Sandbox:Mydah

Associate Editor(s)-in-Chief: Mydah Sajid, MD[1]

Collateral circulation

Overview

Collateral circulation is a network of blood vessels that provide a bypass or alternate conduit of blood flow in a tissue. These specialized blood vessels are naturally present in tissue and undergo adaptive growth and development in response to ischemia. The main function of collateral vessels is to provide an alternate pathway for nutrient and oxygen supply in the case of stenosis or obstruction of the main artery.

Classification

Rentrop devised a grading system to assess the filling of collateral arteries. [7] “Grade 0: no visible filling of any collateral channels Grade I: collateral filling of branches of the vessel to be dilated without any dye reaching the epicardial segment of that vessel Grade 2: partial collateral filling of the epicardial segment of the vessel being dilated Grade 3: complete collateral filling of the vessel being dilated.” Collateral circulation can be classified in the basis of size.[8]

CC0: no continuous connection between donor and recipient artery. 

CC1: continuous, threadlike connection. The diameters of collaterals are ≤0.3 mm. CC2: continuous, small side branch–like size throughout its course. The estimated diameter of CC2 ≥0.4 mm.

Pathophysiology

There are four stages in the development of mature collateral blood vessels from collateral microvasculature. Phase 1 lasts for approximately two days following stenosis or obstruction of the main artery by an embolus. The stenosis of the main artery results in diversion and increase blood flow through small collateral blood vessels. This increases the circumferential diameter of small collateral vessels and augments sheer stress on its walls. The increased stress on the vessel wall causes activation of the Nf-kb gene. [1] There is an increased expression of adhesion molecules on endothelial cells which attracts monocytes at the site of the blocked blood vessels. The monocytes from the bone marrow start accumulating at the extracellular site of collateral vessel formation. The main distinguishing features of this phase is an increase in the permeability of the blood vessel and the transformation of smooth muscle and endothelial cells in the proliferative phase. In the second phase, there is an infiltration of monocytes followed by the release of various cytokines including matrix metallopeptidases, tumor necrosis factor-alpha, platelet-derived growth factors, and vascular endothelial growth factors. There is controlled digestion of extracellular matrix and internal elastic lamina. The cytokines also promote increased proliferation of vascular smooth muscles and endothelial cells. In phase three there is a maturation of smooth muscle cells in uniform circular layer with increase synthesis of elastin and collagen and formation of cell to cell contacts. This results in the formation of a large-caliber blood vessel. In phase four there is dissolution and reduction of small collateral vessels in which there is less blood flow. The collateral vessels which have more flow of blood enlarges and forms mature blood vessels while smaller collateral vessels regress due to decreased flow of blood. [2]