Category: Chest Pain

Don’t ß-Blockade Cocaine Chest Pain

Or, specifically, ignore this evidence that says you can.

There may be some mythology to the hypothesis that non-selective ß-receptor blockade is contraindicated in the setting of cocaine chest pain.  After all, the supporting evidence consists only of small, laboratory case series – and other outcomes-oriented data suggests ß-blockade is cardioprotective, as we already know.  However, this study is a perfect example of inappropriately extending a conclusion from retrospective data.

These authors identified 378 patients from retrospective chart review, selecting patients with chief complaints of chest pain and positive toxicology tests for cocaine.  Unfortunately, urine toxicology tests for cocaine stay positive for days following the initial episode of cocaine use.  Therefore, there is no way from these chart review methods to reliably differentiate the acuity of the cocaine intoxication.  

This is important because a major flaw in retrospective reviews, such as this, is a confounding selection bias.  If all cocaine chest pain patients are not created equal – the neurohormonal effects of cocaine last on the minutes to hours while their drug tests are positive for days – then providers may be selecting patients for beta blocker use/non-use based on acuity information this review cannot detect.  If providers are excluding patients from beta-blockers based on the acuity of their intoxication – as many sensible providers might – and only using beta-blockers in non-acute presentations, then this study may not include any of the population of interest.

The authors’ statement of “We have found that BB use in the acute management of cocaine-associated chest pain did not increase the incidence of MI” cannot be defended as accurate, as it is based on indefensible assumptions.

“Safety of β-blockers in the acute management of cocaine-associated chest pain”
http://www.ncbi.nlm.nih.gov/pubmed/23122421

How Fast Can We Rule-Out AMI?

Six hours?  Two hours?  One hour?  McDonalds’ drive-thru?

This is the paper from Archives of Internal Medicine that’s been making the rounds in the lay press regarding how quickly the ER should be able to detect your AMI with the new highly-sensitive troponins.  This is the APACE, prospective, international, multi-center study evaluating patients with “symptoms suggestive of acute myocardial infarction” and onset within the last 12 hours.

In this cohort, 1247 patients were recruited – and >300 were excluded for either going straight to the cath lab or having “another procedure performed” at the 1-hour time mark – and received hs-cTnT at index, 1, 2, 3, and 6 hours after presentation.  Myocardial necrosis was defined as a hs-cTnT >99th percentile, which for this assay is 14 ng/L, and a diagnosis of acute MI was made by two independent cardiologists upon review of records and lab results.

The authors split their cohort into two groups, a derivation cohort and a validation cohort, and did some statistical wrangling to come up with two cut-off strategies – one for rule-in and one for rule-out.  They were able to make diagnostic decisions on ~76% of their cohort at the one-hour time point, and 52 ng/L at presentation or an increase within an hour of 5 ng/L or more was ~94% specific for AMI.  Likewise, 12 ng/L and an increase less than 3 ng/L at 1 hour was ~100% sensitive for AMI.  The remaining 25% of their cohort was in a non-diagnostic zone.  At 30 days, there was one death in their rule-out cohort, for a 99.8% survival rate.

So, can you use this strategy?  If you feel as though this study is externally valid to your populations and you’re using the same Roche Diagnostics test, you certainly may.  Every piece of data is something you can incorporate to your discussions with a patient regarding diagnostic certainty and risk.  Even an extra hour occupying an ED bed rather than moving out to a chest pain observation facility can significantly impede ED flow, while observation admissions are costly and inconvenient to patients.  The ideal strategy will depend on the capabilities of individual departments.

This study, along with the primary author, are sponsored in part by Abbott, Roche, and Siemens.
www.ncbi.nlm.nih.gov/pubmed/22892889

Vancouver Chest Pain Rule in Tehran

Iran and Canada would be considered by most to be very different places.  However, from a cardiovascular standpoint, it seems they’re not so disparate.


This is a prospective, validation study of the Vancouver Chest Pain Rule.  The Vancouver rule is one of many 2-hour accelerated rule-outs operating under the presumption that all disease can never be detected – sensitivity will never be 100%, but this assumes a context in which a discussion may be had with the patient about outpatient disposition.  Essentially, any patient under 40 years without a history of coronary artery disease and a normal EKG simply gets discharged.  Older than 40 and atypical chest pain is discharged either immediately after a CK-MB < 3.0 µg/L, or receives a 2-hour delta + repeat EKG if > 3.0 µg/L.  Essentially, the rule is designed only to ensure all unusual NSTEMIs are picked up.


In the initial study, the 30-day ACS rate for the discharged group was 1.2%.  In this Iranian study, the 30-day ACS rate of 292 very-low-risk patients is 1.3%.  Two of the four patients meeting criteria for discharge by CK-MB had positive troponins.  Considering CK-MB is nearly considered anachronistic now, most modern EDs would have not have discharged these patients based on troponin testing.  A third patient had EKG changes on the second EKG – which should fail the Vancouver rule, so I’m uncertain why it was included in their very-low-risk group.  Finally, the last patient had an entirely normal evaluation and a subsequent 70% lesion discovered on angiography a week later.  No mention of the hemodynamic significance/relation to ischemia of this lesion is noted.


