ECG Blog #365 — A 30yo with Pericarditis ...

The ECG in Figure-1 was obtained from a previously healthy 30-ish year old man — who presented to medical attention for vasovagal syncope. Based on this initial ECG — the patient was transferred to a PCI-capable center: 

• Do YOU agree with the need for transfer?

Hospital evaluation for this patient was negative for an acute coronary syndrome (ie, CT coronary angiogram was normal — troponin was not elevated — and Echo was negative, with no sign of pericardial effusion). The patient was discharged with a diagnosis of acute pericarditis — and treated with a full course of colchicine and ibuprofen.

• Do YOU agree with the discharge diagnosis and treatment prescribed?

Figure-1: The initial ECG in today's case. Based on this ECG — the patient was transferred to a PCI-capable center. The ultimate discharge diagnosis was acute pericarditis. (To improve visualization — I've digitized the original ECG using PMcardio).

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Editorial NOTE: Today's case was sent to me by Dr. Magnus Nossen from Norway — where the Cabrera Format for ECG recording is used. Given how the internet has changed the world in recent years — virtually all clinicians will periodically encounter different recording formats such as this one. The insert in the lower right portion of Figure-1 highlights the difference in limb lead sequencing with the Cabrera Format:

• Instead of beginning the limb lead display with standard lead I — the Cabrera format begins with the highest lateral lead ( = lead aVL, corresponding to an electrical viewpoint perspective of -30 degrees).
• The right augmented lead is displayed with reversed polarity = lead -aVR (corresponding to an electrical viewpoint perspective of +30 degrees).
• As suggested by the Axis Insert in Figure-1 — the Cabrera Format offers a more logical display of limb lead sequencing, in that there is a gradual progression of equally spaced (at increments of 30 degrees) limb leads, beginning with lead aVL (at -30 degrees) — and continuing until the most rightward frontal plane lead = lead III (at +120 degrees).
• In contrast, the standard U.S. format is not sequential — it views the right augmented lead from the remote perspective of the right shoulder — and it uses unequal spacing between neighboring leads.
• NOTE: The chest leads are unchanged with the Cabrera format. 
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• See ECG Blog #215 — for more on the Cabrera format.

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MY Thoughts on the ECG in Figure-1:

It's important to remember that the ECG in Figure-1 was obtained from a previously healthy 30-ish year old man who presented with an episode of vasovagal syncope — but there is no mention of chest pain in the history!

• Even before looking at today's ECG — the above clinical scenario suggests a low-prevalence likelihood for an acute cardiac event.

I interpreted the ECG in Figure-1 as follows:

• The rhythm is sinus at ~65/minute. All intervals (PR, QRS, QTc) are normal. The frontal plane axis is normal at +75 degrees. 
• There is no chamber enlargement. Although QRS amplitude in lateral chest leads V4 and V5 is generous (with overlap of the S in V3 with the R in V4) — in view of this patient's young age (ie, ~30 years old) — criteria for LVH are not satisfied. 

Regarding Q-R-S-T Changes:

• There are small, narrow Q waves in the inferior and lateral chest leads. These are consistent with normal septal q waves (ie, Normal septal q waves may be seen in the inferior leads when the frontal plane axis is fairly vertical — as it is in ECG #1).
• R wave progression is normal — with transition (where the R wave becomes taller than the S wave is deep) occurring normally between leads V3-to-V4.

Regarding ST-T wave Changes: — ST elevation is present in multiple leads (ie, in leads I-thru-III; and V3-thru-V6). That said — a number of features strongly suggest that this ST segment elevation looks like a benign repolarization variant. These benign-looking features include: 

• ST elevation is gently and smoothly upsloping (ie, "smiley" configuration) in all leads in which it is present. 
• The ST elevation is present in 9/12 leads — such that there is no localization (as is usually present with acute infarction). In particular, in 7 of these leads (ie, in leads -aVR-thru-lead III — and in leads V4-6) — the shape of the ST elevation and peaked T waves is virtually identical (whereas that is rarely the case with acute infarction).
• To emphasize — the inverted T wave in lead aVL of ECG #1 "looks" benign — since the T wave vector often follows close behind the QRS vector (ie, the negative T wave in lead aVL "follows" the negative QRS in this lead) — AND — the size of this inverted T wave is small and not disproportionate to the size of the S wave in this lead. When the frontal plane axis is vertical (as it is in Figure-1) — it is common to see a predominantly negative QRS with shallow T wave inversion in lead aVL.
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• The typical J-point notching that is characteristic of early repolarization is prominently present in lead V4.
• There is no reciprocal ST-T wave depression, as is commonly seen with acute infarction (ie, The inverted T waves in leads V1 and V2 are likely to either be positional or a normal variant).
• The QTc is not prolonged (whereas with acute OMI — the QTc is more likely to be longer).
• R wave progression is entirely normal — and if anything, QRS amplitude is generous in the mid-chest leads (whereas with acute anterior OMI — there is often reduction, if not loss of the initial R wave in anterior leads).
• Finally — Taking a step "back" to look at the tracing in Figure-1 as a "whole" — ST-T wave morphology just "looks" benign!

