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Updated: Aug 14, 2026

Prehospital Thrombolysis: A Manual from Berlin
Published on: November 27, 2013
[Thrombosis in unstable angina. Is there a role for thrombolytic agents?]
P Raynaud1, B Desveaux, G Pacouret
1Clinique Cardiologique, Hôpital Trousseau, Tours.
Insights
Intracoronary thrombosis is a key cause of unstable angina (UA). Thrombolytic treatment shows promise for reducing clots, but further research is needed to confirm benefits and risks.
Area of Science:
- Cardiology
- Vascular Biology
- Pathophysiology
Context:
- Unstable angina (UA) is increasingly linked to intracoronary thrombosis.
- Evidence from pathological, biological, angioscopic, and angiographic studies supports this association.
- Non-obstructive coronary thrombi are frequently observed in UA patients.
Purpose:
- To review the role of intracoronary thrombosis in unstable angina.
- To evaluate the efficacy and safety of thrombolytic therapy for UA.
- To discuss the potential role of transluminal coronary angioplasty and aortocoronary bypass in conjunction with thrombolysis.
Summary:
- Intracoronary thrombosis is a significant etiological factor in unstable angina (UA).
- The frequency of coronary thrombi in UA correlates with the time since the last painful episode, suggesting spontaneous clot lysis.
- While non-randomized studies suggest thrombolysis reduces clots, randomized trials show encouraging but preliminary results, necessitating larger studies.
Impact:
- Highlights the critical role of thrombosis in UA pathophysiology.
- Suggests thrombolytic therapy as a potential treatment strategy for UA.
- Emphasizes the need for further randomized controlled trials to establish the definitive benefits, optimal use, and hemorrhagic risks of thrombolysis in UA, alongside other interventions.
Abstract:
Intracoronary thrombosis is more and more considered as a major etiological factor of unstable angina (UA). The physiopathological diagram from ulceration of the plaque to unstable then stable thrombosis is based on many arguments: pathological (Falk-Fuster), biological, angioscopic (Forrester) and finally angiographic; numerous studies have demonstrated the frequency of non-obstructive coronary thrombi in UA. Their frequency is directly related to the delay in control, in relation with the last painful episode, indicating the spontaneous lysis of the clot. This role suggests the beneficial effect of a thrombolytic treatment. Several non-randomized studies (Vetrovek, Mandelkorn, Gotoh, Vermeer) demonstrate reduction of the clots after thrombolysis. But considering spontaneous lysis, only randomized studies published to date (Gold, Topol and Nicklas) report encouraging results. More extended studies are necessary to specify the beneficial effect and the exact haemorrhagic risk of this treatment and the probable place of additional tests like transluminal coronary angioplasty (TCA) and aortocoronary by-pass.
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