Category Archives: Acute coronary syndromes

ADAPT my management of low risk chest pain? I’m not sure I will…….

Image

Another Friday another JC in Virchester. Lots of chin stroking and pontification on this one.

We looked at the ADAPT trial by Martin Than and colleagues. Essentially they assessed the diagnostic utility of an accelerated protocol using Timi risk score, 0 & 2 hour troponin I measurements for rapid exclusion of cardiac pathology in patients attending the ED with chest pain. I was rubbing my hands on this one. “think of the bed days we can save on the decision unit. Say goodbye to all the 12 hour boredom of the ‘rule out’ MI admission.”

So what did they actually do? Well, over 2 sites in Oz and NZ they assessed 1975 patients attending with chest pain of suspected cardiac origin. They performed baseline and 2 hour Troponin I measurements that were unavailable to clinicians. They performed usual diagnostic protocols and followed patients up for 3 months. Then an adjudication panel apportioned the diagnosis of Major Adverse Cardiac Events at the end of the study period. They subsequently looked back to ask 2 main questions:

Firstly, what was the sensitivity of their accelerated diagnostic protocol (did it catch all the true positives)?

Secondly, if we assume the ADP is highly sensitive and therefore ‘safe’ how many patients would have been potentially dischargeable directly from the ED within 4 hours?

The methodology was pretty sound. Pretest probability for MACE was a little on the low side (15.3%) compared to our prevalence (20%) or other studies (30%). But their use of MACE is in keeping with much of the literature on the topic. The adjudication committee was not independent but we had a long discussion about this and concluded that actually, if they were blind to the Trop I assay, they couldn’t introduce much bias here even if they wanted to. If they underestimated MACE based on some of the more subjective aspects for example, they could potentially heighten the sensitivity of the diagnostic protocol – but this would worsen specificity and consequent diagnostic utility. Thus they would be shooting themselves in the foot.

And what did they find?

An excellent sensitivity of 99.7% (95% CI 98.1 – 99.9)

A dischargeable proportion of 20% using the ADP, with 1 MACE event in this group only (0.25%).

These are very interesting findings from a large, methodologically robust diagnostic study from 2 countries with a distinguished author list.  So, are we going to start applying the findings in practice?  I’m not so sure.  The findings must be taken in context with other concerns about the paper. We only had a few issues, but here they are:

  1. There was no mention of symptom duration at presentation in the cohort. Thus we don’t know how long these patients had had symptoms for prior to presentation. This is important: if most of the 1975 presented at 10 hours then actually, your 2 hour Troponin is predominately a 12 hour Troponin if you use time from symptom onset for your exclusion. We do Troponins 12 hours after symptom onset, but other systems (for example in many American papers) a measure of 12 hours after ED presentation is used.
  2. Their findings have not yet been externally validated. The sensitivity especially is likely to be slightly overestimated in a tightly controlled exploratory cohort. Something to be cautious of.
  3. They used Trop I rather than one of the new all reaching brand new spanking best in show highly sensitive troponin assays.  This might mean that the findings are more immediately relevant if you’re not using a high sensitivity assay, but for us in Europe this is a concern.  The proportion of patients who could be discharged is likely to be lower with a high sensitivity assay.
  4. The proportion of dischargeable patients using this rule was actually not huge at 20%. In the UK, this may be even less (only 7.4% of our patients had a TIMI risk score of 0/7 in previous work).  It follows that the others all end up admitted to some sort of inpatient service. This is a fairly self fulfilling prophecy in terms of investigations and therapeutics, as noted by their figures of 74% ADP negative patients receiving further investigations and 14% recieving therapy of some form.  There are risks with this.  And remember, the actual prevalence is only 15.3% (increased to 18-19% if we discount the ADP positive patients). 60% are still getting a raw deal (full inpatient investigation and treatment with no clear diagnosis at the end) Are we potentially therefore doing more harm by using a strict diagnostic protocol such as this one that will no doubt encourage admission due to the limited specificity?

The accompanying editorial to this paper can be found here and is a really nice summary of how far we have come and how much work still needs to be done on this topic. It also highlights the recent work looking at undetectable HsTnT to exclude MI at the door by a certain Dr Body (who?) and Professor Carley (never heard of him). This kind of work interests me a little more if I am honest.

I want a test which I can use immediately on the young patient with low risk chest pain that will rapidly reassure me about an absence of cardiac pathology. I am happy that Troponin is not this test in the elderly and will often manage them as ACS irrespective of initial trop results.

But if you can find me a way of getting all those 30-40 year olds who wait 12 hours only to be told that they haven’t had a heart attack (no s***) but that we’re not really sure what’s wrong with them,  off my decision ward, then I will applaud you.

Carry on the good work sirs.

dan

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

The problem we have with cardiac chest pain

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