BOTTOM Line: Need for Transfer to a PCI-capable Center?

Considering that the history in today’s case is of a previously healthy 30-ish year old man with an episode of vasovagal syncope, but no chest pain (ie, a “low prevalence likelihood” for acute Occlusion MI) — the above description of ECG findings is my best attempt at explaining why my brain immediately recognized the pattern in ECG #1 as a non-OMI repolarization variant. 

• I saw no need for transfer of the patient to a PCI-capable facility on the basis of this history and the initial ECG.
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• For more on “My Take” regarding the ECG entity of Repolarization Variants — Please check out My Comment at the bottom of the page in the May 23, 2022 post in Dr. Smith’s ECG Blog.

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Factors Against a Diagnosis of Acute Pericarditis:

As stated above — this patient was discharged from the hospital with a diagnosis of acute pericarditis. As a result he was treated with potent medications (that each have potential for side effects) — and told not to work for 4 weeks — as well as being given a medical diagnosis that will stay on his chart. From the information provided — I would not make the diagnosis of acute pericarditis.

• In my experience — acute pericarditis is greatly overdiagnosed! There is a tendency once acute MI is ruled out, to attribute chest pain in a patient with ST elevation to acute pericarditis. Follow-up of many (most) of these patients eventually reveals that they did not have acute pericarditis. To quote Dr. Stephen Smith, "You diagnose pericarditis at your peril" — meaning, that most patients seen in an ED who are given this diagnosis do not have pericarditis.
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• The clinical reality is — Diagnosis of acute pericarditis in an acute setting is often difficult. Inflammatory markers tend to be nonspecific. Assessment of the history for chest pain is subjective — and symptoms are not always pleuritic and positional in nature. Many patients with acute viral pericarditis do not have Echo abnormalitiy (ie, pericardial effusion is often not present). Finally — ECGs in the acute setting are often misinterpreted. (See the Audio Pearl — and Figures 4-thru-8 in the ADDENDUM below for more on the ECG and clinical diagnosis of acute Pericarditis).
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• Cardiac MRI has been increasingly used to assist in diagnosis — although this modality is not always available in the acute setting (Aldweib et al — Curr Cardiol Rev 14(3):200-212, 2018).

PEARL #1: In making the diagnosis — It's important to consider the clinical setting (ie, 80-85% of acute pericarditis in the developed world is idiopathic from presumed acute viral infection). In the "right clinical setting", the one finding that is diagnostic of acute pericarditis — is a pericardial friction rub:

• In my experience over years of consulting on countless internet cases in which the diagnosis of acute pericarditis was put forth — in the overwhelming majority of these cases, no mention of ever having listened for a pericardial friction rub was either made on the chart or included in oral presentation. In my opinion — IF there is no specific mention that "a rub was present (or absent)" — this should be taken as indication that no rub was listened for. And, since short of MRI — a rub is essentially the only clinical finding that may be definitive — Not to carefully listen for a pericardial friction rub is to overlook the best possibility for making the diagnosis (See material in the ADDENDUM below).

Acute Pericarditis: What To Look For on ECG

Distinction between acute Pericarditis vs acute MI vs a Repolarization variant can be challenging! The characteristic ECG finding of acute pericarditis is diffuse ST elevation. While ST elevation with acute MI tends to “localize” (ie, to 1 or more ECG areas — with reciprocal ST depression elsewhere) — the ST elevation with repolarization variants may at times resemble pericarditis when ST elevation is more generalized. That said — consider the following:

• PEARL #2: The History is important. Knowing that your patient was previously healthy, but developed a recent viral infection — and now has distinctly pleuritic and positional chest pain (ie, worse on lying down — and improved on sitting up and leaning forward, so as to “relieve stretch” of the pericardium) — at least increases the likelihood that acute pericarditis might be present. Hearing a “walking on snow” pericardial friction rub in such a patient could confirm your diagnosis, even before you look at the ECG.
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• Regarding Today's CASE: This previously healthy 30-ish year old man presented with syncope — without mention of recent viral infection; pleuritic or positional chest pain; or of the clinician having carefully listened to the chest for a pericardial friction rub. Thus, the clinical setting in today’s case is not really suggestive of acute pericarditis.