A few hundred patients is hardly a definitive validation, but it’s a nice demonstration that 50% of their cohort could have been discharged in two hours – and with the same 30-day event rate as the poor people being made to glow in the CCTA studies.


“Validation of the Vancouver Chest Pain Rule: A Prospective Cohort Study”

Excitement For/Failure of CCTA

The third of the big CT coronary angiography studies from the last year – and, yet again, this is positive for its primary endpoint.


However, that value of that endpoint is another matter – mean length of stay in the hospital.  For the CCTA cohort, that mean was 23.2 hours and the “standard evaluation” was 30.8 hours.  However, more illuminating – and further favoring CCTA – is that the median CCTA evaluation time was 8.6 hours compared with 26.7 hours in the “standard evaluation” group.  Just like in the previous studies, CCTA is faster, and, for some patients, much, much faster.


But, as you can probably gather from that mean/median discrepancy, a substantial cohort in the CCTA group went on to have some pretty extensive downstream testing and prolonged hospital stays.  This means, from a costs standpoint, the two strategies eventually even out.  No significant safety differences were detected between the two strategies.


Now that we’ve seen the full results of ROMICAT II, CT-STAT, and ACRIN-PA, we have a pretty good idea of what this test does.  If you must evaluate these low-risk chest pain patients with imaging of some sort, need to clear them out of your Emergency Department quickly, your cardiology team is excited to take on the false positives, and you’re unconcerned about the downstream harms – then CCTA is the test for you.  If the potential harms, the poor specificity, and the non-functional nature of the test concerns you – then no one will fault you for dragging your feet.


The accompanying editorial gets it right – this is still a test looking for the correct application.  However, we don’t just need a better test – we need a better consensus for whom we’re simply not going to test.


“Coronary CT Angiography versus Standard Evaluation in Acute Chest Pain”

Chest Pain – Here, Your Problem Now

In the United States, a quarter of our medical malpractice payments result from missed myocardial infarctions.  Therefore, in states with sub-optimal liability environments, emergency physicians are stuck in a quagmire of conflicted interests and fear of litigation if a discharged patient has an MI.

Therefore, a common strategy is to make low-risk chest pain Someone Else’s Problem.  And, this article from Archives of Internal Medicine shows the internist evaluating the patient simply makes the same surrender to defensive medicine.  In this retrospective cohort, 2,107 admitted patients underwent 1,474 stress tests during their two-year study period.  Of those 1,474, 12.5% were abnormal.  Of those 184 patients, only 11.6% underwent cardiac catheterization, and a grand total of 9 patients received a revascularization.

So, the authors suggest two salient points:
 – 2,107 admissions to yield 9 (supposedly) beneficial interventions – how crazy is that?
 – What about the 88.4% of patients with abnormal stress tests that didn’t undergo an invasive test within 30 days – why are we using an evaluation strategy we don’t act on?

The authors think we might be able improve upon this practice pattern.

“Outcomes of Patients Admitted for Observation of Chest Pain”
www.ncbi.nlm.nih.gov/pubmed/22566486

The Ehrlanger HEARTS3 Score

I hate using the TIMI score to risk-stratify patients in the Emergency Department.  It wasn’t derived from a question asked in the Emergency Department, but has been co-opted by hundreds of studies as it has some value as part of our common language with inpatient medicine and cardiology teams.  We’re familiar enough with it’s shoehorning into our environment that we can use it to assist in some rough decisions about prognosis, but, clearly a better tool must exist.

A couple years back, the HEART score came out of the Netherlands.  In a small derivation and validation cohort, it did a reasonable job of predicting outcomes, using language and variables more relevant to the Emergency Department.  However, these authors from Ehrlanger in Chattanooga recognized one of the limitations of the HEART score was the somewhat arbitrary “expert” weighting of the various elements.  They therefore undertook a study with the goal of using logistic regression and likelihood ratios of the various included elements to expand the score and modify the weighting.

The good news: they improved the AUC of the scoring system from 0.827 and 0.816 for acute MI and 30-day ACS, respectively, to 0.959 and 0.902.  At the reasonable cut-off, the HEARTS3 score gets up close to ~98% sensitivity with ~60% specificity for 30-day ACS.

The bad news: a complex clinical situation requires a complex clinical decision instrument.  No one will be able to hold this in their head like the NEXUS criteria, the TIMI score, or Wells criteria – if we were even bothering to hold all these hundreds of decision instruments in our heads to start.  Luckily, smartphones, the Internet, and decision-support built-in to electronic health records is making progress towards readily available peripheral brains with which to quickly reference risk-stratification instruments such as this.

