Author + information
- Gérard Finet, MD, PhD⁎ ( and )
- Gilles Rioufol, MD, PhD
- ↵⁎Department of Interventional Cardiology, Hôpital Cardiologique, B. P. Lyon-Monchat, 69394 Lyon Cedex 03, France
We read with interest the paper by Sen et al. (1) proposing a new adenosine-independent index of stenosis severity. It is suggested that negating the need for adenosine-induced hyperemia (2) would increase adoption because of the time savings and reduction in side effects. This sounds like a straw man argument. The main reasons not to measure fractional flow reserve (FFR) most often are financial.
In their paper, the authors present instantaneous wave free ratio (iFR) as the equivalent of FFR, that is, the ratio of 2 hyperemic flows proven to be equal to the ratio of 2 hyperemic pressures. This is definitely not the case. Assuming that the resistance to flow during the wave-free period is equal to the average resistance during maximal hyperemia neglects the role of the coronary microvasculature in controlling blood flow. The wave analysis theory largely explains the flow pattern in the coronary arteries, but not the absolute level of flow, and should not justify the calculation of hyperemic flow parameters from nonhyperemic pressure measurements. Figure 2 of the Sen et al. (1) paper clearly illustrates that the resistance during the wave-free period is markedly higher than the average resistance during hyperemia and that the resistance during this wave-free period varies with the degree of vasodilation. These variations continuously occur in patients in the catheterization laboratory and depend on heart rate, contractility, pre-load, and afterload. So does iFR. The main role of hyperemia is to offset all the mechanisms responsible for the control of myocardial perfusion. Hyperemia is the wind tunnel of coronary stenoses. Sen et al. (1) suggest a wind-free wind tunnel. The reality is that without hyperemia, the force of the wind varies continuously. Of course, some correlation does exist between iFR and FFR, just as the latter correlates with the resting Pd/Pa ratio, with resting gradient and with hyperemic gradient. Yet, this does not indicate a direct relationship with myocardial perfusion. The coefficient of determination, r2 = 0.808 in Figure 6 of Sen et al. (1), indicates that only 80% of iFR variations are explained by the variable FFR. An FFR of 0.60 corresponds to values of iFR ranging from 0.40 to 0.90.
In Figure 10 of Sen et al. (1), the lowest values are approximately 0.07. FFR values below 0.20 do not exist. This further indicates that iFR is not equal to FFR, or it is an error. The latter option is likely because these data points do not appear at all in Figures 6 or 8 of Sen et al. (1).
It therefore may be advisable to wait for additional validation of resting indices like iFR before using them for clinical decision making about revascularization in individual patients.
- American College of Cardiology Foundation