You are. I described my ROAMS strategy (rule out acute myocardial
syndromes) a few years ago here. Take a history. Establish that the pain
could be cardiac; and rule out diagnosable non cardiac causes to manage
appropriately. Do NOT do a trop T before 8 hours. An elevated trop T at
that time is going to indicate actual myocardial damage and hence the
patient needs to come in. The patient with a low probability (stratified as
you wish; TIMI is as good as any but I like GRACE
http://www.outcomes-umassmed.org/grace/ although we don't yet use it, the
calculator is on the screens) can either go for ETT as in Steve Goodacre's
model or an urgent chest pain clinic as in ours.
R
-----Original Message-----
From: Accident and Emergency Academic List
[mailto:[log in to unmask]] On Behalf Of Paul Bailey
Sent: 30 March 2007 07:33
To: [log in to unmask]
Subject: Re: Assessment of possibly ischaemic chest pain
Andy,
We are a unit based in the suburbs of Perth and out patient catchments could
largely be described as working families, predominantly Caucasian. So your
suggestion that our patient population is largely healthy is probably
accurate in part. We also don't have a hard core inner city wino / drug
user / street person population, unlike almost every other ED in the known
world.
We do an admission Trop - the 1:250 rate I'm talking about is when the
admission trop is negative.
Part of the problem is that most of our registrars come from "The Great
White Temple of Healing" down the road that has a much older patient
population. They practice in an identical way in our ED and this is the
source of part (only part) of the problem.
I'm still trying to get a handle on how people are treating soft chest pain
in the 20-39 year old with no risk factors and a normal ECG, but I don't
seem to be getting any replies.
PB
-----Original Message-----
From: Accident and Emergency Academic List
[mailto:[log in to unmask]] On Behalf Of Andrew Webster
Sent: Friday, 30 March 2007 2:24 PM
To: [log in to unmask]
Subject: Re: Assessment of possibly ischaemic chest pain
Paul
Do you do an admission Troponin first, to make an early disposal decision or
do you wait 12 hours to do a single Troponin. If it is the first plan that
is why your rate may be so low.
Alternatively it is all those healthy people in Joondalup, worried about
their atypical chest pain. So you just have a low rate of ACS.
Andy
-----Original Message-----
From: Accident and Emergency Academic List
[mailto:[log in to unmask]] On Behalf Of Paul Bailey
Sent: 30 March 2007 04:05
To: [log in to unmask]
Subject: Re: Assessment of possibly ischaemic chest pain
Thanks Rowley,
But that's not the patient I'm talking about either. I think anyone with a
good story should be taken seriously too. TIMI demonstrated that.
What I'm talking about is the patient with an "atypical" (again, for want of
a better description) history with *no* risk factors. Do you manage a 55
year old different to a 25 year old?
Surely the answer has to be yes, as the prevalence of ACS is going to be
higher in the older patient cohort.
What I'm trying to get out of the group is some sort of feeling for how
"atypical" patients are managed at different age groups.
I've had someone tell me that they admit people to their CDU who have good
stories, normal ECGs and risk factors. And have a 10% positive troponin
rate.
That to me seems to be a very risk tolerant approach as these patients are,
in fact, "high risk" from a clinical scoring point of view as far as we can
tell and I think a troponin rate like that - positive in 10% - means that we
are talking about different groups of patients.
I can tell you that the positive troponin rate of patients who are admitted
to our equivalent of CDU is in the order of 1:250. Which means that we are
investigating a lot more patients than you are.
What I'm trying to get a feel for is who you send home and who you keep in
the low risk group to try and make sense of why our negative troponin rate
is so high. It must, surely, mean that we are admitting a very low risk
cohort for prolonged CDU workup.
PB
-----Original Message-----
From: Accident and Emergency Academic List
[mailto:[log in to unmask]] On Behalf Of Rowley Cottingham
Sent: Friday, 30 March 2007 7:11 AM
To: [log in to unmask]
Subject: Re: Assessment of possibly ischaemic chest pain
No, my reply was not talking about that group either, but the soft
group. I'm not sure I'd want to set a lower age limit, just as we don't
set an upper age limit for thrombolysis. A junior coming to me with a 30
year old male with a good history will be listened to seriously. Setting
limits simply curtails and abrogates clinical judgement - if she's 25
she can't possibly have coronary artery disease. Sure it may be rare,
but to muddle two separate threads so are C1 fractures but that doesn't
stop us hunting for them. For example from an old paper:
Am J Cardiol. 1987 Apr 1;59(8):750-5.
Magnitude and determinants of coronary artery disease in
juvenile-onset, insulin-dependent diabetes mellitus. Krolewski AS,
Kosinski EJ et al.
The risk of premature coronary artery disease (CAD) and its
determinants were investigated in a cohort of 292 patients with
juvenile-onset, insulin-dependent diabetes mellitus (IDDM) who were
followed for 20 to 40 years. Although patients with juvenile-onset IDDM
had an extremely high risk of premature CAD, the earliest deaths due to
CAD did not occur until late in the third decade of life. After age 30
years, the mortality rate due to CAD increased rapidly, equally in men
and women, and particularly among persons with renal complications. By
age 55 years the cumulative mortality rate due to CAD was 35 +/- 5%.
This was far higher than the corresponding rate for nondiabetic persons
in the Framingham Heart Study, 8% for men and 4% for women. Angina and
acute nonfatal myocardial infarction followed a similar pattern, as did
asymptomatic CAD detected by stress test, so that their combined
prevalence rate was 33% among survivors aged 45 to 59 years. Age at
onset of IDDM and the presence of eye complications did not contribute
to risk of premature CAD. This pattern suggests that juvenile-onset
diabetes and its renal complications are modifiers of the natural
history of atherosclerosis in that although they profoundly accelerate
progression of early atherosclerotic lesions to very severe CAD, they
may not contribute to initiation of atherosclerosis.
> *From:* Dr Paul Bailey <[log in to unmask]>
> *To:* [log in to unmask]
> *Date:* Wed, 28 Mar 2007 17:19:45 +0800
>
> Thanks Rowley,
> I think we have all seen STEMIs in patients in their twenties. I
> know I
> certainly have. It is my experience that they usually present with
> florid
> ECG changes and you are in no danger of sending them home.
>
> That's not the group I'm talking about.
>
> It's more the 'atypical' (for want of a better term) chest pain that
> *could*
> be ischaemic in the patient with a normal or softly abnormal ECG.
>
> Surely, in the end, it gets down to risk and reward - not unlike the
> SAH /
> LP etc conversation we all had last year that Tim made a great
> contribution
> to.
>
> Saying that you have seen an AMI in a 21 year old are you implying
> that you
> send all 21 year olds with chest pain and no diagnosable cause
> through a
> late troponin protocol?
>
> I'm interested to know what everyone is doing to these low risk
> patients.
>
> FYI cocaine has historically not been a big factor in Western
> Australia, but
> it is certainly on the rise.
>
> In answer to your question of where have all the MIs gone? I have a
> personal theory that they have all gone to the cath lab many months
> pre infarct. Totally unsupported by anything other than a gut
> feeling.
/Rowley./
