Deciding Who To Investigate For ACS: The Problem Of ‘Coronary Bridge’

It seems to me that many emergency physicians struggle to understand exactly how we’re supposed to be managing patients with suspected cardiac chest pain.  The first, and arguably most important question, is about who we should investigate in the first place.

The confusion is understandable as there are mixed messages coming out of the literature.  On the one hand, we have to be very cautious as we know that atypical symptoms don’t rule out an acute coronary syndrome (ACS).  We really don’t want to miss ACS as we know that patients who are inadvertently discharged have a worse prognosis than similar patients who are admitted.  What’s more, missed diagnosis of ACS is one of the leading causes of medical litigation.  On the other hand, we get constant negative feedback from inpatient specialties who may feel that we admit too many patients for suspected ACS and others who feel that we may be overusing troponins.  After all, less than 25% of the patients we admit for investigation will actually turn out to have ACS.  So what are we to do?

The value of symptoms and signs

Amal Mattu recently provided some great guidance in a fantastic Medscape article.  He sums up with 3 key pearls of wisdom: (1) Though there are factors that reduce the likelihood of ACS, don’t rely on them – none of them risk stratify the patient to the level of ‘no risk’; (2) If you do discharge a patient with chest pain, make your practice as defensible as possible by documenting as many of the ‘low risk’ factors as possible; (3) Beware of factors known to increase the likelihood of ACS (like pain radiating to both shoulders/arms or to the right shoulder/arm, vomiting, sweating and exertional pain).  I certainly echo these sentiments.  Following a recent conversation on Twitter, I thought it would be useful to expand further on my thoughts.  (Further than you can in a 140 character Tweet!)

Dr. Mattu’s Medscape article referred to my paper in Resuscitation, entitled ‘Symptoms and signs in the emergent diagnosis of acute coronary syndromes’.  In this paper, we reported some interesting findings.  First, there are a number of ‘typical’ symptoms that don’t seem to alter the probability of acute myocardial infarction (AMI) very much at all.  This included pain radiating to the left shoulder or arm, which did not significantly increase the likelihood of AMI or adverse events over the following 6 months. Pain located in the left anterior chest actually made the diagnosis of AMI less likely.  On the other hand, certain atypical symptoms turned out to make the diagnosis of AMI more likely.  This included, notably, pain radiating to the right shoulder or arm!  No features were useful to help rule out an AMI.  For example, 19% of patients who described their pain as sharp or stabbing in nature were either having AMI or developed a major adverse cardiac event within 6 months.  That’s not much of a rule out!  A pleuritic nature to the pain did not significantly alter the probability of AMI or adverse events at all.

There were some more interesting findings in our study.  Patients who were observed to be sweating in the ED were, more often than not, having AMI.  The probability of AMI was, in fact, 59%.  The positive predictive value of sweating observed in the ED is even higher than that of ischaemic ECG changes.  That’s pretty powerful.  AMI was diagnosed in 40% of patients with an initial systolic blood pressure <100 mmHg; 41% of patients who reported vomiting; and 35% of patients whose pain radiated to the right arm or shoulder.  So these are fairly powerful positive predictors, given that we started with a pre-test probability of 18%.  They are things we should be quite concerned about, if present, although of course they should be taken in conjunction with everything else.

So when can we rule out ACS without tests?

It’s time to re-iterate something important: no symptoms or signs can be used alone to rule out ACS.  Let’s be clear about that.  Just because a patient describes the pain as stabbing in nature doesn’t mean you can relax.  Just because it’s worse on inspiration doesn’t mean you can’t relax.  If it’s not worse on exertion, you can’t relax.  Of course, if the patient has sharp, stabbing pain that only appears on inspiration and is located only in a well localised point in the left lateral chest wall, you can relax – you’re clearly not going to suspect ACS.  We do have to retain some common sense.  Document the clinical context carefully and you shouldn’t be criticised.  However, when things aren’t as clear, when you’re relying simply on the fact that the pain is worse on inspiration (alone), stabbing in nature (alone), indigestion-like or whatever else to justify your decision not to investigate the patient for ACS, then to quote Amal Mattu at ICEM 2012, “you should slap yourself before someone else does”.

The golden rule

In practice, therefore, I can suggest 3 things that you ought to remember when considering how to manage patients presenting to the ED with chest pain:

  1. There are patients you can identify as having a high probability of AMI.  Ischaemic ECG changes, sweating observed, vomiting reported, pain radiating to the right arm or both arms, and hypotension all identify high risk groups.  These patients clearly need investigation
  2. There are patients you can rule out immediately who clearly don’t have ACS.  They have other causes for their pain that can be objectively identified, or their history is so clearly non-cardiac that it would be ludicrous to investigate them.
  3. Then there’s the middle group of patients, who aren’t in either of these ‘high probability’ or ‘clearly non-cardiac’ groups.  Investigate these patients.  They could have ACS and you really don’t want to miss it – for the patient’s sake and for your own.

