The patient groups were identical in their clinical characteristics. Serum levels of the aminoterminal propeptide of type III collagen increased rapidly on infusion of the thrombolytic agents, with the maximal mean increases of 44% and 16% in the streptokinase and TPA-treated groups, respectively. Levels of the carboxyterminal propeptide of type I collagen did not change during the thrombolytic therapy. A transient decrease occurred in the type I propeptide concentration at postinfarction day 2, and this decrease was followed by a secondary increase at days 4 to 6 in both patient groups studied. We conclude that thrombolytic agents stimulate the breakdown of interstitial collagen and that the collagen-degrading activity of TPA is lower than that of streptokinase. This factor may contribute to the relatively higher rethrombosis rate seen after TPA, because exposed collagen in the affected vascular wall stimulates thrombosis formation. On the other hand, increased collagen degradation followed by inhibition of collagen synthesis in the infarcted myocardium might increase the risk for cardiac rupture, especially after streptokinase treatment.
Peuhkurinen
K
K
Department of Medical Biochemistry, University of Oulu, Finland.
Risteli
L
L
Jounela
A
A
Risteli
J
J
D000991:Antithrombins / Q000032:analysis; D003094:Collagen / Q000096:biosynthesis / Q000187:drug effects / Q000378:metabolism*; D003328:Coronary Thrombosis / Q000209:etiology; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005340:Fibrinogen / Q000032:analysis; D005343:Fibrinolytic Agents / Q000009:adverse effects / Q000627:therapeutic use*; D005500:Follow-Up Studies; D006342:Heart Rupture, Post-Infarction / Q000209:etiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy* / Q000378:metabolism; D010446:Peptide Fragments / Q000097:blood; D010960:Plasminogen Activators / Q000009:adverse effects / Q000627:therapeutic use*; D011347:Procollagen / Q000097:blood; D012008:Recurrence; D013300:Streptokinase / Q000009:adverse effects / Q000627:therapeutic use*; D010959:Tissue Plasminogen Activator / Q000009:adverse effects / Q000627:therapeutic use*
D000991:Antithrombins; D005338:Fibrin Fibrinogen Degradation Products; D005343:Fibrinolytic Agents; D010446:Peptide Fragments; D011347:Procollagen; C041876:procollagen Type III-N-terminal peptide; C042813:procollagen type I carboxy terminal peptide; D005340:Fibrinogen; D003094:Collagen; D013300:Streptokinase; D010960:Plasminogen Activators; D010959:Tissue Plasminogen Activator