FFR is based on the hemodynamic principle of pressure drop when fluid or blood flows across a narrowed segment (similar to Bernoulli principle). If there is more than 25 % pressure drop across the lesion under maximum hyperemic condition (or steady-state) it is counted as significant.(FFR is .75)
Now, if the distal vessel is supported by collaterals, what happens?
When a vessel in question, is supplied by well-formed distal collaterals, it will prevent this pressure drop and hence lesion is underestimated. Similarly, if the donor artery has a suspicious intermediatory lesion, the FFR across it is falsely low, and overestimates the lesion.The distal pressure drop here is not because of the lesion but due to rapid collateral flow into the recipient artery.
Let us take a hypothetical case. In a post anterior MI 90 % LAD lesion receiving well-formed collateral from RCA which also has a 70 % proximal lesion.
- First, fix a lesion in the recipient artery and then reassess donor artery.
- This is especially important in LAD CTO
- If you open up CTO, a lesion in RCA might become insignificant and may not require intervention.
FFR overestimates lesion in the donor artery. Under-estimates lesion severity in the recipient artery.
FFR as a concept has suffered a conceptual as well as situational issues (Left main, bifurcation blues, ACS confounders, Adenosine antics! etc) . Hence,we have moved to IFR, CT-FFR, QFR, IMR, etc.(Sorry to say this, even these modalities are struggling to become a practical tool for the true physiological assessment of a lesion)
I used to tell my students, do a stress test if we encounter 70 to 90 % single-vessel lesion (or even multivessel ). If it comes negative or if the patient has good exercise capacity, it is a non-invasive marker of adequate FFR and avoids an Intervention.
I wish , we can call the humble stress test as poor(smart) man’s FFR.