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Posts Tagged ‘ifr’

FFR is the ultimate hemodynamic test that measures the physiological Impact of lesions. Just pass a manometer tipped wire across the lesion and note the pressure drop (with or without Adenosine) All you have to remember is two cut off values  .8 for FFR and .9 for IFR. Abracadabra . . . yes you got the answer , whether to proceed with PCI or not? It’s as simple as that. We are no longer blind to physiology to which many coronary purists often criticize us.

ffr ifr fame study

Coronary physiology simplified

Now , answer this question.

Is FFR heart rate dependent? If yes, how significant it is?

This simple question on coronary physiology caused the maximum distress  to  a large expert cardiologist group

Some of the answers

  1. No, it doesn’t.
  2. I think it may be affected.
  3. Yes for sure, but it’s not significant
  4. Yes, it’s an important limitation

My Answer

It has to be yes, right, however minimal it may be. My interpretation of truth in FFR is, it can have a massive influence* . (*Unless you are sure (we can never be ) about achieving maximum hyperemia or this hyperemia is the same as physiological exercise.) In fact, the whole concept of FFR lies in the fact that it should induce enough HR raise that should be used as a surrogate marker for maximum hyperemia. Ideally, like stress testing, we need to test FFR at maximum heart rate and minimal heart rate. The difference could be documented as FFR max-min. This will throw new light into the physiology of microcirculation.

Should we need to create a heart rate corrected FFR?

Yes , I think we need to do it or else should report at what HR we are reporting the FFR. If FFR falls at a high heart rate and maintains at low it implies a significant lesion. So don’t get fooled with FFR of .9 measured at an inadequate heart rate.

IFR to replace FFR : On what basis?

Meanwhile, new generation coronary flow quantification tool IFR jettisoned Adenosine and simply measure diastolic instantaneous flow at resting state. This makes a mockery of coronary physiology, without a true debate about heart rate dependence of trans-lesional flow.

Impact on clinical practice

Even as we struggle to answer the fundamental question of the influence of Heart rate on FFR, many landmark studies had been done. They have ratified FFR as the most physiological modality to assess coronary lesion. Important guidelines have been written based on these studies. No one will ever know, the true impact on the current cardiology care,  had we included heart rate adequacy /correction as an essential criteria in those FAMEd studies we hype about.

Counterpoint.

All is well with FFR.It has been tested with various heart rates.

FFR at peak hyperemia means there is no further HR rate induced potential microvascular reserve. So a properly administered optimal Adenosine augmented FFR should not bother the HR variability. (But its only theory)

If FFR is ok . . . IFR should not be ok is it not?, For the simple reason, there is no hyperemia in IFR , what is the use of knowing resting flow reserve (RFR)

Reference

 

Postamble with a slice of History 

FFR is as old as the concept of PTCA. In fact, the original balloons used by the great Gruentzig’s * had a central port for pressure recording through which he measured both proximal and distal pressure curves to guess the significance of obstruction. After each inflation, he checked  whether both curves are drawn together which he speculated to indicate a successful procedure physiologically.

*What a stunning scientific mind the father of Interventional cardiology was blessed with, still inadequate for the Nobel committee to get convinced.

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