Category: Chest Pain

Can We Trust Our Computer ECG Overlords?

If your practice is like my practice you see a lot of ECGs from triage. ECGs obtained for abdominal pain, dizziness, numbness, fatigue, rectal pain … and some, I assume, are for chest pain. Every one of these ECGs turns into an interruption for review to ensure no concerning evolving syndrome is missed.

But, a great number of these ECGs are read as “Normal” by the computer – and, anecdotally, are nearly universally correct.  This raises a very reasonable point as to question whether a human need be involved at all.

This simple study tries to examine the real-world performance of computer ECG reading, specifically, the Marquette 12SL software. Over a 16-week convenience sample period, 855 triage ECGs were performed, 222 of which were reported as “Normal” by the computer software. These 222 ECGs were all reviewed by a cardiologist, and 13 were ultimately assigned some pathology – of which all were mild, non-specific abnormalities. Two Emergency Physicians also then reviewed these 13 ECGs to determine what, if any, actions might be taken if presented to them in a real-world context. One of these ECGs was determined by one EP to be sufficient to put the patient in the next available bed from triage, while the remainder required no acute triage intervention. Retrospectively, the patient judged to have an actionable ECG was discharged from the ED and had a normal stress test the next day.

The authors conclude this negative predictive value for a “Normal” read of the ECG approaches 99%, and could potentially lead to changes in practice regarding immediate review of triage ECGs. While these findings have some limitations in generalizability regarding the specific ECG software and a relatively small sample, I think they’re on the right track. Interruptions in a multi-tasking setting lead to errors of task resumption, while the likelihood of significant time-sensitive pathology being missed is quite low. I tend to agree this could be a reasonable quality improvement intervention with prospective monitoring.

“Safety of Computer Interpretation of Normal Triage Electrocardiograms”
https://www.ncbi.nlm.nih.gov/pubmed/27519772

The Chest Pain Decision Instrument Trial

This is a bit of an odd trial. Ostensibly, this is a trial about the evaluation and disposition of low-risk chest pain presenting to the Emergency Department. The authors frame their discussion section by describing their combination of objective risk-stratification and shared decision-making in terms of reducing admission for observation and testing at the index visit.

But, that’s not technically what this trial was about. Technically, this was a trial about patient comprehension – the primary outcome is actually the number of questions correctly answered by patients on an immediate post-visit survey. The dual nature of their trial is evident in their power calculation, which starts with: “We estimated that 884 patients would provide 99% power to detect a 16% difference in patient knowledge between decision aid and usual care arms”, which is an unusual choice of beta and threshold for effect size – basically one additional question correct on their eight-question survey. The rest of their power calculation, however, makes sense “… and 90% power to detect a 10% difference in the proportion of patients admitted to an observation unit for cardiac testing.” It appears the trial was not conducted to test their primary outcome selected by their patient advocates designing the trial, but in actuality to test the secondary outcomes thought important to the clinicians.

So, it is a little hard to interpret their favorable result with respect to the primary outcome – 3.6 vs 4.2 questions answered correctly. After clinicians spent an extra 1.3 minutes (4.4 vs 3.1) with patients showing them a visual aid specific to their condition, I am not surprised patients had better comprehension of their treatment options – and they probably did not require a multi-center trial to prove this.

Then, the crossover between resource utilization and shared decision-making seems potentially troublesome. An idealized version of shared decision-making allows patients to participate in their treatment when there is substantial individual variation between the perceived value of different risks, benefits, and alternatives. However, I am not certain these patients are being invited to share in a decision between choices of equal value – and the authors seem to express this through their presentation of the results.

These are all patients without known coronary disease, normal EKGs, a negative initial cardiac troponin, and considered by treating clinicians to otherwise fall into a “low risk” population. This is a population matching the cohort of interest from Weinstock’s study of patients hospitalized for observation from the Emergency Department, 7,266 patients of whom none independently suffered a cardiac event while hospitalized.  A trial in British Columbia deferred admission for a cohort of patients in favor of outpatient stress tests.  By placing a fair bit of emphasis on their significant secondary finding of a reduction in observation admission from 52% to 37%, the authors seems to indicate their underlying bias is consistent with the evidence demonstrating the safety of outpatient disposition in this cohort.  In short, it seems to me the authors are not using their decision aid to help patients choose between equally valued clinical pathways, but rather to try and convince more patients to choose to be discharged.

