The human coronary collateral circulation
1Cardiology, University Hospital, Bern, Switzerland. christian.seiler@insel.ch
Insights
Promoting the growth of large coronary collateral arteries (arteriogenesis) is key for patients with coronary artery disease (CAD) who cannot be revascularized. This approach improves blood flow and patient outcomes.
Area of Science:
- Cardiovascular Medicine
- Vascular Biology
- Interventional Cardiology
Background:
- Coronary collateral arteries provide alternative blood supply to ischemic myocardium.
- Well-developed collaterals in coronary artery disease (CAD) patients reduce infarct size and improve survival.
Purpose of the Study:
- To explore the role and therapeutic promotion of coronary collateral arteries in CAD.
- To differentiate between arteriogenesis and angiogenesis for therapeutic benefit.
Main Methods:
- Assessment of collateral flow during vascular occlusion using pressure- or velocity-derived collateral flow index.
- Investigated factors promoting collateral growth, including granulocyte-colony stimulating factor and augmented coronary flow velocity.
Main Results:
- Collateral arteries preventing ischemia are present in about one-third of CAD patients.
- Collateral flow sufficient to prevent ischemia is at least 25% of normal flow.
- Infarct size is determined by occlusion time, area at risk, and collateral supply.
Conclusions:
- Therapeutic strategies should focus on promoting arteriogenesis (large artery growth) over angiogenesis (capillary sprouting).
- Monocyte/macrophage activation via granulocyte-colony stimulating factor or increased coronary flow velocity can promote collateral artery development.
Background:
Coronary collaterals are an alternative source of blood supply to myocardium jeopardized by ischaemia. Well-developed coronary collateral arteries in patients with coronary artery disease (CAD) mitigate myocardial infarcts and improve survival.
Methods And Results:
Collateral arteries preventing myocardial ischaemia during brief vascular occlusion are present in 1/3 of patients with CAD. Among individuals without relevant coronary stenoses, there are preformed collateral arteries preventing myocardial ischaemia in 20-25%. Collateral flow sufficient to prevent myocardial ischaemia during coronary occlusion amounts to double dagger25% of the normal flow through the open vessel. Myocardial infarct size, the most important prognostic determinant after such an event, is the product of coronary artery occlusion time, area at risk for infarction and the inverse of collateral supply. Coronary collateral flow can be assessed only during vascular occlusion of the collateral-receiving artery. The gold standard for coronary collateral assessment is the measurement of intracoronary occlusive pressure- or velocity-derived collateral flow index expressing collateral as a fraction of flow during vessel patency. Approximately one of five patients with CAD cannot be revascularized by percutaneous coronary intervention or coronary artery bypass grafting. Therapeutic promotion of collateral growth is a valuable treatment strategy in those patients.
Conclusions:
Promotion of collateral growth should aim at inducing the development of large conductive collateral arteries (i.e. arteriogenesis) and not so much the sprouting of capillary like vessels (i.e. angiogenesis). Large conductive collateral arteries appear to be effectively promoted via the activation of monocytes/macrophages by means of granulocyte-colony stimulating factor or of augmenting coronary flow velocity.
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