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Assessment of the coronary collateral circulation by intracoronary pressure measurements was first described a decade ago and has rapidly become a clinically accepted standard for quantification of collateral flow. The pressure-derived collateral flow index (CFI) expresses collateral flow in relation to normal maximum myocardial perfusion and is calculated by simultaneous measurement of aortic (Pa), central venous (Pv) and coronary wedge (Pw) pressures, where CFI = (Pw − Pv)/(Pa − Pv). In addition to these pressure gradients, collateral flow is determined by the resistances of collateral vessels and the myocardial microvasculature. Therefore, a flow index can only be derived from pressure measurements during conditions of maximum vasodilatation, when all resistances are minimised and held constant. Maximal and steady-state hyperaemia can be induced by administration of pharmacological agents such as adenosine or papaverine, which cause reproducible vasodilatation of resistance vessels.
CFI is assessed during transient coronary occlusion, which often induces myocardial ischaemia. The resulting hypoxia and accumulation of metabolites minimise microvascular resistance and therefore exogenous pharmacological vasodilators are often omitted during measurement of CFI. However, the depth of ischaemia and consequent effectiveness of the endogenous hyperaemic stimulus depend on a variety of anatomical, cellular and vascular factors, including collateral supply itself. Well-collateralised myocardium becomes less ischaemic1 and this may attenuate the endogenous vasodilative stimulus during coronary occlusion. We hypothesised …