In a sense, it represents offering patients a menu of options where overtreatment is one of them.  If a dyspneic patient meets PERC, we don’t offer them a visual aid where a CTPA is an option – and that shouldn’t be our expectation here, either.  These authors have put in tremendous effort over many years to integrate many important tools, but it feels like the end result is a demonstration of a shared decision-making instrument intended to nudge patients into choosing the disposition we think they ought, but are somehow afraid to outright tell them.

“Shared decision making in patients with low risk chest pain: prospective randomized pragmatic trial”
http://www.bmj.com/content/355/bmj.i6165.short

Don’t CTPA With Your Gut Alone

Many institutions are starting to see roll-out of some sort of clinical decision-support for imaging utilization. Whether it be NEXUS, Canadian Head CT, or Wells for PE, there is plenty of literature documenting improved yield following implementation.

This retrospective evaluation looks at what happens when you don’t obey your new robot overlords – and perform CTPA for pulmonary embolism outside the guideline-recommended pathway. These authors looked specifically at non-compliance at the low end – patients with a Wells score ≤4 and performed with either no D-dimer ordered or a normal D-dimer.

During their 1.5 year review period, there were 2,993 examinations and 589 fell out as non-compliant. Most – 563 – of these were low-risk by Wells and omitted the D-dimer. Yield for these was 4.4% positivity, compared with 11.2% for exams ordered following the guidelines. This is probably even a high-end estimate for yield, because this includes 8 (1.4%) patients who had subsegmental or indeterminate PEs but were ultimately anticoagulated, some of whom were undoubtedly false positives. Additionally, none of the 26 patients that were low-risk with a normal D-dimer were diagnosed with PE.

Now, the Wells criteria are just one tool to help reinforce gestalt for PE, and it is a simple rule that does not incorporate all the various factors with positive and negative likelihood ratios for PE. That said, this study should reinforce that low-risk patients should mostly be given the chance to avoid imaging, and a D-dimer can be used appropriately to rule-out PE in those where PE is a real, but unlikely, consideration.

“Yield of CT Pulmonary angiography in the emergency Department When Providers Override evidence-based clinical Decision support”
https://www.ncbi.nlm.nih.gov/pubmed/27689922

All Glory to the Triple-Rule-Out

The conclusions of this study are either ludicrous, or rather significant; the authors are either daft, or prescient. It depends fundamentally on your position regarding the utility of CT coronary angiograms.

This article describes a retrospective review of all the “Triple-Rule-Out” angiograms performed at a single center, Thomas Jefferson University Hospital, between 2006 and 2015. There were no specific circumstances under which the TRO were performed, but, grossly, the intended population were those who were otherwise being evaluated for an acute coronary syndrome but “was suspected of having additional noncoronary causes of chest pain”.

This “ACS-but-maybe-not” cohort totaled 1,192 patients over their 10 year study period. There were 970 (81.4%) with normal coronary arteries and no significant alternative diagnosis identified. The remaining, apparently to these authors, had “either a coronary or noncoronary diagnosis that could explain their presentation”, including 139 (11.7%) with moderate or severe coronary artery disease. In a mostly low-risk, troponin-negative population, it may be a stretch to attribute their symptoms to the coronary artery disease – but I digress.

The non-coronary diagnoses, the 106 (8.6%) with other findings, range from “important” to “not at all”. There were, at least, a handful of aortic dissections and pulmonary emboli picked up – though we can debate the likelihood of true positives based on pretest odds. However, these authors also credit the TRO with a range of sporadic findings as diverse as endocarditis, to diastasis of the sternum, and 24 cases of “aortic aneurysm” which were deemed important mostly because there were no priors for comparison.

The authors finally then promote TRO scans based on these noncoronary findings – stating that, if a traditional CTCA were performed, many of these diagnosis would likely be missed. Thus, the paradox. If you are already descending the circles of hell, and are using CTCA in the Emergency Department – then, yes, it is reasonable to suggest the TRO is a valid extension of the CTCA. Then again, if CTCA in the acute setting is already outside the scope of practice, and TRO is an abomination – carry on as if this study never existed.

“Diagnostic Yield of Triple-Rule-Out CT in an Emergency Setting”
http://www.ncbi.nlm.nih.gov/pubmed/27186867

The High-Sensitivity Troponin Ennui

They’re coming. It’s inevitable. They have yet to be approved in the the United States, but every year the news is the same: they’re coming.

