{"title":"FIBRINOLYSIS WAS REPLACED BEFORE IT WAS UNDERSTOOD.","authors":"Victor Gurewich, David Segarnick","doi":"10.1159/000542197","DOIUrl":null,"url":null,"abstract":"<p><p>Introduction Fibrinolysis is often wrongly believed to be due to tissue plasminogen activator (tPA) alone. Instead, both endogenous plasminogen activators are required, but only a mini bolus of tPA is needed to initiate fibrinolysis. This is due to tPA's unique high fibrin affinity binding site located on the fibrin D-domain. Both activators are present in all normal plasma, consistent with both being involved in biological fibrinolysis, which is also the model for optimal therapeutic fibrinolysis. Methods This uses a sequential combination of a 5 mg mini bolus of tPA followed by an infusion of proUK (40 mg/hr) for 90 minutes. This treatment is both highly effective and free of side effects. Results By contrast, due to a misunderstanding of fibrinolysis, tPA is often administered alone. This requires doses of 90-100 mg of tPA over 60 minutes, which is neither very effective nor safe, due to a risk of bleeding complications from the lysis of hemostatic fibrin by tPA's fibrin affinity. Due to this problem, fibrinolysis was replaced by interventional procedures, like percutaneous coronary intervention (PCI), which is much slower, limited to clots larger than the catheter, but is generously reimbursed by third party payers.</p>","PeriodicalId":9391,"journal":{"name":"Cardiology","volume":null,"pages":null},"PeriodicalIF":1.9000,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cardiology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1159/000542197","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
引用次数: 0
Abstract
Introduction Fibrinolysis is often wrongly believed to be due to tissue plasminogen activator (tPA) alone. Instead, both endogenous plasminogen activators are required, but only a mini bolus of tPA is needed to initiate fibrinolysis. This is due to tPA's unique high fibrin affinity binding site located on the fibrin D-domain. Both activators are present in all normal plasma, consistent with both being involved in biological fibrinolysis, which is also the model for optimal therapeutic fibrinolysis. Methods This uses a sequential combination of a 5 mg mini bolus of tPA followed by an infusion of proUK (40 mg/hr) for 90 minutes. This treatment is both highly effective and free of side effects. Results By contrast, due to a misunderstanding of fibrinolysis, tPA is often administered alone. This requires doses of 90-100 mg of tPA over 60 minutes, which is neither very effective nor safe, due to a risk of bleeding complications from the lysis of hemostatic fibrin by tPA's fibrin affinity. Due to this problem, fibrinolysis was replaced by interventional procedures, like percutaneous coronary intervention (PCI), which is much slower, limited to clots larger than the catheter, but is generously reimbursed by third party payers.
期刊介绍:
''Cardiology'' features first reports on original clinical, preclinical and fundamental research as well as ''Novel Insights from Clinical Experience'' and topical comprehensive reviews in selected areas of cardiovascular disease. ''Editorial Comments'' provide a critical but positive evaluation of a recent article. Papers not only describe but offer critical appraisals of new developments in non-invasive and invasive diagnostic methods and in pharmacologic, nutritional and mechanical/surgical therapies. Readers are thus kept informed of current strategies in the prevention, recognition and treatment of heart disease. Special sections in a variety of subspecialty areas reinforce the journal''s value as a complete record of recent progress for all cardiologists, internists, cardiac surgeons, clinical physiologists, pharmacologists and professionals in other areas of medicine interested in current activity in cardiovascular diseases.