Collateral circulation

Collaterals, or collateral circulation, refer to an endogenous network of pre-existing anastomotic vessels that provide alternative blood flow pathways when a primary artery is occluded [1, 13, 15]. These "natural bypasses" are found in multiple tissues, with coronary collaterals in the heart and pial (leptomeningeal) collaterals in the brain being the most clinically significant [3, 6, 13]. In the event of acute ischemia, such as a stroke or myocardial infarction, these vessels undergo a physiological process called arteriogenesis, characterized by significant outward remodeling and lumen expansion to maintain perfusion in the ischemic penumbra [1, 13, 14]. This process is driven by mechanical forces like fluid shear stress and molecular signaling pathways involving growth factors such as vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), and the CXCL12/CXCR4 signaling axis [1, 10, 13, 21]. Therapeutic strategies aimed at enhancing this network, termed collateral therapeutics, seek to salvage at-risk tissue and improve long-term clinical outcomes [5, 6, 14]. Understanding the genetic and molecular determinants of collateral status is crucial for patient risk stratification and the development of pro-arteriogenic pharmaceutical agents [4, 16, 17, 20].

Other names

Collateral vesselsAnastomotic vesselsLeptomeningeal collateralsPial collateralsCoronary collateralsNatural bypass vessels

Promotion of arteriogenesis and collateral vessel recruitment through the stimulation of endothelial cell proliferation, macrophage-mediated vascular remodeling, and nitric oxide-dependent vasodilation [1, 7, 8, 13, 14, 15].