Category: Chest Pain

Testing For Pulmonary Embolism is More Harmful Than Helpful

This is, in my opinion, the most conceptually important article I have read in the few months I’ve been posting to this blog.

This is where Dr. Newman and Dr. Schriger, outstanding clinicians and analysts of data, present a compelling case regarding the diagnosis and treatment of pulmonary embolism.  In brief, the authors try to estimate, based on the limited evidence, both the benefits and harm of diagnosis and treatment of pulmonary embolism.  In their review, very few patients were found to benefit from treatment of pulmonary embolism – the existing evidence is weakly supportive of anticoagulation.  Additionally, they show a great many patients were harmed by excessive testing and treatment of clinically unimportant pulmonary embolisms.

This is, while a complicated opinion piece, a lovely summation in a nutshell of the concept that finding more “disease” does not equal better outcomes.  And, depending on the risks of testing and treatment – the barbaric contrast, radiation, and rat poison that diagnosis of PE typically entails – more people would be alive today if we all stopped testing for pulmonary embolism.

This is not unique to pulmonary embolism – this is partly the same issue we encounter with overtesting our low-risk chest pain patients, particularly with CTA.  What this means – and, of course, subject to legal challenge in our bizarre society – is that with our current methods of detection and treatment, society would be better off as a whole if we missed a few pulmonary embolisms in order to find and treat the few clinically relevant ones.  The only shame in this article is that not nearly enough people will read it and take it to heart.

http://www.ncbi.nlm.nih.gov/pubmed/21621091

Heart Fatty Acid Binding Protein

A nice comparison of the sensitivities and specificities of the various biomarkers for acute myocardial infarction at ~3.5 hours after symptom onset.  Each biomarker was set at the 95th or 99th percentile based on manufacturers definitions for their reference table, and then they also show ROC curves and calculate AUCs for each.

Essentially, none of the biomarkers is completely adequate for ruling out AMI given the constraints of their study.  Their best combination, for both sensitivity and specificity, is combining the heart fatty acid binding protein and the troponin – which they state provides an NPV of 95.6%, outperforming the “triple rule out” of troponin, CKMB, and myoglobin at 92.1%.  Interestingly, they also state that if they used clinical risk stratification, they could select a population in which HFAP and troponin together get up to 96.9% NPV…showing that regardless the resources we throw at the problem of “low risk chest pain”, it is an absolutely Quixotic quest to definitively rule out every MI in the Emergency Department.  3% of their “very low risk” population that was biomarker negative with the best sensitivity they could muster ended up ruling in for AMI during their subsequent hospital stay.  They only way we’re going to prevent healthcare from becoming bankrupt is increasing our levels of acceptable risk.

As a side note, this article gets the award for “best vs. least professional” title so far this year.

http://www.ncbi.nlm.nih.gov/pubmed/21561701

Chest Pain and Recent Negative Stress Test

If your hospital is anything like our hospital, you have tons of low- and intermediate-risk chest pain.  Every one is stressful, but hopefully you have a friendly hospitalist, or better yet, an ED-run chest-pain unit that gives you a place for observation admissions.  They go there, get their rule-out, and get some sort of provocative test, as discussed in the most recent AHA guidelines.  The test is negative, they go home.

…and then they come back a week later with the same symptoms.

This is a great paper to have in your pocket when you need to justify why this patient still needs to be ruled out; I heard about it when it was mentioned on the April EM:RAP during the low-risk chest pain discussion.  Patients with negative stress tests may still be diagnosed with CAD on angiography – 20.7% incidence of CAD in their cohort which had negative or non-diagnostic stress within 3 years – and 7.8% were diagnosed with AMI.

