It is my opinion that the medical discovery of pericarditis as a disease entity has actually caused overall net harm to human beings. I see and review so many cases in which the notion of “pericarditis” leads to patient harm that it has become a four-letter diagnosis to me. With the exception of extremely rare cases of significant pericardial effusions made hemorrhagic by thrombolytics (only 2 cases witnessed in an entire career by one of the world's leading experts who reviews thousands of cases around the world), almost no one has any significant complication of uncomplicated pericarditis (unlike myocarditis, complicated pericarditis with significant pericardial effusions, etc.), and whatever small symptomatic benefit true pericarditis patients receive from NSAIDs and/or colchicine is completely overshadowed by the harms of erroneously diagnosing pericarditis.

Pericarditis is almost a wastebasket diagnosis of exclusion, barely more important than costochondritis (and treated in basically the same way). If I were pericarditis, my only reason to exist would be to trick emergency physicians and cardiologists into missing Occlusion MIs and other real pathologic processes. If you correctly diagnose 99 patients with pericarditis and misdiagnose 1 Occlusion MI as pericarditis, you have failed your goal of protecting patients from emergencies. The harm of missing a single Occlusion MI far outweighs the harms of missing pericarditis.

The simplest solution for Emergency Medicine: Just say no to diagnosing uncomplicated pericarditis in the ED.

I remember what it was like before I learned this the hard way. I remember how fun and interesting it was as a medical student to suggest that someone might have pericarditis. I remember being fascinated by finding PR depression. I remember learning this fascination from physicians of all levels of experience who were somehow visibly happier about their job after diagnosing pericarditis. It's difficult to understand why this diagnosis is so tempting to make.

In my experience, the harms of pericarditis come in two major phenotypes:

1. A patient with Occlusion MI (and more rarely, other important diagnoses such as PE, dissection, etc.) is misdiagnosed as having “pericarditis” as the reason for their chest pain and ECG abnormalities.
2. A patient with a baseline ECG with normal variant STE but without any dangerous pathology is misdiagnosed as having pericarditis, thereby preventing the physicians from learning that the ECG was simply the baseline normal variant, and labeling the patient with a history of “pericarditis”, such that future visits are more likely to be considered also due to pericarditis, leading to unnecessary pericarditis treatment and premature diagnostic closure each time the patient presents with any complaint of the chest or abdomen.

Here are some examples of Occlusion MI misdiagnosed as pericarditis:

• Watch what happens when “pericarditis” and morphine cloud your judgment
• You Diagnose Pericarditis at your Peril (at the Patient's Peril!)
• Is it MI or pericarditis?
• Inferolateral ST elevation might be pericarditis, but not with Reciprocal ST depression in aVL

The inspiration for writing this post, however, was a recent case I witnessed highlighting the second phenotype: a patient who had normal variant STE, who was misdiagnosed as pericarditis despite no actual pathology. I have seen this countless times now, at every institution I have been so far. It always seems to happen the same way.

Here's the formula:

1) Patient presents complaining of chest pain, who happens to have a baseline ECG that looks scary in some way to providers who do not have ECG interpretation skill beyond that which our current paradigm requires (the ECG usually shows early repolarization a.k.a. baseline variant ST elevation).

2) The providers see chest pain plus abnormal ECG (usually meeting STEMI criteria), and activate the cath lab (sometimes they know it is a false positive but feel they are beholden to the paradigm, other times they are truly convinced it is pathological).

3) The cath shows normal coronaries, or at least no culprit. Troponins are all negative.

4) The physicians now struggle to reconcile the fact that the ECG looks scary to them, and the patient received false positive emergent cath lab activation (something that they consider embarrassing to be done for a “baseline” ECG), therefore the ECG is not the patient's baseline, so they must find a reason to both explain the patients symptoms and maintain their belief that the ECG is truly pathologic like their guidelines and their training have taught them.

5) The description of the patients symptoms in the chart suddenly changes. Pain that was exertional is now suddenly pleuritic. Pain that was once documented as dull and pressure-like is now sharp and positional, better when sitting up. Sick contacts with low grade undocumented fevers who were not mentioned earlier are suddenly swarming around the patient in the days leading up to presentation. Sometimes even phantom friction rubs are auscultated on day 2 in the most egregious scenarios.

6) Now that the history and ECG “abnormalities” have aligned, the patient is diagnosed with pericarditis. Ibuprofen and colchicine are given, and the patient's pain universally improves. The patient is told they had “pericarditis,” and that they are at risk for getting it again someday.

7) The patient has their next episode of non-cardiac chest pain for whatever reason, anytime later in life. They present to the ED, this time with “a history of pericarditis”. Of course, this would make ACS, PE, and dissection less likely because this patient has a history of pericarditis, so no need to look for those.

8) Back to step #1 and repeat indefinitely. After the third iteration or so, start calling it “chronic pericarditis” and consider adding biologic anti-inflammatory agents or chronic steroids, etc.

