ECG Cases 27 Pericarditis – Diagnosis of Exclusion

In this ECG Cases blog we present 9 patients who had widespread ST elevation on their ECG and explain our 3-step approach to the diagnose of pericarditis. Which of these patients with widespread ST elevation had pericarditis?

Written by Jesse McLaren; Peer Reviewed and edited by Anton Helman. November 2021

9 patients presented with chest pain and widespread ST elevation. Which had pericarditis?

Case 1: 50yo with 1 hour chest and left shoulder pain, normal vitals

Case 2: 50yo with 5 hours of epigastric burning. Serial ECGs:

Case 3: 55yo with one hour of chest pain. Normal vitals. Serial ECG:

Case 4: 35yo with one hour of chest pain. Normal vitals

Case 5: 75yo with one day pleuritic back pain radiating to the chest and right arm. Normal vitals

Case 6: 80yo with autoimmune disease on immunosuppressants, presenting with 4 days of pleuritic chest pain and fever. Normal vitals except temperature 38.2. Old the new ECG:

Case 7: 70yo history of diabetes, lupus and PE, with positional and pleuritic chest pain, normal vitals

Case 8: 50yo with pleuritic chest pain. Normal vitals

Case 9: 25yo with recurring chest pain, previously diagnosed and treated for pericarditis, presenting with non-pleuritic chest pain without viral prodrome. Normal vitals. Old ECGs from previous diagnoses of pericarditis, and new ECG.

Pericarditis: A diagnosis of exclusion

According to guidelines, the clinical diagnosis of pericarditis can be made with two of the following:

• History: chest pain, typically sharp and pleuritic, improved by sitting up and leaning forward
• Physical: pericardial friction rub
• ECG: widespread ST elevation or PR depression
• POCUS: pericardial effusion

Additional supporting findings include inflammatory markers (CRP, ESR, WBC) and pericardial inflammation on imaging (CT, CMR).[1] This definition can lead to the assumption that chest pain + widespread ST elevation = pericarditis. But in undifferentiated chest pain patients presenting to the emergency department, conditions that improve with NSAIDs (like chest wall pain, or most cases of pericarditis) should be low on our differential. Pericarditis is a retrospective diagnosis of exclusion.

STEP 1: Exclude life-threatening conditions

The first step is to exclude life-threatening conditions. Pulmonary embolism can produce pleuritic chest pain, aortic dissection can produce chest pain + pericardial effusion, and acute coronary occlusion can present with atypical pain [2], as well as widespread ST elevation—including wraparound or distal LAD occlusion causing antero-inferior ST elevation, or inferolateral Occlusion MI. ST elevation has a differential diagnosis (ELEVATIONS mnemonic), and widespread ST elevation is not specific for pericarditis. Other signs attributed to pericarditis are PR depression or TP downsloping (Spodick’s sign). But as a recent study found, these “were both statistically associated with pericarditis, but that either could be seen in STEMI.”[2] STEMI criteria do not reliably identify acute coronary occlusion and differentiate it from pericarditis, because many Occlusion MIs don’t meet STEMI criteria while many cases of pericarditis do. ST morphology does not differentiate either: while convex ST elevation excludes pericarditis, many occlusion MIs have initially concave elevation. The vector of ST elevation is more helpful: the diffuse inflammation of pericarditis causes ST elevation along the main vector of ventricular depolarization (II>III) whereas most inferior OMI are caused by RCA occlusion resulting in STE III>II. But STE II>III can also result from circumflex occlusion.

