Collateral circulation

Middle cerebral artery embolectomy remains controversial in the acute treatment of stroke. Patients who may benefit from this procedure are those who have good collateral circulation and can be operated on within the first few hours after the onset of symptoms. 

The diameter and length of obstructing lesions and the influence of pressure drop across an area of stenosis also affect coronary blood flow and function of the collateral circulation. Dynamic coronary obstruction can occur in normal vessels and vessels with stenosis in which vasomotion or... 

Much work has been done in the area of vascular growth factors to create collateral circulation, but so far clinical efforts have fallen short of predictions. The new field of cell transplantation may provide the necessary milieu and may be more effective at inducing neovascularization in ischemic myocardium. Fibroblast growth factor in... 

Acquired hyperammonemia Liver disease is a common cause of hyperammonemia in adults. It may be a result of an acute po cess, for example, viral hepatitis, ischemia, or hepatotoxins. Cirrhosis of the liver caused by alcoholism, hepatitis, or biiary obstruction may result in formation of collateral circulation around the liver. As a result, portal blood is shunted directly rto the systemic circulation and does not have access to the ter. The detoxification of ammonia (that is, its conversion to urea) is, therefore, severely impaired, leading to elevated levels of cicu lating ammonia. 

It is not clear why some individuals develop a collateral circulation sufficient to compensate for their ischemic vascular disease whereas others do not, Certainly, features such as the extent of the disease and the time frame over which the ischemia develops are contributing factors. However, other previously unconsidered variables appear to play important roles. 

Schultz A, Lavie L, Hochberg I, et al, Inter-individual heterogeneity in the hypoxic regulation of VEGF significance for the development of the coronary artery collateral circulation. Circulation 1999 100 547-552,... 

Buschmann I, Schaper W. The pathophysiology of the collateral circulation (arteriogenesis). J Pathol 2000 190 338-342. 

Some patients may undergo rapid irreversible injury to larger regions of brain, presumably due to poor collateral circulation. These patients may present with large acute DWI lesions that are of similar size to the acute PI lesion (non-mismatch pattern, see Fig. 3.3). It has been suggested that this group of... 

The posterior communicating artery offers significant variations in size and is often not sufficiently visible in MRA. If it is utilized for a collateral circulation, it can increase in signal and size, but lacking detection in MR angiography in patients with proximal stenosis does not permit an assessment of the lack of collateral flow (Hartkamp et al. 1999 Hoksbergen et al. 2003). 

The anterior cerebellar artery (AICA) is normally the thinnest cerebellar artery and in MR angiographies is often insufficiently depicted. The superior cerebellar artery on the other hand can almost constantly be identified and anomalies such as duplications are mostly recognized on MR angiographies (Uchino et al. 2003). For the numerous anomalies and potential collateral circulations see specific literature (Osborn and Anderson 1977). 

In many instances TOF-MRA provides indirect indicators on collateral circulation at the level of the circle of Willis. While the anatomic conditions for collateral circulation can be studied, the recognition... 

Preliminary studies of collateral circulation in high grade stenoses or occlusions using ultra fast dynamic MRA with temporal resolution in the range of a second did show delayed contrast enhancement in the affected vascular territory, but did not provide relevant additional information compared with conventional MRI and perfusion techniques probably due to the reduced spatial resolution (Wetzel et al. 2001). A dedicated analysis of collateral circulations, especially extra-intracranially, is still the domain of DSA as far as the exact depiction of anatomical connections is of importance. If the exact anastomotic vascular anatomy is not of primary interest, the collateral supply is better determined by MR perfusion techniques. 

Chronically impaired perfusion reserve tends to occur when one or both internal carotid arteries are stenosed by at least 50% of the luminal diameter (Brice et al. 1964 DeWeese et al. 1970 Schroeder 1988), or are occluded, and the collateral circulation is inadequate (Powers et al. 1987 Kluytmans et al. 1999). In this situation, the brain is vulnerable to any fiirtber fall in cerebral perfusion pressure and cerebral metabolism is begiiming to become impaired, with the appearance of structural abnormalities on MRI (van der Grond et aL 1996 Isaka et al. 1997 Derdeyn et al. 1999). 

Rutgers DR, Klijn CJ, Kappelle LJ et al. (2004). Recurrent stroke in patients with symptomatic carotid artery occlusion is associated with high-volume flow to the brain and increased collateral circulation. Stroke 35 1345-1349... 

It is conceivable that patients with impaired cerebral reactivity and raised oxygen extraction fraction are at particular risk of stroke without surgery, and that this impairment can be corrected by carotid endarterectomy, but the studies have been too small to be sure (Schroeder 1988 Naylor et al. 1993b Yonas et al. 1993 Hartl et al. 1994 Yamauchi et al. 1996 Visser et al. 1997 Silvestrini et al. 2000 Markus and Cullinane 2001). Also, we do not know what proportion of strokes in patients with recently symptomatic severe carotid stenosis are actually caused by impaired cerebral reactivity, either as a direct result of low flow or perhaps indirectly as a result of an inadequate collateral circulation to compensate for acute arterial occlusion if it should occur. Nor do we know whether the risk of surgery is higher in these patients and so whether, on balance, carotid endarterectomy will indeed reduce stroke risk any more than in those without impaired reactivity. 

Endothelin may also have a role in ischaemic stroke. Endothelin, released after ischaemia caused by thrombo-embolic occlusion of a cerebral vessel, could propagate further infarction by constricting the collateral circulation. Much less information is available on endothelin in ischaemic stroke but endothelin levels are raised in animal models of focal ischaemia [183] and in ischaemic stroke patients [184]. 

Confirmation of collateral circulation (e.g. umbilical vein, veins of the gall-bladder wall) or flow reversal with centrifugal refluxes... 

Fig. 7.5 Portal hypertension with pronounced collateral circulation in an area with adhesions ( spontaneous Talma effect)...

Indirect splenoportography via the femoral artery is not only very important, but also low-risk. (s. p. 182) Using radiography, the arterial branches of the abdominal aorta initially become visible, followed by the spleen, the splenic vein and the portal vein together with its afferent veins and collaterals. This procedure provides information on (7.) localization of vascular resistance-related hypertension, (2.) cause of portal hypertension (in individual cases), (3.) patency and diameter of the respective vessel, 4.) extent of collateral circulation, (5.) hepatopetal or hepatofugal direction of flow in the portal vein, and 6.) shunt capacity of the splenic vein or superior mesenteric vein. (s. p. 182)... 

Portacaval collaterals represent the final stage of pressure-induced changes to the portal vessels. Initial dilation of the small portal vein branches is followed by the development of meandering vessels. This produces a compensating gain in vascular volume. In the long term, however, the thin-walled portal vessels are unable to withstand the elevated portal venous pressure. As a result, portacaval anastomoses form, which ultimately culminate in varices and frequently also in extensive collateral circulation. In addition to this, the portal vein itself occasionally develops different degrees of ectasia. 

However, this reaction is generally accompanied by fibrosis and increased elasticity of the vessel wall. Portal hypertension leads to the dilation and reopening of veins which connect the portal vein system to the superior or inferior vena cava. Hence collateral circulation develops in the region of the oesophagus and gastric fundus as well as in the intestinal tract, retroperito-neum, lungs, spleen and kidneys, and at the anterior abdominal wall. (s. p. 253) (s. tab. 14.10) (s. figs. 7.5 14.11, 14.12 16.9)... 

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