Thread by @ProfDFrancis

Yesterday I clicked on a link on Twitter, and then didn't get to see the content as I had to do boring stuff instead.

Anyway, today after I closed some browser tabs I saw this on my screen.

I was annoyed because obviously some Industry SpinMeister had hijacked my browser with tedious twaddle.

"I must remember to update my Antivirus."

Just before I closed the browser tab, ready to wash my eyes out with alcohol to minimise the damage from reading drivel, I noticed this.

"Ah, this Soares mischief-maker has done a Poldermans, writing an article of absolute gibberish and then stuck David Brown's name on! Haha, unlucky for David!"

I couldn't help reading a little of it, purely for the Schadenfreude, knowing David would be desperately disassociating himself from it shortly.

It started off in conventional manner. You could easily imagine a panel of high priests intoning it solemnly in an ESC guideline.

But then it took an entirely unexpected turn for the dreary hagiography I assumed it was to be.

Some analytical thought! This is a break with tradition, if Soares is an ESC sock-puppet.

You know how you can't mention the Tiannenmen Square Incident in Chinese Media?

Equally, you can't publically discuss the "Great Migration" in polite cardiological society. It is taboo.

The Long March of the Red Army in the 1930's is extensively pictorialised.

South African Boers pour romanticism into "Die Groot Trek" of the 1830's Voortrekkers.

But of the Great Migration of '75-'80, paintings there are none

Only then did I fully grasp the title. So this was actually going to be an *interesting* article about FFR, not just one saying how it will save the whale and prevent global warming and bring us eternal bliss etc.

Another body blow for poor FFR.

If your microvasculature does not open up much with adenosine, your lesion will look mild on FFR.

Conversely, if your microvasculature is veryy healthy, e.g. coro flow surges 4-6 fold with adenosine, then even a minor lesion have positive FFR.

Something good about FFR, at last. If you suffer from uncontrollable urges to stent anything you see, it can help you put in less stents.

Francis Industries is shortly to launch its own technology which does this without adenosine.

The Instantaneous Handsfree Ratio.

Easily mistaken for a simple straightjacket, this technology is far more advanced. It uses Wavelet Theory and Big Data and Other Mysterious Stuff, to help you resist the temptation to stick that stent in.

ihFR reps will be in touch with you all soon.

And FAME 2 doesn't get a free-pass here.

There's a 5th thing perhaps worth pointing out.

All this "FFR guided" business needs to stop.
People interpret this as "Measure the FFR and be guided by it".

I don't blame people for interpreting it this way, since the FAME-2 paper:

says this in the first line of the Methods of the Abstract.

In reality, this was a lie.

In a small minority of patients, for some stenoses the eyeball was used. FFR was not measured but simply written down as 0.5 because the lesion looked so impressive.

I sympathise with that.

In ORBITA, "all" meant "all" and "measured" meant "measured". Four of 200 patients received suspected dissections and received immediate stenting.

In fact that is why poor @rallamee gets confused when asked "What proportion of ORBITA patients had ischaemia?"

@rallamee Originally, she decided to take the purist approach to avoid the FAME-2 embarrassment.

"For the 4 patients who had lesions so tight that the wire caused a dissection, strictly speaking we don't know whether they had ischaemia, so I will say they are a 'no'."

This gave 94%.

@rallamee Then people said "Helloooo!?!?! In FAME 2 the whole study's positivity came out of the people with made-up values, who had obviously extremely tight or already occluded vessels. They counted these super tight ones as 'yes'."

"... So you are certainly *still* conservative in your counting, compared with FAME-2 if you count ONLY the ones SO TIGHT that they actually DISSECTED."

She eventually accepted this and went to "96%".

Nowadays she is super-complete in her answer and says "94 to 96%".

Anyway, the message is, there are some lesions out there which are so tight that, outside a research study, you would not want to pass a pressure wire just out of curiosity.

In FAME-2, which not only a research trial, but was SPECIFICALLY a trial ALL ABOUT MEASURING FFR, and therefore should be the trial most eager in the entire world to measure FFR, they STILL couldn't bring themselves to do it in all patients.

The patients with lesions so buttock-clenchingly tight that even FAME-2 investigators, advertising *measurement* rather than eyeball assessment, couldn't bring themselves to measure,

*those* patients do not tell us anything about *measuring* FFR in moderate lesions.

So all we need from the FAME-2 people is the answer to the simple question. In the approximately 90% of patients in whom they did what the first line of the NEJM Abstract Methods said they did, measure FFR in *all* stenoses, what was the outcome.

They have been asked repeatedly, and have never answered.

This is not a trivial distinction.

The lesions considered so severe as to not be measurable for FFR, were as anatomically mild as 40%, as shown in the scatterplot here:

Source:

ahajournals.org/doi/pdf/10.116…

And an elegant conclusion.

Full article here. Still in Proof stage. sciencedirect.com/science/articl…