English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Therapeutic fibrinolysis has used tissue plasminogen activator (tPA) since 1987 based on the belief that tPA was alone responsible for fibrinolysis. This was, however belied by clinical experience with tPA as well as experimental findings showing that fibrinolysis required both biological activators. In the clinic, it was never possible to show that tPA was more effective than the previous activator, streptokinase (SK), despite comparative mega trials in acute myocardial infarction (AMI) in which the only significant difference found was that tPA caused more intracranial hemorrhage (ICH) than SK. Eventually, this experience with tPA resulted in tPA as well as fibrinolysis being discredited and replaced by percutaneous coronary intervention (PCI) whenever possible. In ischemic stroke, fibrinolysis with tPA remains the standard. By contrast, the endogenous, physiological system induces fibrinolysis with both tPA and urokinase plasminogen activator (uPA). The native form of uPA is a proenzyme, prouPA, and tPA and prouPA have complementary modes of action making them synergistic in combination. This combination was once tested clinically in 101 AMI patients who were given a mini bolus of tPA (5 mg) followed by a modest infusion of prouPA. Compared with the results in the best of the tPA trials, this combination regimen almost doubled the infarct artery TMI-3 patency rate and reduced the mortality rate six-fold. The findings are a testimony to the therapeutic potential of the endogenous paradigm of fibrinolysis compared with current monotherapy.

THERAPEUTIC FIBRINOLYSIS WITH TPA FAILED BECAUSE TPA’S MECHANISM OF ACTION WAS MISUNDERSTOOD