Appropriate for risk stratification and clinical studies ACS indicates acute coronary syndrome; AP, angina pectoris; CFI p , pressure-derived collateral flow index; CFI v , velocity-derived collateral flow index; CPI, collateral perfusion index; CTO, chronic total (coronary) occlusion; and LV, left ventricle. threshold of 11 heartbeats accurately distinguishes between collateral supply sufficient or insufficient to prevent myocardial ischemia during a brief occlusion (sensitivity of 88%, specificity of 81% 28 ; Table 2).
Quantitative Coronary Pressure and Doppler Sensor MeasurementsIn addition to their principle angiographic results, Rentrop et al 27 first described an angioplasty balloon occlusion model using the ratio between distal coronary occlusive or wedge pressure (P occl ) and aortic pressure (P ao ), which correlates with angiographic collateral score groups in patients with 1-vessel CAD (Table 2). 29 In 1987, Meier et al 30 found that a P occl ≥30 mm Hg accurately predicted the presence of spontaneously visible or recruitable collaterals. However, P occl is not dependent only on the amount of collateral flow to the occluded vascular region. Determinants of P occl are the driving pressure across collateral pathways (ie, the pressure difference between the coronary pressure in the collateral supplying and receiving artery), the venous back pressure (central venous or right atrial pressure), but also extravascular pressure related to compression of intramural vessels by cardiac contraction and to transmission of diastolic LV pressure to the epicardial circulation. 31 In this context, in that of microembolization of the collateral-dependent vascular area, P occl should not be used for collateral assessment in the acute coronary syndrome because collateral function is substantially overestimated. In the setting of chronic CAD, LV filling pressure has, however, no influence on P occl unless it exceeds values of 30 mm Hg.In 1993, Pijls et al 32 provided the experimental basis for the determination of maximum coronary and myocardial fractional blood flow by coronary pressure measurements; importantly, the contribution to myocardial blood flow by collateral pathways was assumed negligible. In this study, microvascular resistance during pharmacologically induced hyperemia was postulated to be constant and minimal and, thus, no longer dependent on the degree of epicardial stenoses. As a consequence, coronary pressure should directly reflect coronary flow, the former of which is more easily obtainable during invasive examination than the latter. Therefore, myocardial flow Q distal to a stenosis (the sum of flow through the stenotic vessel plus collateral flow as assumed to be zero) relative to myocardial flow without the stenosis Q N (Q/ Q N =fractional flow reserve, FFR) could be calculated on the basis of distal coronary pressure and aortic pressure both after subtraction of central venous backpressure (CVP). The model was tested in dogs, whereby Doppler-derived measurements of stenotic coronary flow Q s to norm...