Although, the observed improvements are probably more a result of their preposterously high initial admit rate.
The HEART score, already evangelized in multiple venues, is a tool for risk-stratifying chest pain patients in the Emergency Department. Its advantage over other, competing scores such as GRACE and TIMI, is its specific derivation intended for use in the Emergency Department. This trial, of note, is one of the first to do more than just observationally report on its effectiveness. These authors randomized patients to the “HEART Pathway” or “usual care”. The HEART Pathway was a local decision aid, combining the HEART score and 0- and 3-hour troponin measurements. Patients with low-risk HEART scores (0 to 3) were further recommended to treating clinicians for discharge from the Emergency Department without additional testing. The primary outcome was rate of objective cardiac testing, along with other secondary outcomes related to resource utilization. Patients were also followed for 30-day MACE, with typical endpoints for cardiovascular follow-up.
With 141 patients each arm, the cohorts were generally well-balanced – specifically with regard to TIMI score >1 and accepted cardiovascular comorbidities. Stunningly, 78% of the usual care cohort was hospitalized at the index visit. Thus, the mere 60% hospitalized in the HEART pathway represented a massive improvement – and, such difference likely played a role in the 57% vs. 68% reduction in objective cardiac testing within 30 days. 17 patients suffered MACE, all at the index visit – and, even though the trial was not powered for safety outcomes, none occurred in the “low risk” patients of the HEART cohort.
The authors go on to state strict adherence to the HEART pathway could have eked out an additional 6% reduction in hospitalization. Certainly, in a nearly 80% admit rate environment, scaling back to a 54% rate is an important reduction. But, considering only 6% suffered an adjudicated MACE, there remains a vast gulf between the number hospitalized and the number helped. Some non-MACE patients probably derived some benefit from their extended healthcare encounter as a result of better-tailored medical management, or detection of alternate diagnoses, but clearly, we can do better.
“The HEART Pathway Randomized Trial – Identifying Emergency Department Patients With Acute Chest Pain for Early Discharge”
The problem with HEART and ADAPT/EDACS is they don't focus on the relevant group of patients. We care about the 'unstable angina' group. Not the troponin-positive group (we don't miss those). The vast majority of MACE patients are identified by troponins, and the contribution of the clinical tools touted by HEART and EDACS are minimal, if that.
For HEART, 91% of AMIs were identified on presentation by troponins. Only 12 of the 2441 patients (<0.5%) had AMI not identified by initial troponins (6-week follow-up). And here's the kicker: HEART missed 9 of them!
(Of the MACE outcomes, AMI is more meaningful than PCI and CABG.)
For EDACS/ADAPT, all but 38 of 1974 patients had MACE identified by troponins. ECG identified another 5, meaning the clinical tool was left to operate on 33 patients. So for ADAPT/EDACS:
1. Troponins missed MACE in only <2% of enrolled chest pain patients, about 1.5% if you include ECG (all MACE, not just missed MI).
2. There were only 33 patients remaining upon whom logistic regression was applied to determine the oh so important clinical variables.
Ryan, I don't have this small study you just reviewed in front of me, but question: how many 'unstable angina' (Trop neg, MACE pos) patients were there?
My guess is, like the prior studies, there were not nearly enough to determine that a clinical tool+trop/ECG is smarter than me+trop/ECG. Nor enough to worry about.
* 'smarter than me' is grammatically incorrect (irony), but I'm not sure the straight vertical line (I) in 'smarter than I+trop/ECG' would be interpretable.
** In EDACS, they used 37 clinical variables for the regression, but strangely did not include 'exertional component' in the set. It's rare for a trop/ECG negative patient to really worry me, but a good history of exertional CP will do it (unstable angina red flag, anyone?).
In the HEART pathway Mahler cohort, there were 8 MACE – 7 AMIs and 1 revascularization. All occurred at the index visit, and all were in the "high risk" population by HEART. It doesn't break down whether they were "high risk" due to troponin elevation or not.
But, yes, your point regarding troponins is well-taken. The vast majority of patients in the ED for chest pain, regardless of risk category, once they rule-out in the ED, they have very low 30-day MACE. Two negative troponins would have qualified 92% of this HEART cohort for discharge – with a sensitivity for MACE of 87.5%. The sensitivity might not look so great until you look at the overall prevalence and see the NPV of two negative troponins was 99.2%. From a practical standpoint, that's a <1% miss rate – which isn't "zero miss", but it's pretty darn good.
And, again, these risk-stratification methods mostly miss the point – they're for protecting clinicians, not for helping patients. A good system of integrated follow-up refers appropriate patients for secondary evaluation after AMI rule-out in the ED, and it's not a MACE when appropriate secondary testing identifies an ischemic stenosis or a high-grade proximal lesion. What we're looking for, as you say, true "unstable angina" – where the patient drops dead before they can work through appropriate follow-up testing – is not explicitly what these studies are precisely trying to detect/prevent. The good news is, especially with newer troponin assays interpreted correctly, it's vanishingly rare. These are, to some extent, the patients Stephen Smith wants to detect by doing CCTA occasionally in the ED.