High-sensitivity troponins have been both lauded and mocked from various perspectives. The literature is replete with examples of expedited rule-outs in the Emergency Department owing to their improved lower limit of detection for myocardial injury. However, every study touting the benefits of improved sensitivity has begrudgingly or worse acknowledged the correspondingly diminished specificity.

This, then, is a randomized trial of reporting either a conventional troponin assay result or a high-sensitivity troponin assay result, with a multitude of patient-oriented short- and long-term outcomes measured. The specific assays used here were either a c-TnT with a threshold of detection of 30 ng/L, or a hs-TnT with a threshold of detection of 3 ng/L. Clinicians caring for patients were randomized to making care decisions based on one, without knowledge of the other.

For all the various propaganda for and against high-sensitivity troponins, this trial is highly anticlimactic. There were, essentially, no changes in physician behavior resulting from the additional information provided by the more sensitive assay. No fewer patients were admitted, similar numbers of ultimate downstream tests occurred, and there were no reliable differences in long-term cardiac or combined endpoint outcomes.

The only outcome of note is probably consistent with what we already knew: any circulating troponin portends worse outcomes. This may be most helpful in directing the long-term medical management of those whose troponin levels were previously undetectable with a conventional assay; these patients clearly do not have the same virtually-zero risk as a patient with undetectable troponin levels. Indeed, troponin levels alone were a better predictor of long terms outcomes than the Heart Foundation Risk Stratification, as well.

I’ll let Judd Hollander sum it up in his most concise – with a link to much more verbose – terms:

“Randomized Comparison of High-Sensitivity Troponin Reporting in Undifferentiated Chest Pain Assessment”
http://circoutcomes.ahajournals.org/content/early/2016/08/09/CIRCOUTCOMES.115.002488.abstract

Perpetuating the Flawed Approach to Chest Pain

Everyone has their favored chest pain accelerated diagnostic risk-stratification algorithm or pathway these days.  TIMI, HEART, ADAPT, MACS, Vancouver, EDACS – the list goes on and on.  What has become painfully clear from this latest article, however, is this approach is fundamentally flawed.

This is a prospective effectiveness trial comparing ADAPT to EDACS in the New Zealand population.  Each “chest pain rule-out” was randomized to either the ADAPT pathway – using modified TIMI, ECG, and 0- and 2-hour troponins – or the EDACS pathway – which is its own unique scoring system, ECG, and 0- and 2-hour troponins.  The ADAPT pathway classified 30.8% of these patients as “low risk”, while the EDACS classified 41.6% as such.  Despite this, their primary outcome – patients discharged from the ED within 6 hours – non-significantly favored the ADAPT group, 34.4% vs 32.3%.

To me, this represents a few things.

We are still have an irrational, cultural fear of chest pain.  Only 11.6% of their total cohort had STEMI or NSTEMI, and another 5.7% received a diagnosis of “unstable angina”.  Thus, potentially greater than 50% of patients were still hospitalized unnecessarily.  Furthermore, this cultural fear of chest pain was strong enough to prevent acceptance of the more-aggressive EDACS decision instrument being tested in this study.  A full 15% of low-risk patients by the EDACS instrument failed to be discharged within 6 hours, despite their evaluation being complete following 2-hour troponin testing.

But, even these observations are a digression from the core hypothesis: ADPs are a flawed approach.  Poor outcomes are such the rarity, and so difficult to predict, that our thought process ought be predicated on a foundation that most patients will do well, regardless, and only the highest-risk should stay in the hospital.  Our decision-making should probably be broken down into three steps:

  • Does this patient have STEMI/NSTEMI/true UA?  This is the domain of inquiry into high-sensitivity troponin assays.
  • Does the patient need any provocative testing at all?  I.e., the “No Objective Testing Rule”.
  • Finally, are there “red flag” clinical features that preclude outpatient provocative testing?  The handful of patients with concerning EKG changes, crescendo symptoms, or other high-risk factors fall into this category.

If we are doing chest pain close to correctly, the numbers from this article would be flipped – rather than ~30% being discharged, we ought to be ~70%.

“Effectiveness of EDACS Versus ADAPT Accelerated Diagnostic Pathways for Chest Pain: A Pragmatic Randomized Controlled Trial Embedded Within Practice”

Let’s Get Inappropriate With AHA Guidelines

How do you hide bad science?  With meta-analyses, systematic reviews, and, the granddaddy of the them all, guidelines.  Guidelines have become so twisted over the recent history of medicine the Institute of Medicine had to release a statement on how to properly create them, and a handful of folks have even gone so far as to imply guidelines have become so untrustworthy a checklist is required for evaluation in order to protect patients.

