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./
