[ WARNING – These are a bunch of scribbled, fairly rough unedited notes on the SMART EM podcast on stress testing. I was on a rather crowded bus in north wales at the time and I was sharing the seat with a mid-sized dog (seriously you can read about it here…) so it is likely full of inaccuracies and comedy autocorrects so buyer beware…]
2010 AHA guidelines are a philosophy of chest pain
AHA recommend EST first line. Other stuff is for people with a reason (ie DSE for poor mobility)
Bausfield 1918 one of the first reports of ECG use to diagnose ischemia.
1950 was first common use of EST for diagnosis
(?) Cuhn 1970 was first to use cath as gold standard. Looking for obstructive cardiac disease.
CAS study showed that in all comer chest pain referred for CABG only 20% had stenosis. Given that CABG is only done for a proportion (left main, triple vessel).
They actuallly used this info to skip the EST and go straight to cath in classic stories.
Goldman 1982 thought EST didn’t add enough. History and enzymes to direct you to angio +/- CABG
Universal agreement that low risk shouldn’t get anything.
Duke treadmill score publihsed 1981. A more nuanced way of Reading the EST and applying it. Adds 5% accuracy. Used it to prognose death not CAD. This is a change. Goldman and everyone else talked about prediction of CAD. But they used prediction of death to prod toward angio.
1998 Frolicker (?) published best EST study. Everyone who got EST got angio here (no WU bias). Sens 45% spec 85%. Need to know the rule in rate overall though.
Now people start using it on in patient following Q wave mi. EST here able to predict left main and triple vessel; it predcted CABG with some use.
What the hell is unstable angina?
– it has morphed and drifted over time.
– unstable angina are often now nstemi.
– non q wave mi would be a term from then.
– they overlap is the key point.
1977 one guy stated that you should not do EST on unstable angina/nstemi.
Butman and Wilcox (… snigger…) EST 72 hrs after unstable angina. Showed that 0.5% had an MI after EST. Therefore (in their eyes) it’s safe. Now it’s ok to do EST in everyone. (both q wave and unstable angina).
Larssen published data set of mi and unstable angina. 20% stemi and the others would be mi by today’s satndards.of the unstable 20% death/MI in a year.
The lasrssen paper is the one that repeatedly gets cited to justify stressing unstable angina pts before the leave the hospital.
1994 AHCPR guideline suggests EST wihtin 72 hrs is safe and should be done for unstable angina.
1997 first AHA guide on EST in unstable angina. Say that unstable angina either progress to mi/death or settle to be stable. They presume these are high risk pts and suggest EST is to point toward CABG. They are not trying to diagnose CAD – they already presume this.
So what about low risk ED chest pain?
– Late 80s “accelerated diagnostic protocols” in ED to pick up mi in not classic acute mi.
– suggests this was done to reduce admission at the front door.
– also the litigation issue.
Pope 2000 is the quoted one for missed mi rate and quoted to say that missed mis have double mortality rate. Of the 11000 pts they brought ALL of them back for a 2nd visit. They found 11 mis on second visit( this was the 2%) Overall 1 in 550 was a missed MI. There is a risk adjustment done to find the mortality difference. The raw numbers are equal.
Now EST does not predict revascularisation, it causes it.
Back to the beginning. The reason the aha says do this is
– convenience
– avoid admission
– predict short term mortality/mi
It does not do that.
Now it is trying to find people whom ECG and enzymes missed.
Gibbler chest pain unit study.
– some people got EST while the ckmb was being done
– some mis were not classed as mi and they probably were.
– very few mi overall.
It did not give us the Test that we need – to exclude cad in the 2%
When you look at the outcomes remember that they’re composite and most of the composite is made up of EST causing angio.
There is a question as to whether the angios that are done actually save lives and prevent mi needs addressed
Reinforces the old message that the low risk ed chest pain is truly very low risk.
New candian study in annals shows that if you don’t do the EST it’s ok. No one dies, no one has an mi.
Using the diagnostic properties you convert 1% risk to 0.7% risk. And this isn’t even a risk of anything we’re worried about.
Reasonable summary of evolution of approach to problem, though needs framing. The framing is forming the question so that somewhere in all the data is the answer. So EP needs three questions answered:
1) Is this patient having an MI?—troponin +ECG ( see Mills (Edinburugh) in JAMA.for really interesting study)
2) If no, is this patient’s symptom caused by ischemia?–multiple ways to answer this but if it is a genuine question ETT is best test for EP because although it is not best at diagnosis it is excellent at prognosis and therefore allows safe discharge and is cheap, has no radiaton and takes one hour max start to finish. Needs structured interpretation–i.e. Duke score.–see Manini in Journal of Emergency Medicine.
3) Is there anyone I can just send home without further testing? Asia Pacific study from July 2011 and Hess (Ottawa) “North American Chest Pain Rule” in Feb Annals give simple criteria but risk for Major Cardiac Events is 1-2%.
Thanks for the comments and impressed you persevered through all the mis-spelt notes!
That JAMA paper was a little weird. I wrote about it previously here:
http://emergencymedicineireland.com/2011/06/07/implementation-of-a-sensitive-troponin-i-assay-and-risk-of-recurrent-myocardial-infarction-and-death-in-patients-with-suspected-acute-coronary-syndrome-jama-2011305121210-1216/
Where I’ve worked they use treadmills all the time, i suspect cause we haven’t a better alternative but it’s really not as good as most people think it is. I’m pretty sure I send most of my rule out ACS patients home with out any stress testing, and I imagine that’s fairly common practice in the UK/Ireland. Most of the time that’s because there’s a clear alternate diagnosis or the story is so atypical it doesn’t sound like ischemia heart disease at all.
I’m aware in the US it’s quite a different story and pretty much everyone gets a provocative test.
From what I could work out (and I may have read it wrong) in that Hess study, only 6 out of 2700 chest pain patients died. only 170 of the 2700 were MIs. It seems like the whole cohort was immensely low risk.
what is your current thinking? for ACS- PCI, Unstable angina- pci vs medical management -seems to be equal or benefit for medical. And for NSTEMI? and if benefit for invasive then what is the time frame? I predict that in 3 years it will be simplified to this….STEMI or STEMI equivalent=invasive therapy, all else should have medical management.
to be honest it doesn’t much matter what I think, the cardiologists will do what they like – they’ll be the ones making that call. The tihngs I think matter are aspirin, rule out and lytics/cath lab activation. I’m quite apathetic to a lot of the rest of ACS management – everything else doesn’t seem to be that important. heparin may do nothing, never mind the GP2/3b inhibitor thingies. Plavix v Prasugrel – i’m just not that impressed by either.