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Updated: Aug 8, 2025

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
Published on: May 28, 2019
[Managing patients with left ventricular thrombosis after acute myocardial infarction: current evidence,
Francesca Giordana1, Giulia Bugani2, Massimiliano Camilli3
1U.O.C. Cardiologia, Azienda Ospedaliera Santa Croce e Carle, Cuneo.
Insights
Left ventricular thrombosis (LVT) incidence has decreased post-myocardial infarction. Embolic events remain a concern despite anticoagulation, with Vitamin K antagonists preferred over newer agents.
Area of Science:
- Cardiology
- Thrombosis Research
Context:
- Left ventricular thrombosis (LVT) incidence has declined due to improved revascularization and antithrombotic therapies post-acute myocardial infarction.
- Embolic events are the primary complication of LVT, even with oral anticoagulation.
- LVT pathogenesis involves Virchow's triad: endothelial damage, blood stasis, and hypercoagulability.
Purpose:
- To review the current understanding of left ventricular thrombosis (LVT) following acute myocardial infarction.
- To discuss diagnostic modalities and therapeutic strategies for LVT.
- To evaluate the role of screening and prophylactic anticoagulation.
Summary:
- Diagnostic tools for LVT include contrast-enhanced echocardiography and cardiac magnetic resonance.
- Thrombi typically form within two weeks post-myocardial infarction, limiting the utility of serial imaging.
- Vitamin K antagonists are the current standard of care; direct oral anticoagulant efficacy is unproven. Prophylactic anticoagulation shows limited evidence.
Impact:
- Highlights the evolving landscape of LVT management after myocardial infarction.
- Underscores the persistent risk of embolic complications.
- Informs clinical practice regarding diagnostic screening and therapeutic choices for LVT.
Abstract:
The incidence of left ventricular thrombosis (LVT) after acute myocardial infarction has declined significantly in recent decades, thanks to advances in the field of revascularization and antithrombotic therapy. Despite oral anticoagulation, embolic events are the most feared complication of LVT. From a pathophysiological point of view, the development of LVT depends on Virchow's triad, that is, endothelial damage caused by myocardial infarction, blood stasis due to left ventricular dysfunction, and hyper-coagulability determined by inflammation. The diagnostic modalities of LVT include transthoracic echocardiography preferably implemented by contrast administration, and cardiac magnetic resonance. Most thrombi develop in the first 2 weeks after acute myocardial infarction, so the role of systematic screening with short to medium term repeated imaging appears limited. Vitamin K antagonists remain the cornerstone of therapy, since the effectiveness of direct oral anticoagulants remains to be established. Only weak evidence supports the routine use of prophylactic anticoagulant therapy, even in high-risk patients.
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