Related Experiment Video

Updated: Aug 23, 2026

Prehospital Thrombolysis: A Manual from Berlin
05:52

Prehospital Thrombolysis: A Manual from Berlin

Published on: November 26, 2013

[Pharmacologic therapy in failed thrombolysis: sequential infusion of tirofiban. Pilot study with 47 patients]

Alfredo Vetrano1, Maurizio Catanzaro, Fabrizio Corsini

  • 1Dipartimento di Cardiologia, Azienda Ospedaliera San Sebastiano di Caserta, Via Palasciano, 1, Corso Tescione, 81100, Caserta.

Monaldi Archives for Chest Disease = Archivio Monaldi Per Le Malattie Del Torace
|June 24, 2004
PubMed

Insights

Glycoprotein IIb/IIIa inhibitors like tirofiban offer a feasible and safe approach for ST-elevation myocardial infarction patients when thrombolysis fails. This strategy may provide clinical benefits for high-risk individuals undergoing rescue angioplasty.

Area of Science:

  • Cardiology
  • Interventional Cardiology
  • Pharmacology

Background:

  • Thrombolysis is a primary treatment for ST-elevation myocardial infarction (STEMI).
  • Failure of thrombolysis necessitates alternative reperfusion strategies.
  • Glycoprotein IIb/IIIa inhibitors are being explored as adjunctive therapy before rescue angioplasty.

Purpose of the Study:

  • To evaluate the feasibility, safety, and efficacy of using tirofiban as a bridge to rescue angioplasty in STEMI patients with failed thrombolysis.
  • To assess the clinical outcomes of this strategy in a high-risk patient subgroup.

Main Methods:

  • A prospective study involving 47 consecutive STEMI patients who received tirofiban after failed thrombolysis.
  • Comparison with a historical control group of 48 STEMI patients treated two years prior without tirofiban or rescue angioplasty.
  • Tirofiban was administered at a full regimen dose.

Main Results:

  • The use of tirofiban as a bridge to rescue angioplasty was found to be feasible and safe.
  • Preliminary data suggest a potential clinical benefit in this high-risk STEMI population.
  • Further investigation is warranted to confirm efficacy.

Conclusions:

  • Tirofiban administration before rescue angioplasty is a viable option for STEMI patients unresponsive to initial thrombolysis.
  • This approach appears safe and may improve outcomes in patients with failed reperfusion.
  • This strategy addresses a critical unmet need in managing complex STEMI cases.

More Related Videos

Tracking Fibrinolysis of Chandler Loop-Formed Whole Blood Clots Under Shear Flow in An In-Vitro Thrombolysis Model06:16

Tracking Fibrinolysis of Chandler Loop-Formed Whole Blood Clots Under Shear Flow in An In-Vitro Thrombolysis Model

Published on: April 19, 2024

Related Concept Videos

Venous Thrombosis III: Interprofessional Care01:29

Venous Thrombosis III: Interprofessional Care

Venous thrombosis requires effective prevention and treatment strategies to improve patient outcomes and reduce potential complications.Prevention StrategiesHealthcare providers must prioritize preventing venous thromboembolism (VTE) for all adult patients upon admission. Interventions depend on bleeding and thrombosis risk, medical history, current medications, diagnoses, planned procedures, and patient preferences. Patients on bed rest should change positions every two hours and, if not...
Pulmonary Embolism II: Diagnostic Studies and Interprofessional Care01:29

Pulmonary Embolism II: Diagnostic Studies and Interprofessional Care

Diagnosing Pulmonary EmbolismDiagnosing pulmonary embolism (PE) involves clinical assessment and advanced imaging tests. The preferred diagnostic tool is the spiral (helical) CT scan or CT angiography (CTA), which uses intravenous contrast media to visualize the pulmonary vasculature and identify emboli.A ventilation-perfusion (V/Q) scan is an alternative for patients unable to receive contrast media. This scan includes both perfusion and ventilation scanning. Perfusion scanning involves...
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists01:23

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...