Ask any medical student (when they are sober) the clinical features of an Acute Coronary Syndrome they’ll look at you funny for a bit, then talk of severe, left sided chest pain radiating through to the arm, they might add in diaphoresis, or pulmonary oedema. If you’ve got a real nugget that might carry on talking about risk factors, relief from GTN and ‘pain like previous MI’ making a cardiac cause more likely.
You’d probably tell them they were right.
I remember hearing the first description of a chest pain history in a big lecture theatre as a first year medical student, and it was pretty much that.
We’ve always been taught that Histories Are Important, we are taught these by rote, by repetition and by exposure to lots of real world cases. They are the narrative that gives us the pathology our patients experience. So it’s implicit that the clinical features of those histories are equally important, and give us a sense of the probability of the disease in question. I doubt I’m alone in labouring to commit ‘red flag symptoms’ to memory for exams, or general day to day work.
Now in my last post I got in a bit of a tiz about the HEART score, and about how the definition of a suspicious history was a little vague. Now the history component of the HEART score is just worth 0,1, or 2 points out of 10. So if histories were as important as my old professor said why does the component only make up a maximum of 20% of the score?
Thats because the classical chest pain history is not a very good predictor of ACS.
Let that sink in. You have been taught that histories are important, they’re the key to finding the pathology. Sometimes when the diagnosis is essentially a clinical one (eg appendicitis) that still holds true. However when you have a good quality gold-standard test (eg a Troponin) things become different. You can test the history, and the chest pain history is not very good at all.
In 2001 Prof Steve Goodacre published a study looking at the clinical features of people with low risk chest pain (normal ECG, no initial trop rise), seeing if any particular features had a predictive effect. Previous research up to this point suggested left arm pain, diaphoresis, a 3rd heart sound and hypotension predicted acute myocardial infarction, but these studies were done prior to the advent of Troponin.
He conducted a big single centre prospective trial of patients over 25 with chest pain, no known CAD, and a normal initial workup. He followed his patients up over 6 months looking for AMI and MACE. He had a ACS rate of 9.1% in his cohort of 893 patients.
If I were to ask you ‘where do most people who have an NSTEMI complain there pain is coming from?’ You’d probably point somewhere over the left side of your chest.
Taken from table 4 – Univariate Analysis of Predictors of ACS (Goodacre 2001)
Would you suggest pain in both arms? What about pain in the right arm being more suggestive of AMI than pain in the left? That’s what Prof Goodacre found, though his confidence intervals are wide, and some of his findings were not statistically significant.
Now if we look at some his multivariate analysis results we can see that he only really found 3 good predictors. Pain in both arms, exertional pain and a tender chest wall (this was a good negative predictor). How many people have you admitted because ‘they had pain at rest’?
|Pain in both arms||4.07||4.9||1.3-19.4||0.02|
|Tender chest wall (as negative predictor)||0.3||0.2||0.05-0.97||0.045|
“We also found no evidence that the site of pain, the presence of nausea, vomiting, or diaphoresis, and the duration of the pain were at all useful in predicting whether the pain was likely to be cardiac or not”
Despite him having a pretty big sample of low risk, non cardiac chest pain he probably still didn’t have a big enough sample to look at what he wanted to look at. This dataset was taken from another study primarily looking at the feasibility of a rapid chest pain assessment service. I guess thats why theres no sample size calculation.
Lets look at my next study. I love this study, it’s come out of manchester. Prof Body included everyone over 25 who attended with suspected cardiac chest pain, treating clinicians completed a standard form with tick boxes for clinical features. All patients had a 12 hour troponin and follow up at 48 hours, 30 days and 6 months. His primary outcome measure was AMI and secondary outcome was MACE at 6 months. So we’ve got a slightly different risk profile to the Goodacre study.
They analysed the results from 796 patients, and got 100% follow up. I feel they had a slightly higher AMI rate of 18.6% (n=148) for initial presentation. At 6 months they had a MACE rate of 22.9% (n=179).
The Odds ratios for AMI for individual clinical features are below.
A few things to point out. Sweating and abdominal pain seemed to be good predictors of AMI, as did reported N+V (which was not predictive in Prof Goodacres cohort). Pain location that was in both arms predicted AMI more than pain in the left (and pain in the right was slightly better than left). My favourite one though is that if the pain was described as ‘like their previous MI’ patients were less likely to have AMI.
Body didn’t find any excellent predictors of AMI. His best ones were observed sweating, both arm/shoulder pain, and hypotension.
|Sweating Observed||36.5 (28.7-44.8)||94.3 (92.2 – 96.0)||59.3 (48.5 – 69.5)||86.7 (83.9 – 89.1)||6.39 (4.38 – 9.33)||0.67 (0.28 – ).46)|
|Reported Vomiting||16.2 (10.7 – 23.2)||94.8 (92.7 – 96.3)||41.4 (28.6 – 55.1)||83.2 (80.3 – 85.8)||3.09 (1.89 – 5.05)||0.88 (0.82 – 0.95)|
|Pain in both shoulders||13.5 (8.5 – 20.1)||94.8 (92.7 – 96.3)||37.0 (24.3 – 51.3)||82.8 (79.8-85.4)||2.58 (1.53-4.34)||0.91 (0.85-0.96)|
|Same as previous ischemia||22.3 (15.9-29.9)||69.4 (65.7 – 73.0)||14.3 (10-19.5)||79.7 (76.1 – 82.3)||0.73 (0.53-1.01)||1.12 (1.01-1.24)|
|Right arm/shoulder pain||18.9 (13.0 – 26.2)||91.8 (89.4 – 93.8)||34.6 (24.4 -46.0)||83.2 (80.3 – 85.9)||2.31 (1.52 – 3.53)||0.88 (0.81 – 0.96)|
Taken from Table 3 of Body (2010) Characteristics of each predictive clinical feature as a diagnostic test for AMI
So in two good quality studies of chest pain characteristics we get right arm pain more predictive of AMI than left arm pain. We can’t with any degree of accuracy state that someones epigastric burning pain isn’t cardiac in origin, and a classical heavy central pain radiating to the jaw or arm isn’t predictive of AMI or 6 month MACE at all.
Caveats. You’ve got lots of hypothesis tests going in both of these studies. Maybe too many, given the sample size and the rarity of the condition we are looking for. A bigger sample would increase the accuracy certainly.
So should we stop talking to people about their chest pain? Of course not, however we need to be very careful at excluding ACS based on the chest pain history alone. Using something like the HEART score is probably more accurate, safer for your patient and safer for your registration.