Posts Tagged ‘ffr’

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.


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)



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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Even as we make rapid strides in  conquering coronary atherosclerosis by all those fancy gadgets , the  fundamental coronary  hemodynamic principle   is poorly understood . Hence  there is no surprise  for the  “perennial ambiguity”  in the indication  and effectiveness of  coronary revascularization .

Why the hell ,   reliving  a  coronary obstruction  may  not provide the   expected hemodynamic benefit  or do not prevent future  heart attack  in many ?    One of my patients  asked ?

I told him . Wait , do not get  excited , we also do not know  . . .We are just beginning to understand mysteries of coronary  circulation.

It is a well documented fact  ( but a  debatable )   that  lesser the  severiity of a  lesion more likely it is prone for an acute coronary  event .( Vulnerability , shearing stress or is it a simply a statistical mirage !) While the  vulnerability aspect is  complex , the hemodynamic  impact of  coronary  lesions  is   relatively better  understood. Here is  an important  documentation from Dr B . K  Koo from  Seoul , South Korea  who has elegantly shown the behavior of  fractional flow reserve (FFR ) in various grades of  stenosis  .This study was done in jailed side branches following PCI.

FFR  shows a surprise   relationship  with severity of coronary stenosis  . Even severe lesions showed equal if not more flow  reserve ?

and mild lesions might have lost all its reserve.

 How is it possible ?  Can it be true ?

Yes , it is indeed a  fact . God generally  keeps a stong link between anatomy and physiology  , structure and function . But he adds a rider and keeps  a reserve in every  human cell   meant for  emergency  back up . FFR is  one aspect of this , we have  partially discovered .  When we fail to understand this we are bound to get confused and make a wrong decision in cath lab.

Simply stated ,  flow across a coronary  artery is much more depedent on the status of microvascualture  than the hurdles they face in the epicardial highways !

Link to this original article from JACC .

How to do the FFR procedure ?


Soon to follow . . .  If less severe lesions are more  dangerous why we are ignoring it in cath lab ?

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