Regardless, despite this new modern era, we have yet another guideline – this time from the American Heart Association – that deviates from our dignified ideals.  This guideline is meant to rate appropriate use of advanced imaging in all patients presenting to the Emergency Department with chest pain.  This includes, for their purposes, imaging to evaluate nSTEMI/ACS, suspected PE, suspected syndromes of the aorta, and “patients for whom a leading diagnosis is problematic or not possible”.

My irritation, as you might expect, comes at the expense of ACS and “leading diagnosis is problematic or not possible”.  The guidelines weighing the pros and cons of the various options for imaging PE and the aorta are inoffensive.  However, their evaluation of chest pain has one big winner: coronary CT angiograms.  The only time this test is not appropriate in a patient with potential ACS is when the patient has a STEMI.  They provide a wide range of broad clinical scenarios to assist the dutiful reader – all of which are CCTA territory – including as every low/intermediate risk nonischemic EKG and troponin-negative syndrome, explicitly even TIMI 0 patients.

Their justification of such includes citation of the big three – ACRIN-PA, ROMICAT II, and CT-STAT – showing the excellent negative predictive value of the test.  Indeed, the issues with the test – middling specificity inflicted upon low disease prevalence, increased downstream invasive angiography and revascularization of questionable value – are basically muttered under the breath of the authors.  Such dismissive treatment of the downsides of the test are of no surprise, considering Harold Litt, of ACRIN-PA and Siemens, is part of the writing panel for the guideline.  I will, again, point you to Rita Redberg’s excellent editorial in the New England Journal of Medicine, refuting the foundation of such wanton use of CCTA in the emergency evaluation of low-risk chest pain.

The “leading diagnosis is problematic or not possible” category is just baffling.  Are we really trying to enable clinicians to be so helpless as to say, “I don’t know!  Why think when I can scan?”  The so-called “triple rule-out” is endorsed in this document for this exact scenario – so you can use a test whose characteristics for detection of each entity under consideration are just as degraded as your clinical acumen.

Fantastically, both the Society of Academic Emergency Medicine and the American College of Emergency Physicians are somehow co-signatories to this document.  How can we possibly endorse such fragrant literature?

“2015 ACR/ACC/AHA/AATS/ACEP/ ASNC/NASCI/SAEM/SCCT/SCMR/ SCPC/SNMMI/STR/STS Appropriate Utilization of Cardiovascular Imaging in Emergency Department Patients With Chest Pain”
http://www.ncbi.nlm.nih.gov/pubmed/26809772

CTCA in the ED, Getting Less Sexy By The Day

As I’ve written before, the CT coronary angiograms is a funny test.  The idea of having a non-invasive method of detecting previously unknown coronary artery disease is compelling.  The practical application, however, has been limited by a low specificity – further exacerbated by those encouraging its use in a population with low pretest probability.

However, the few major studies regarding it tend to view CTCA in a favorable light – the result of comparing CTCA-based strategies to modern over-triage and over-testing of potential acute coronary syndrome.  These studies, ACRIN-PA and ROMICAT, showed significant improvements in direct discharge from the ED and in length-of-stay, not so much due to being a superior strategy of benefit to patients, but by obviating unnecessary care inflicted upon them.

The general gist of this trial is framed in the “era of high-sensitivity troponins” – referring to new developments in assays allowing a safer rapid rule-out in the Emergency Department.  This trial, as opposed to the others, also occurs in the Netherlands, a setting in which direct discharge from the ED is no anathema.  The “standard care” arms of ACRIN-PA and ROMICAT-2 had discharge rates from the ED of ~20% or less, while this trial discharges nearly 60%.  Yet, despite such recklessness displayed in this trial, these patients are ultimately just as safe.  And, when such an insanity-reduction initiative is undertaken, the advantages of CTCA diminish.

And, frankly, nearly all low-risk patients can be discharged safely from the Emergency Department.  The appropriate urgent follow-up test, if any, is a trickier proposition – and CCTA may yet be appropriate for some.  However, as a routine, ED-based strategy, it should probably be considered low-value care.

“Coronary CT Angiography for Suspected ACS in the Era of High-Sensitivity Troponins”
http://content.onlinejacc.org/article.aspx?articleID=2479881

Still Making Sense of High-Sensitivity Troponin

Figuring out the value of a troponin measurement is both simple, and complicated.  Big numbers are still straightforward and trouble.  Small numbers – and even smaller still – are increasingly difficult to parse.