As noted earlier — the ECG in Figure-1 does show ST elevation in 9/12 leads. That said — the distribution and nature of this ST elevation is a bit atypical for acute pericarditis (See ADDENDUM below for details):

• PEARL #3: With acute pericarditis — the 3 leads that do not typically show ST elevation are the “right-sided” leads (ie, leads III, aVR and V1). However, in Figure-1 — it is lead aVL instead of lead III that shows T wave inversion. (NOTE: Because today’s ECG is recorded with the Cabrera format — the negative aVR lead that shows ST elevation would correspond to ST depression and T wave inversion in a positive aVR lead).
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• PEARL #4: With acute pericarditis —  the shape of the ST-T wave in lead II tends to look much more like the ST-T wave shape in lead I (instead of like ST-T wave shape in lead III — as is seen in Figure-1).
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• PEARL #5: The RATIO of the amount of ST elevation to T wave amplitude in lead V6 should be less than 0.25 (ie, height of the ST elevation, as measured from the end of the PR segment to the J-point — should be less than 1/4 of the height of the T wave in lead V6). I illustrate HOW this RATIO is arrived at in Figure-2, which I have adapted from the 3/10/21 post in Life-In-The-Fast-Lane. Applying this measurement technique in Figure-3 to today’s tracing — the ST/T Wave Ratio = 0.20. This is less than the 0.25 ratio cutoff point — and therefore not suggestive of acute pericarditis.
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• PEARL #6: There is virtually no PR depression at all in ECG #1. While significant PR depression is not a specific ECG finding with acute pericarditis — the lack of any PR segment deviation at all is a factor against the likelihood of acute pericarditis.

Figure-2: Illustration of how the ST segment to T wave ratio is calculated — adapted from Life-In-The-Fast-Lane (See text).

Figure-3: Calculation of the ST/T wave ratio in lead V6 from today's case. The ratio is 0.20 — which is not suggestive of pericarditis.

Putting It All Together:

To Emphasize — Nothing is perfect. There are always exceptions to clinical generalities (ie, A patient with baseline ST-T wave repolarization changes may on top of this, develop a case of acute pericarditis). That said — taking all factors from today’s case into account, my thoughts are the following:

• The clinical presentation of this previously healthy 30-ish year old man does not suggest a likelihood of either acute OMI or acute pericarditis.
• The initial ECG looks like a benign repolarization variant. Transfer to a PCI-capable Center seems unnecessary.
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• CASE Follow-Up: Serial troponins from today's patient were negative. Echo was completely normal, and without pericardial effusion. CT Coronary Angiogram showed no sign of underlying coronary disease. In the absence of a history of positional and/or pleuritic chest pain — and in the absence of a pericardial friction rub — evidence in support of a diagnosis of acute pericarditis is lacking. The patient was seen in follow-up and told that his initial diagnosis was mistaken. He gladly returned to work the next day. 

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Acknowledgment: My appreciation to Magnus Nossen (from Fredrikstad, Norway) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation
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• ECG Blog #215 — Reviews the Cabrera Format (and explores potential advantages of this more logical anatomical sequencing).
• ECG Blog #114 — Reviews another case using the Cabrera format.
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• ECG Blog #208 — Reviews the ECG Diagnosis of Acute Pericarditis.
• My Comment (at the bottom of the page in the December, 13, 2019 post in Dr. Smith's ECG Blog) — regarding potential use with pericarditis of the ST/T Wave Ratio in Lead V6.
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• My Comment (at the bottom of the page in the May 23, 2022 post in Dr. Smith's ECG Blog) — regarding Repolarization Variant Patterns.
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• ECG Blog #193 — for review of the concept of “OMI” ( = Occlusion-based Myocardial Infarction) — and why this term should replaced the outdated STEMI paradigm. 
• ECG Blog #337 and ECG Blog #294 — relevant related Blog posts on the importance of the OMI paradigm (in preference to the outdated STEMI paradigm).

 

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ADDENDUM (2/24/2023):

• The Audio Pearl below reviews the Cabrera Lead Format ...

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ECG Media PEARL #32 (7:30 minutes Audio) — reviews the Cabrera ECG Format — and doing ECGs at a recording speed of 50 mm/second.

 

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ECG Media PEARL #25 (9:50 minutes Audio) — Pearls & Pitfalls regarding the ECG diagnosis of Acute Pericarditis.

In the following 5 Figures — I post written summary from my ECG-2014-ePub on the ECG diagnosis of Acute Pericarditis.

• CLICK HERE — for a PDF of this 9-page file on Pericarditis that appears in Figures-4-thru-8.
• An additional criterion that has sometimes been cited as helpful for making the diagnosis of acute Pericarditis — is the ST/T Wave Ratio in Lead V6 (Please see My Comment at the BOTTOM of the page in the December 13, 2019 post of Dr. Smith's ECG Blog).

Figure-4: How to make the diagnosis of acute Pericarditis (ie, use of the History and Physical Exam).

Figure-5: ECG findings (4 Stages of acute pericarditis — with attention on diagnostic Stage I). How helpful is PR depression?

 

Figure-6: PR depression (Continued). Spodick’s sign. Acute MI vs Pericarditis vs Repolarization variants?

 

Figure-7: Acute MI vs Pericarditis. ECG findings with acute Myocarditis. Pericarditis vs Early Repolarization?

 

Figure-8: Pericarditis vs Early Repolarization? (Continued).