[Role of coronary risk factors in blood thrombogenicity and acute coronary syndromes]
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Updated: Aug 30, 2026

Coronary Progenitor Cells and Soluble Biomarkers in Cardiovascular Prognosis after Coronary Angioplasty
Published on: January 28, 2020
Antonia Sambola1, Valentín Fuster, Juan José Badimon
1Servicio de Cardiología, Hospital de Terrassa, Barcelona, España. asambola@yahoo.com
Insights
Systemic risk factors contribute to endothelial dysfunction, leading to atherosclerotic disease and acute coronary syndromes (ACS). Targeting tissue factor (TF) offers a new therapeutic strategy for ACS by reducing blood thrombogenicity.
Area of Science:
- Cardiovascular Science
- Pathophysiology
- Molecular Biology
Context:
- Endothelial dysfunction is a key mechanism in atherosclerotic disease and acute coronary syndromes (ACS).
- Systemic risk factors like diabetes, hypercholesterolemia, and smoking promote a pro-thrombotic state.
- Superficial plaque erosion contributes to ACS in a significant proportion of patients.
Purpose:
- To explore the link between systemic risk factors, endothelial dysfunction, and thrombotic complications in ACS.
- To investigate the role of tissue factor (TF) in heightened thrombogenicity associated with risk factors.
- To identify potential therapeutic targets for ACS based on TF inhibition.
Summary:
- Systemic risk factors impair endothelial function, promoting atherosclerotic plaque instability and thrombotic complications in ACS.
- These risk factors increase blood thrombogenicity, partly through elevated circulating tissue factor (TF) levels, which activate the coagulation cascade.
- This heightened thrombogenicity, driven by TF, exacerbates thrombus formation, triggering ACS events.
Impact:
- Highlights the importance of aggressive management of cardiovascular risk factors.
- Suggests that inhibiting tissue factor (TF) expression could be a novel therapeutic strategy for treating ACS.
- Opens new research avenues for developing targeted therapies to prevent or treat ACS.
Abstract:
Recent advances in basic science have linked some systemic risk factors to endothelial dysfunction which gives rise to atherosclerotic disease and triggers the progression of thrombotic complications. Superficial erosion of the stenotic plaque can be observed in one-third of acute coronary syndromes (ACS). In these cases the presence of classic risk factors such as diabetes mellitus, hypercholesterolemia and smoking favor a state of "vulnerable blood" or high risk. Increased thrombogenicity can exacerbate thrombus formation and is able to trigger an ACS. The vessel endothelium regulates contractile, mitogenic and thrombotic activities of the vessel wall. Risk factors impair both homeostasis and hemostasis of the vessel wall and promote inflammatory signals. Platelet and monocyte activation favors the expression of tissue factor (TF), thus triggering the coagulation cascade with thrombin generation and clot formation. Increased blood thrombogenicity linked to classic risk factors may be associated with circulating TF levels which are much higher than those observed in healthy subjects without risk factors. These observations not only emphasize the usefulness of aggressive management of risk factors but open a new avenue for future studies to devise therapeutic strategies to treat ACS by inhibiting TF expression.
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