Let's see an example case play out.

Step #1

A middle aged male with a history of single-vessel CAD (1 stent in the LAD years ago) presented to Janus General complaining of chest pain. I was in the room during the HPI, and I can attest to the fact that the patient described the chest pain as intermittent exertional chest discomfort lasting 5-20 minutes, but it was also worse with inspiration when it was present. He had no pain at the time of evaluation. These episodes had been coming off and on for two weeks, and the day of presentation he had an episode while doing some light yard work. His vitals and physical exam were normal. Pain and other anginal equivalents were completely absent at the time of evaluation.

Here is his triage ECG:

This ECG shows sinus rhythm with a normal QRS and normal variant STE in II, III, aVF, and V4-V6. The QRS in lead aVL is predominantly negative, and thus the T-wave would already be expected to be negative in this lead, as well as the obligatory reciprocal minimal STD. This is an ECG that contains no evidence of acute ischemia to experienced ECG interpreters.

However, it meets STEMI criteria, as there is 1mm STE in II, III, and aVF. Because of our current guidelines, it is appropriate to consult cardiology for emergent cath for a patient with known CAD presenting with exertional chest pain and an ECG that meets STEMI criteria.

Let's compare to a baseline. He had many prior ECGs on file, none of which were during acute chest pain as far as I could tell (and none of the following were during his visit when he received a stent).

Baseline 1

Baseline 2

Baseline 3

Some of these prior ECGs show STE in the inferior and lateral leads, some show a negative T-wave in lead III, etc. Beginners respond appropriately with the concern for a “dynamic change” or a “change from baseline” when looking at the current presentation ECG, but these are all simply normal variant ECGs. Patients with early repolarization have variability in repeat ECGs over time and with different lead placement, according to our experience and several longitudinal studies [1,2]. With experience these changes are all just expected shades of normal variants. Just like we propagate the simplified lie that STEMI vs. NSTEMI is how we separate full occlusions from partial occlusions, we also like to tell ourselves that a baseline ECG should be THE BASELINE, and should never have any change in any aspect, otherwise that equals a “dynamic change” and therefore has to be pathologic (otherwise we would have to admit that baseline ECGs are dynamic and then learn to differentiate normal variants form abnormal variants). Rather than challenging the current paradigm of ECG interpretation, we can simply say that the patient must have had pericarditis.

Step #2

The providers recognized that the patient was now asymptomatic, and that the ECG was unlikely to represent true ischemia. However, they were faced with a patient with known CAD with exertional chest pain and an ECG that technically meets formal STEMI criteria, so they very appropriately called the interventionalist to review the case with them immediately. The interventionalists focused on the STE and the patient's history of CAD, and activated the cath lab.

Step #3

The cath revealed no culprit lesion:

Left main: normal

LAD: proximal 10% stenosis at site of prior stent

LCX: normal

RCA: normal

Three serial troponins were negative. Echocardiogram was completely normal, without wall motion abnormalities, LVH, or effusion. No more serial ECGs were recorded.

Steps #4-6

Watch as the HPI transforms before your eyes.

Pre-cath cardiology HPI:

“…male with a pmhx of CAD s/p LAD stent, HLD, who presents with 2 weeks of decreased exercise tolerance and dyspnea with exertion which has progressed. The patient was doing yard work when he felt acute onset chest discomfort, dyspnea, and the general sensation that there was something wrong.”

Post-cath cardiology HPI the next day:

“…presents after 2 weeks of pleuritic chest pain”

“etiology of pain likely pericarditis given the classic symptoms (sharp pain, worse with inspiration, better while leaning forward)”

“improved after receiving ibuprofen and colchicine, will continue ibuprofen for 1-2 weeks and colchicine for 3 months”

A formal diagnosis of pericarditis is now in the chart, despite not meeting the “formal diagnosis” (typically the diagnosis is said to require at least two of: typical chest pain, pericardial friction rub, typical electrocardiographic progression, and pericardial effusion)[3]. This patient actually had zero of these four criteria (using the original HPI).

Learning Points:

The major mechanism of harm of pericarditis usually starts in the mind of the practitioner rather than the pericardium of the patient.

Use our carefully collected cases of pericarditis and OMIs misdiagnosed as pericarditis to learn how to think about pericarditis in the ED, and how to distinguish them with the help of the ECG.

You diagnose pericarditis at the peril of yourself and your patient.

References:

1. Kambara et a. Long-term evaluation of early repolarization syndrome (normal variant RS-T segment elevation). American Journal of Cardiology 1976;38(2):157-61.
2. Mehta et al. Early repolarization on the scalar electrocardiogram. American Journal of the Medical Sciences 1995;309(6):305-11.
3. LeWinter. Acute pericarditis. New England Journal of Medicine 2014;371(25):2410-6.

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Pendell Meyers

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