Thread by @SukhNijjer

#ISCHEMIA Thread: I gave a quick hot take during #AHA presentation & haven’t had time to expand on it. Queue some collected thoughts (albeit without gifs & references) on some responses I've seen to the study. Hats off to @alenghat for the great graphic on applying the study

@alenghat Be warned, I am being reductive and, some may say, provocative. You may not agree with me because you practice in a different way, your local system, and “in your experience etc”. Also, your test is better, I’m sure. Accepting that, read on. #ISCHEMIA

@alenghat Everyone in #ISCHEMIA had “ischemia” measured by a variety of means, and some went to cath, and some had revasc with PCI and a good percentage of CABG. There’s a lot of crossover too.

@alenghat Regardless of how it was done, what was done, precise changes in MI etc, we can agree that all had #ischemia by standard conventional techniques used around the world. And yet no difference in major events & no signal of difference despite good levels of ischemia

Therefore a reductive approach is to say “ischemia” (as currently tested & used in study), does NOT help guide outcomes either way. #ISCHEMIA is a strategy study after all - what strategies work in managing the prerequisite to get into the study.

Some may say, well we need non-invasive ischemia testing to understand symptoms - is it Angina? Really? Are all symptoms related to ischemia on non-invasive testing? You’ll all have seen patients with no symptoms, yet “ischaemia” on testing, and Vice Versa.

For the patient with ischemia on a scan but no symptoms and no CAD & normal microvascular resistance, are you still saying they have angina? After all you said you did the non-invasive test to see if they have angina / understand symptoms.

Then there are those with atypical symptoms. We have seen those with atypical pains, positive ischemia test, stenoses treated, ischemia confirmed to be gone by repeat test, but atypical pains continue (likely pain was non-cardiac but there was ischaemia!).

A patient with frequent convincing angina may have “negative test” but may have true ischemia, so we rely on symptoms. There is a degree of error in all imaging tests, so we miss the cause. Others have lots of Sx & ischemia & when normal Coros we suggest microvascular issues

But the key end of such thoughts, is that:
Ischemia, as currently detected, and symptoms
are not as closely related as you think. #ischemia

Some may say we need Non-invasive imaging to guide OMT. Really? Angina is a clinical diagnosis of reproducible chest pain. We’ve all seen patients with angina and no ischemia, but proven CAD. Are you saying they shouldn’t get OMT? Based on what?

Some say OMT helps reduce ischemia: does it really? I’ve not seen data that shows beta-blockers reduce the measurable ischemia on a given test. How about ACE-I? (I’ve not seen it but I’m sure someone will find something and appropriately hound me)

How about those with convincing angina but negative stress test, do you stop the OMT? Its still angina though.

How about those with a large ischaemic burden but no symptoms. Are you adding additional tablets even though no symptoms. What are you achieving? Better symptom control? Lower blood pressure and more side effects?

So, based on these thoughts, the decision to give medicines based specifically on an imaging modality also doesn’t make much sense.

A further painful issue, is that ischemia testing was developed as a way of deciding who went to the cath lab or not. It was validated against presence of sometimes quite mild CAD. And now, we relying on functional imaging without assessing the plaque/atherosclerotic burden.

For me, the #ISCHEMIA challenges the validity of non-invasive functional imaging in determining the care of patients who we think have angina. It challenges all aspects of #Cardiology & hence all the hand wringing from all corners (please note - in stable patients).

So if you want to adopt the study findings and really apply EBM in its truest form, we have take the information & adapt it in a way that makes sense as a gestalt within context of a given patient & you being a Doctor.

Rather than just doing what they did in the trial, let’s boil it to its core. So if “ischemia” doesn’t matter and doesn’t alter outcome (even when severe, as detected by conventional means), then lets change the paradigm. Lets go for CTCA directly.

If you have a patient in whom there is high likelihood of CAD & symptoms consistent with angina, give them all OMT. Done. If young-ish & kidney function is good, do a CTCA. How you interpret the CTCA is key for the next step to avoid over investigating

If CTCA done and no CAD, then hurrah! Consider microvascular disease if convincing ongoing symptoms not relieved by the good news. In which case, try a variety of medical approaches in knowledge that there
is no good blinded data to guide Rx, (so it’s probably all Ok)

If there is moderate CAD, but no LMS (and I’ll add proximal LAD), then continue OMT (aspirin, statin, beta-blocker) and observe response. Avoid ischemia testing in the first instance as it didn’t alter outcomes. If ongoing symptoms, then reasonable to do so.

If CAD with severe proximal LAD/LMS, then define coronary anatomy with invasive angiogram. Consider invasive physiology where there is doubt (helps defer safely). You don’t need to proceed to revasc but may intensify OMT. If ongoing symptoms or clinical change, then revasc.

So really we can stop spinning the magnets & turn off the gamma cameras. The dobutamine can be put back in the cupboard. I'm sure the imaging Doctors would rather focus on the complex issues like Sarcoid, not guessing if there is a perfusion defect or subtle wall motion change.

If you feel triggered or annoyed by this thread, relax, it’s just words on a screen. You can ignore them. I'll apologise in advance.