This article sets out to examine the physiological consequences of percutaneous intervention at a microvascular level. The effect of vessel occlusion on the myocardium is determined by the duration of ischaemia, the amount of tissue supplied and the tolerance of the myocardium at a cellular level. In addition, the extent to which angioplasty affects physiological processes depends on the degree of preexisting ischaemia and the interventional substrate, e.g. chronic total occlusions or unstable lesions in the context of an acute coronary syndrome.

Many of the assumptions made regarding the effect of percutaneous intervention on coronary physiology are based on vessel ligation in animal models, which may incompletely reflect mechanisms at play in the pro-thrombotic, pro-inflammatory milieu commonly associated with ischaemic heart disease.

The effect of intervention on coronary flow is complex. It is appreciated that blood flow is determined not only by the degree of epicardial obstruction, but equally by the status of the microvasculature and available collateral support.

Dichotomous physiological responses have been demonstrated whereby in some studies flow has been shown to increase post intervention while in others there is clear impairment of microvascular flow and an increase in microvascular resistance. Available data do not explain entirely why one mechanism predominates under individual circumstances, but it likely reflects the balance of vasoconstrictive and vasodilatory mechanisms together with the degree of luminal obstruction.

Reactive Hyperaemia
It has been shown that following restoration of flow in a previously obstructed vessel, an increase in blood flow above basal levels frequently occurs – a phenomenon known as reactive hyperaemia. This adaptive phenomenon is believed to repay the oxygen debt of the ischaemic episode.

Reactive hyperaemia is mediated by myogenic responses to changes in shear stress and the metabolic conditions – provoked by the preceding ischaemia – and occurs virtually instantaneously. Adenosine, nitric oxide (NO) and the potassium adenosine triphosphate (ATP) channel are all believed to be involved. It is thought that the myogenic response is predominantly controlled by NO-related mechanisms, while activation of the potassium ATP channel mediates the metabolic response. Heterogeneity of this response has been observed with it being most pronounced in the sub-endocardial vessels and least in the sub-epicardium reflecting the degree of ischaemia. Similarly the relative contribution of myogenic and metabolic stimulation appears to vary according to vascular size. The smallest vessels (<50μm) are most sensitive to metabolic factors, the intermediate arterioles (50–80μm) are most sensitive to myogenic activation and the large arterioles (>80μm) respond to flow-induced dilatation.