What does seem to be true, at least: the closer to zero, the better.

This is a multi-center evaluation of a 0- and -1hour troponin delta strategy, based on a hs-cTnT from Roche.  These authors prospectively enrolled 1,458 patients with chest pain of peak intensity within 6 hours.  Samples were then taken at 0, 1, 2, and then at least 4 hours after presentation.  The outcome of interest was an independently adjudicated final diagnosis of acute myocardial infarction.  And, this study probably shows just about what every similar study has shown: initial sensitivity is ~90%, with marginal increases as additional time points are added, while specificity suffers predictably due to the nature of the assay.

However, there are a couple concerning potential sources of bias.  The authors enrolled 1,458 patients – but exclude 176 of them from analysis for a variety of reasons.  In a study trying to catch rare events to demonstrate near-100% sensitivity, over 10% of patients dropping out is an important consideration.  There were also issues with slow enrollment, compared to previous studies, and the patient flow diagram is extremely sparse.  Over two years, the centers involved likely had many thousands of chest pain presentations.  No information regarding the missed enrollments is presented.

There are also issues with the adjudication downstream, which was based on the results of various follow-up examinations as well as, oddly enough, a different troponin assay: s-cTnI-ultra.  213 (17%) patients received a final diagnosis of AMI, while 167 (13%) received a diagnosis of unstable angina.  The clinical significance of their definition of unstable angina remains unclear to me – myocardial ischemia without cellular injury associated with chest pain at rest.  The authors reference these UA patients as being at low risk for poor long term outcomes, which seems clinically discontinuous with the sort of “critical near-occlusion” working definition I’m familiar with for true UA.  Regardless, the safety of their strategy is only reasonable if UA is a relatively benign catch-all diagnosis for troponin-negative chest pain, so I will accept their categorization.

There were also diverse and perverse conflicts-of-interest described with the manufacturer of the assay involved.

Regardless, as previously stated, these data are consistent with prior demonstrations – so, yes, using these assays at presentation, or as 1- or 2-hour deltas in the Emergency Department, will result in a very low miss rate when paired with low pretest likelihoods of disease.  Furthermore, anything missed by these assays will be such a minute injury pattern as to be extremely low-risk for short term cardiac mortality.

Yes, Virginia, you can discharge chest pain.

“Multicenter Evaluation of a 0-Hour/1-Hour Algorithm in the Diagnosis of Myocardial Infarction With High-Sensitivity Cardiac Troponin T”
http://www.annemergmed.com/article/S0196-0644(15)01501-2/abstract

What Did We Find On Stress Testing?

The so-called “provocative” testing advocated by the American Heart Association for every patient with chest pain of possible ischemic origin has been the thistle in our salad for many years.  They are the nidus for the crystallization of countless chest-pain observation units in our Emergency Departments.

And, they are one of lowest-yield venues in medicine.

Last year, I reported on a set of 1,754 biomarker-negative patients undergoing stress testing in Rhode Island, only 20 of which were true positives.  This latest report follows-up the stress testing outcomes from the ASPECT and ADAPT cohorts in New Zealand.  Of the 1,483 patients enrolled with negative biomarkers, 749 ultimately underwent exercise tolerance testing – 32 of which were positive, 22 of such had stenosis of greater than 70%.  Including index admission and 1-year follow-up of the study cohort, 20 of these received some form of revascularization (PCI or CABG).  In addition, there were 66 equivocal and 103 submaximal stress tests contributing to a total of 70 episodes of invasive coronary angiography, 32 of which identified stenosis >70%.

This is slightly higher yield, overall, than the previously reported U.S. cohort.  Most likely, this is due to patients in this study being almost a decade older – almost 60 years on average – and having median TIMI score of 2, compared with the U.S. stress test population having a TIMI of 0.  But, clearly, a cohort referred for stress testing resulting in only a 4.8% initial revascularization, including just 36 of 93 referred for coronary angiography, is not an effective use of healthcare resources.  And, this presumes the interventions performed as a result of stress testing provide some incremental morbidity or mortality benefit.

There are certainly patients for whom the various types of stress testing, non-invasive coronary angiography, and invasive angiography are each appropriate – but clearly we need to dramatically improve the specificity of our selection criteria.

“The incremental value of stress testing in patients with acute chest pain beyond serial cardiac troponin testing”