When you add negative troponins and the negative stress from the previous visit, you’ve met the guidelines and standard of care to say they did not have acute myocardial ischemia and you cannot induce ischemia on provocative testing, and they are risk-stratified into a group of patients very unlikely to have ACS in the next 30 days/60 days/6 months.  However, you get that high NPV because you’re performing these tests on a low-risk population, not because the sensitivity of those tests, particularly stress testing, is good enough.  While this patient likely does not need another provocative test – although, depending on individual factors, they may be candidates for angiography of some sort – if their story is concerning for cardiac etiology, they still need enzymatic rule-out.

http://www.ncbi.nlm.nih.gov/pubmed/21079714

ASPECT 2-Hour Rule-Out

Low-risk chest pain – if your ED doesn’t already have a chest pain unit set up for you to painlessly move patients through their enzymatic and non-invasive testing, you’re probably trying to find safe ways to discharge your chest pain patients home to avoid the repetitive calls to an unsympathetic hospitalist.  Problem is, without some kind of imaging or functional study, you’re going to invariably get burned.  This is another one of the TIMI-score-plus-X attempts at risk-stratifying patients in a prospectively applied dry run of their protocol.  It’s TIMI 0 patients plus normal EKG plus negative zero and two-hour CKMB/troponin/myoglobin.  Basically, 10% of their chest pain cohort fit this essentially zero-risk profile and were enzymatically ruled out.  And 0.9% (0.02 to 2.1%) of this slam-dunk non-cardiac group came back with an MI within 30 days.

Now, for a rational person who thinks that we’re spending altogether too much money and resources to capture every last potential cardiac event – that sounds pretty reasonable.  Home with follow-up.  The problem is, the non-invasive testing in basically the same sort of low-risk cohort, whether stress or CTA, the negative tests have 6+ month event-free periods.  So, the standard of care is unfortunately moving away from “no heart attack today!” to prognosticating distant events.

The other great thing about this article was their mini systematic review where they say there’s 115 of these prediction rules in the literature in the last fifteen years.  Clearly someone everyone wants, but also something we can’t get right….

http://www.ncbi.nlm.nih.gov/pubmed/21435709

The Cost-Effectiveness of Cardiac CTA

I was really hoping this would be a great article that convinced me that my hesitancy towards cardiac CTA is unfounded.  I feel, based on the literature, that we’re misusing cardiac CTA – or at least, the current generation of technology and reconstruction methods aren’t leading us in the right direction.  Angiography, whether radiographic or invasive, describes anatomy, and then we use the anatomy as our basis whether to attribute chest pain to cardiac causes or not.  Many situations, this works – the STEMI goes to the cath lab and the occlusion correlates with symptoms.  But, we’re trying to use CTA in our low-risk population to draw conclusions about the etiology of chest pain – and it’s much harder to say someone’s troponin-negative and EKG non-specific chest pain comes from a stenosis of a certain percentage.

The problem with their article is that they completely underestimate the number of false-positives cardiac CTA is generating.  There are several articles out there showing that the population considered for cardiac CTA is generally a population that just does great in follow-up, and that the number of negative follow-up studies generated after cardiac CTA – nuclear stress and invasive angiography – tend to far outnumber the number of positives.  They base their cost estimates on numbers that just don’t reflect reality, and I just can’t believe that cardiac CTA is a test that saves money and gives me better answers compared to functional cardiac testing.  If you wanted to use it as a screening tool for identifying a population that needs aggressive secondary-prevention of progressive atherosclerotic coronary disease, it would do great at that – but we know that plenty of ACS comes from ruptured plaque and hemodynamically insignificant disease, and someone who had a “negative” cardiac CTA that morning doesn’t preclude them from needing an enzymatic rule-out.

http://www.ncbi.nlm.nih.gov/pubmed/21427336

Patient Reported Symptoms in STEMI and NSTEMI

Here’s an article with a lot of great numbers to keep you from sleeping well at night.  It’s a prospective look at the symptoms patients present with when their eventual diagnosis is STEMI or NSTEMI.  6.4% of their STEMI patients and 5.6% of their NSTEMI patients didn’t complain of any chest symptoms (pain, pressure, etc.).  There’s a lot of arm pain, epigastric pain, shoulder pain, and then multiple anginal-equivalents on their list of symptoms, but it’s a great example showing that if you write off ACS in your patients without chest pain, you’re going to get burned – 1 in 16 STEMIs in their cohort.  Even better, only 45.1%/53.9% of their patients thought their symptoms were cardiac related, which probably means there’s a population of STEMIs just sitting at home figuring they’ll feel better in the morning….

http://www.ncbi.nlm.nih.gov/pubmed/21338424