Coronary Bridge

In my first job as a Senior House Officer in Emergency Medicine, one of my seniors told me about a hospital he used to work at.  The main road leading to and from the hospital ran across a bridge.  They apparently named it ‘Coronary Bridge’, after the number of patients who suffered a cardiac arrest there having just been inadvertently discharged from the ED with a missed myocardial infarction.

We do need to reduce unnecessary admissions for cardiac chest pain.  We do, however, need to do this in an evidence based manner, with a validated rule out strategy.  I’m certainly not suggesting that we throw common sense out of the window and investigate everyone.  But next time you consider discharging your patient with ‘vague’ or ‘atypical’ chest pain just because it’s ‘vague’ or ‘atypical’, consider whether you really want to take the chance that your patient won’t make it across ‘Coronary Bridge’.  We want to reduce admissions – but let’s do it safely and scientifically.

Rick Body

Cite this article as: Rick Body, "Deciding Who To Investigate For ACS: The Problem Of ‘Coronary Bridge’," in St.Emlyn's, July 11, 2012,

7 thoughts on “Deciding Who To Investigate For ACS: The Problem Of ‘Coronary Bridge’”

  1. Slap yourself before someone else does – lol!

    Seriously though, in that mid-range grey-zone booby-trapped group, is there a one-size-fits all investigation strategy? Or is there a way to further risk stratify them so that eg single negative troponin would be good enough as a rule-out? Should we be treating all this middle group for “ACS” – aspirin? clopi? fondaparinux? or can we treat some with higher risk and not others?

    1. Hi Kirsty! To be honest, I think that deserves a whole different article by itself. There isn’t a one size fits all right now because there’s massive variation in practice. In fact, we’ve been planning an international survey to document exactly how much variation there is in practice right now.

      You’re being very Bayesian suggesting that a single troponin might rule out in low risk patients! Actually, if anything, you’d need at least a 2-hour troponin in low risk patients, though. Martin Than from New Zealand ran the ASPECT and ADAPT studies. ADAPT showed that serial troponins over 2 hours in TIMI risk score 0 patients had a high negative predictive value. That deserves another article in itself, though, so watch this space for more!


  2. It seems that myocardial ischaemic events, similar to many other aspects of medicine, are complex for a number of reasons. First, excluding AMI does not of itself exclude ACS. So using papers that assess the use of symptoms and signs to manage risk for AMI, still leaves you with the need to manage ACS risk. And that’s the second issue. Most of medicine is about risk management. It is inherently fallible and therefore individuals will fail from time to time. For the moment, expecting an absolute outcome is probably unreasonable, which is something that both doctors and patients need to understand and accept. That does not mean we should ot strive for perfection, just that we should not be surprised when it does not always happen.

  3. Hi Matthew,

    It’s a great point about unstable angina. Having the primary outcome as AMI does leave out the issue of unstable angina and we thought about that carefully in the design of the manuscript. The problem is that there’s no accepted reference standard for unstable angina. Take a look at the ESC guideline – there’s no robust way for differentiating between troponin negative patients who have (a) non-coronary disease/illness, (b) stable angina and (c) unstable angina. The key differentiator, particularly between (b) and (c), is the history. If we evaluate the predictive value of the patient’s history using a reference standard that includes the patient’s history, then we’d have incorporation bias and would probably overestimate the predictive value of certain historical features. (Because we’d be using them to decide whether the patient had unstable angina). For AMI, we have robust guidelines on how to make the diagnosis so we can be more objective.

    What we’re most worried about with the patients with unstable angina is that they may go on to develop AMI or an adverse event in the near future. That’s why we don’t want to miss that diagnosis. Ultimately, therefore, our secondary outcome was adverse events within 6 months of follow up.

    I agree about the element of risk stratification. There is, of course, no such thing as ‘no risk’. There never will be. Some of our patients will unfortunately go on to develop adverse events no matter how good we are. Of course, we know that – both patients and doctors are mortal, after all! As doctors, we don’t want to subject our patients to any risk – that’s natural. However, some level of risk is inevitable whatever we decide about the disposition of our patient. Even admitting patients to hospital for further investigation is associated with small but significant risks. Our job is to carefully balance those risks and do all we reasonably can to achieve the most favourable outcome for the patient.

    Rick Body

  4. To be sure, every effort must be made to understand ACS. What most of us fail to admit, however, is that there comes a point where legal expediency trumps all other reasons to investigate an atypical chest pain.
    This acknowledgement tells me out scientific progress must go hand in hand with tort reform, offering safe harbor for docs who adhere to theist up to date data, yet don’t wish to overburden the system.

  5. Is sweating a sign of AMI or are sweaty people more likely to have an AMI – I couldn’t figure is out from your blog?!

  6. Pingback: Cardiology Case 04: An unusual ECG - St.Emlyn's

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