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Updated: Jun 4, 2026
In Vitro Model of Coronary Angiogenesis
Published on: March 10, 2020
Physical coronary arteriogenesis: a human "model" of collateral growth promotion
Rolf Vogel1, Tobias Traupe, Valérie Stolt Steiger
1Departmentof Cardiology, University Hospital, Bern, Switzerland.
Insights
Minimizing myocardial infarction size is key for coronary artery disease patients. Physical arteriogenesis, like external counterpulsation, promotes collateral artery growth, potentially reducing infarct size and cardiovascular mortality.
Area of Science:
- Cardiovascular research
- Biomedical engineering
- Translational medicine
Background:
- Myocardial infarction size significantly impacts patient outcomes in coronary artery disease.
- Reducing infarct size is a primary goal to decrease cardiovascular mortality.
- Arteriogenesis, the growth of collateral arteries, is a promising strategy for infarct size reduction.
Observation:
- Tangential fluid shear stress is a known trigger for arterial remodeling and collateral growth in experimental models.
- External counterpulsation (ECP) applied to the lower legs during diastole generates shear stress in coronary arteries.
- Cardiac transplant recipients serve as unique human models to study physical coronary arteriogenesis.
Findings:
- Two cardiac transplant recipients demonstrated progressing and regressing clinical arteriogenesis in response to physical stimuli.
- External counterpulsation induces endothelial shear stress, a key factor in promoting coronary collateral artery growth.
- Review of clinical studies supports feasible forms of physical arteriogenesis for managing coronary artery disease.
Implications:
- Physical arteriogenesis presents a potential non-invasive therapeutic strategy to reduce infarct size and improve outcomes in coronary artery disease.
- Understanding the mechanisms of physical arteriogenesis can lead to novel treatments for cardiovascular diseases.
- Further clinical investigation into physical arteriogenesis is warranted to optimize its application in patient care.
Abstract:
In patients with coronary artery disease, the size of myocardial infarction mainly determines the subsequent clinical outcome. Accordingly, it is the primary strategy to decrease cardiovascular mortality by minimizing infarct size. Promotion of collateral artery growth (arteriogenesis) is an appealing option of reducing infarct size. It has been demonstrated in experimental models that tangential fluid shear stress is the major trigger of arterial remodeling and, thus, of collateral growth. Lower-leg, high-pressure external counterpulsation triggered to occur during diastole induces a flow velocity signal and thus tangential endothelial shear stress in addition to the flow signal caused by cardiac stroke volume. We here present two cases of cardiac transplant recipients as human "models" of physical coronary arteriogenesis, providing an example of progressing and regressing clinical arteriogenesis, and review available evidence from clinical studies on other feasible forms of physical arteriogenesis.
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