It still needs external validation, but this is one of the tools seeming to have the greatest potential I’ve recently seen

“Improving risk stratification in patients with chest pain: the Erlanger HEARTS3 score”
http://www.ncbi.nlm.nih.gov/pubmed/22626816

Everyone Is On the Cardiac CT Bandwagon

The NEJM is on the wagon with their recent publication.  Annals of EM has been publishing all the ROMICAT trials.  And, not to be outdone, the American College of Cardiology is publishing the CT-STAT trial – a head to head comparison between coronary CT angiogram in the Emergency Department and stress perfusion imaging.

The endpoint of interest, however, is length of stay – and by association total index visit costs – rather than accuracy or safety.  And, in this sense, it was successful.  The primary difference in LOS was the length of time it took to perform the CT or stress test, which was approximately 4 hours quicker in the CT group.  ED costs were also lower, somehow, presumably billing for an observation code while awaiting the stress test and results.

However, what the authors don’t include are the total downstream costs and time of additional testing after the Emergency Department visit.  The stress test group had 34 abnormal or non-diagnostic scans, while the CT group had 64.  27 patients in the stress group underwent additional testing vs. 51 in the CT group – mostly stress tests that were subsequently normal – and none of these costs or times are included in their analysis.  I imagine if these extra tests are included in their analysis, the cost difference shrinks or disappears.

It seems to be a trend to advertise more than CT angiography actually delivers.

Several authors are sponsored by Siemens.

“The CT-STAT (Coronary Computed Tomographic Angiography for Systematic Triage of Acute Chest Pain Patients to Treatment) Trial”
www.ncbi.nlm.nih.gov/pubmed/21939822

ADAPT 2-Hour Rule Out

I’ve had a couple questions recently about accelerated rule-out strategies – considering they’re in the ACEP Guidelines, but the AHA seems to endorse a viewpoint that any suspicion for cardiac chest pain needs to be taken to its bitter end with a provocative test.  Unfortunately, an all-in strategy doesn’t mesh quite as well with reality where the costs are astronomical, and the yield abysmal.

Conveniently, this is another recent study highlighting the use of two sets of biomarkers, two hours apart – using conventional troponin assays.  This is an observational cohort study in Australia and New Zealand investigating the feasibility of their stratification instrument, with the endpoints of “Major Adverse Cardiac Events” within 30 days – an endpoint that, for once, excludes revascularizations.  Specifically, the decision protocol being evaluated includes:
 – Negative troponins at 0 and 2 hours from presentation.
 – No new ischemic changes on ECG.
 – TIMI Score of zero.

Of their 1,976 enrolled patients, 392 met these criteria and were followed for 30 days.  Their single miss was reported as an nSTEMI with two initially negative troponins who subsequently had a positive 12-hour troponin.  Therefore, their sensitivity for 30-day MACE is statistically 98.1% to 99.9%.  This is one of the eight patients in the low-risk cohort who underwent a revascularization procedure in the course of their routine care.

Essentially, using a normal EKG, two negative sets of enzymes, and a risk-stratification instrument – TIMI, Geneva, etc. – the evidence out there lets you have a discussion with the patient regarding their overall risk for a poor outcome.  If you’re stuck in a zero-miss environment, then any of these 2-hour protocols will be of no use – they all have a non-negligible miss rate.  But, if you have a grey area to work with, and an otherwise relatively low-risk patient, a quick two-hour troponin helps you catch a few extra fish you otherwise would have missed.

“2-Hour Accelerated Diagnostic Protocol to Assess Patients With Chest Pain Symptoms Using Contemporary Troponins as the Only Biomarker The ADAPT Trial”
www.ncbi.nlm.nih.gov/pubmed/22578923

A Chest Pain Disposition Decision Instrument

This article has three things I like – information graphics, informed patients, and an attempt to reduce low-yield chest pain admissions.  Unfortunately, in the end, I’m not sure about the strategy.

This is a prospective study in which the authors developed an information graphic attempting to illustrate the outcome risks for low-risk chest pain presentations.  They use this information graphic as the intervention in their study population to help educate patients regarding the decision whether to be observed in the hospital with potential provocative stress testing, or whether they would like to be discharged from the Emergency Department to follow-up for an outpatient provocative test.  They were attempting to show that use of this decision aid would lead to increased patient knowledge and satisfaction, as well as reduce observation admissions for low-risk chest pain.

The good news: it definitely works.  Patients reported increased knowledge, most were happy with the decision instrument, and a significantly increased proportion elected to be discharged from the Emergency Department – 58% of the decision aid group wanted to stay vs. 77% of the “usual care” arm wanted to stay.

My only problem: this study truly exposes the invalidity of our current management of chest pain.  If these patients are low-risk and they’re judged safe enough for the outpatient strategy in this study – why are any of them being offered admission?  Of course, it’s probably because they don’t have timely follow-up, and AHA guidelines dictate stress testing urgently following the index visit.  But, truly, in an ideal world, few (if any) of these low-risk patients – such as the one who ruled in by enzymes – should be offered admission.

But, other than that, I’m all for information graphics and patient education techniques to include them in a shared decision-making process!

“The Chest Pain Choice Decision Aid : A Randomized Trial”
www.ncbi.nlm.nih.gov/pubmed/22496116