Is the coronary physiology of bypass grafts different from that of the native coronary artery? Comment on the “Hemodynamic evaluation of coronary artery bypass graft lesions using fractional flow reserve”

Coronary blood flow is controlled by three resistances; epicardial conduit, precapillary arteriolar, and intramyocardial capillary microvascular resistance. When atherosclerosis increases the normally negligible resistance of the epicardial arteries, the myocardial oxygen-supply demand relationship is challenged. As the epicardial resistance (read stenosis obstruction to flow) further increases, coronary reserve is reduced, ultimately resulting in ischemia which may require revascularization often with coronary bypass grafting. After surgery, the bypass conduit should act in a similar fashion to the native low resistance epicardial vessel. However, the assessment of a stenosis in a CABG conduit is complicated by several features which include: (1) the potential for competing flow (and pressure) from both the native and conduit vessels; (2) the presence of collaterals from long-standing native coronary occlusion; and (3) the potential for microvascular abnormalities due to ischemic fibrosis and scarring, preexisting or bypass surgery-related myocardial infarction or chronic low flow ischemia. In the absence of these complicating features, the theory of FFR should apply just as much to a lesion in a saphenous vein graft to the right coronary artery feeding a normal myocardial bed as a lesion in the native right coronary. However, to prove this point requires some effort. An attempt to demonstrate whether FFR of lesions in coronary bypass grafts can be useful compared FFR in 10 SVGs and the myocardial perfusion imaging results [1]. The 10 male patients were studied some unknown time after CABG with multiple vessels bypassed. All SVGs had at least >50% narrowing and three had >70% narrowing. The sensitivity, specificity, positive and negative predictive values and accuracy of FFR < 0.75 for detecting ischemia on MPI was 50, 75, 33, 85, and 70% and for detecting >70% angiographic narrowing was 33, 71, 33, 71, and 60% respectively (r 5 0.1, P 5 ns). The authors conclude that the use of FFR to assess physiologic significance of SVG lesions is feasible and provides acceptable specificity and negative-predictive value compared with stress perfusion imaging. While my enthusiasm for all things coronary physiologic is well known, I respectfully must disagree with this conclusion. Certainly the physiologic examination of saphenous vein grafts is a worthy subject which has not been previously reported. However, the presentation of such a small number of data points cannot be statistically or clinically reliable. The MPI agrees with the FFR in 7/ 10 patients and only in 6/9 for those with lesions in SVGs supplying the inferior myocardial territory. Only one SVG to D1 was included with the FFR of 0.76 and normal MPI. The technique of MPI further limits my confidence. Of the 10 patients, the MPI stressors were mixed with adenosine in six, dipyridamole in two, and dobutamine in two patients, numbers to small to have uniform results and the tests were not all performed in their center. Although the perfusion abnormality was large in four patients and six patients had transient ischemic dilatation, we do not know what the corresponding FFR was. Sensitivity and specificity based on only 10 patients must be taken with a grain of salt. Moreover, how do we interpret the MPI scar/ischemia designation? It is worthwhile to recall the report of Ragosta et al. [2] who demonstrated that MPI in patients with