Coronary collateral circulation

Collateral vessels are accessory vascular channels which provide perfusion distal to an obstructed native coronary artery. Even in the normal myocardium, inter- and intracoronary collaterals exist at all levels of vessel sizes except the capillaries.6 In certain species (for example, humans and dogs), they are present even in the neonatal heart. In the unstimulated state, collaterals are 40 p,m in diameter and often only one cell layer thick. In the stimulated state, they may have diameters as large as 1 mm, and histologically they are similar to a myocardial arteriole.

There are considerable species differences in localisation and extent of intercoronary collaterals, which have to be taken into account when comparing results of different studies. The dog and the guinea pig have a relatively well developed collateral circulation. Pigs (similar to humans without coronary artery disease) have practically no anatomically demonstrable collaterals. Consequently, acute coronary occlusion leads very quickly to transmural infarction.

There are species differences not only in native (pre-existent) collaterals but also in transformed (developed) collaterals. In the human and porcine heart, collaterals develop predominantly in the subendocardium, and these look histologically like abnormally thin-walled arteries. By contrast, collaterals in canine hearts develop only in a narrow subepicardial zone around the edge of the zone that is potentially ischaemic. These collaterals generally exhibit significantly higher resistance than the vessels that they have replaced, although they are not nearly as flow limiting as the collaterals that develop in humans with ischaemia.

The factors that induce the transformation from the unstimulated to the stimulated state are largely unknown. Ischaemia seems to be a very powerful stimulus for the development of coronary collaterals.7 Several experimental findings would, however, suggest that ischaemia of the cardiac myocyte may not necessarily be a prerequisite for the stimulation of collateral growth:7 8 (1) growing segments of collaterals that are relatively far removed from areas of tissue hypoxia; (2) progressive ameroid induced coronary artery stenosis leading to the development of collaterals in the surrounding subepicardium even though subepicardial perfusion is not necessarily impaired; and (3) lack of defined time or spatial relationship between presumed ischaemia and collateral growth.

There is evidence that an inflammatory response may be the primary stimulus for collateral growth.8 As a result of the lack of preformed arteriolar connections between superficial and deeper vascular territories in humans, a progressive stenosis of large epicardial vessels is likely to cause ischaemia-induced local micronecroses. The subsequent inflammatory response produces angiogenic mitogens mediated by macrophages/monocytes that trigger collateral growth. Thus, in humans (unlike the dog and like the pig) development of subendocardial collateral plexus appears to be a result of true angiogenesis. Reduction in arterial inflow at rest may be the predominant trigger mechanism. Other factors such as coronary occlusion, anaemia, and hypoxia have also been shown to stimulate collateral growth.9

Well developed canine collateral vessels do not vasoconstrict in response to a-adrenergic agonists. Sympathetic activation is therefore unlikely to cause collateral vasoconstriction. There is, however, thromboxane A2 mediated vasoconstriction induced by platelet activating factor (PAF) in mature canine coronary collaterals.10 As myocardial ischaemia can rapidly increase lyso-PAF (the precursor of PAF) by as much as 50%,11 collateral dependent myocardial areas may well be susceptible to PAF-induced vasoconstriction and decrease in blood flow.

Although the protective role of coronary collaterals in humans has been debated in the past, prospectively collected data provide evidence that the collateral circulation limits the degree of ischaemia and improves survival during controlled intracoronary balloon occlusion, and after coronary artery spasm, acute myocardial infarction and post-coronary artery bypass graft closure.9 Thus, in humans the coronary collateral circulation appears to constitute an important alternative source of blood supply to "jeopardised" myocardium.

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