The most useful sign in identifying inferior Occlusion MI and excluding pericarditis is reciprocal ST depression in aVL: in pericarditis there should only be reciprocal ST depression in aVR (opposite II), whereas inferior OMI produces reciprocal ST depression in aVL. New primary ST depression in aVL (i.e not from LBBB/LVH/WPW or old MI), is 99% sensitive for inferior OMI (much greater than STEMI criteria) and 100% specific for excluding pericarditis.[4] So rather than anchoring on one finding to rule in pericarditis (eg widespread ST elevation, concave elevation, or PR depression), any abnormal finding should exclude it—including Q waves or loss of R waves, 5mm of ST elevation, convex ST segments, reciprocal change other than aVR, or abnormal T waves during ST elevation (as opposed to the T wave inversion that develops after ST segments normalize).[5]

STEP 2: Exclude complications of pericarditis

If life-threatening diagnoses have been excluded and pericarditis remains the main provisional diagnosis, the next step is to exclude complications. Guidelines recommend trop/CK and echo for all cases of pericarditis to assess for myocarditis and large pericardial effusions; coronary angiography for suspected myocarditis to exclude acute coronary occlusion; and searching for underlying causes in those with major risk factors (fever>38, subacute course, large pericardial effusion, cardiac tamponade, failure to respond to NSAIDS). Hospital admission is recommended for high-risk patients with major risk factors or minor risk factors (myocarditis, immunosuppression, trauma, and oral anticoagulants).[1]

STEP 3: Exclude whether ST elevation is a normal variant

If life-threatening causes have been excluded and complications of pericarditis have been excluded, the last step is excluding whether the ST elevation is simply a normal variant—and whether the diagnosis of pericarditis can be excluded altogether. This is to prevent patients with benign chest pain and early repolarization on ECG from getting labeled with pericarditis and unnecessarily treated with colchicine and high dose NSAIDs for weeks, and possibly steroids if their symptoms persist or recur. Early repolarization can have concave ST elevation in the inferolateral leads as well, but it is proportional to tall R waves and tall T waves, whereas in pericarditis the ST elevation is disproportionate: a ST/T ratio > 0.25 in the lateral leads I/V5-6 favours pericarditis whereas ST/T<0.25 favours early repolarization.[5]

Back to the cases

Case 1: wraparound LAD occlusion

• Heart rate/rhythm: normal sinus rhythm
• Electrical conduction: normal conduction
• Axis: normal axis
• R-wave: normal R wave progression
• Tall/small voltages: normal voltage
• ST/T waves: concave ST elevation V2-6 (with terminal QRS distortion in V3) and inferiorly, with reciprocal STD in aVL

Impression: there is widespread concave ST elevation with STE II>III. But the patient is a 50yo with acute chest pain, and the ECG has massive (5mm) anterior ST elevation and reciprocal ST depression in aVL. EMS took the patient directly to the cath lab: 99% mid LAD occlusion, first trop I was 26ng/L (upper limit of normal), and peak was 7,000.

Discharge ECG had preserved R waves and reperfusion T wave inversion:

Case 2: mid LAD occlusion

• H: from normal sinus to sinus tach
• E: normal conduction
• A: normal axis
• R: late R wave progression
• T: normal voltages
• S: anterior ST elevation V1-5 which is becoming convex

Impression: the second ECG has some PR depression in II. But the patient is a 50yo with epigastric pain, and the ECG has anterior ST elevation becoming convex, with hyperacute T waves. On POCUS there was a corresponding anterior regional wall motion abnormality, so cath lab activated, with ECG-to-Activation time of 40 minutes. 100% mid LAD occlusion, first trop I was 3,000ng/L (normal <26) and peak 50,000.

Case 3: circumflex occlusion

• H: from normal sinus to borderline sinus bradycardia
• E: normal conduction
• A: normal axis
• R: normal R wave progression
• T: normal voltages
• S: borderline inferolateral ST elevation (II>III) with hyperacute T waves, development of Q wave and convex ST segment in III, dynamic reciprocal change in aVL and ST depression in V2 (first ECG has high placement of V2, which has been corrected in second ECG)

Impression: there’s widespread concave ST elevation with II>III. But the patient is a 55yo with acute chest pain, and the ECG includes acute Q waves, convex ST segments, reciprocal change in aVL and ST depression in V2—all of which exclude pericarditis and confirm infero-postero-lateral OMI. Cath lab activated, with an ECG-to-Activation time of 13 minutes: 99% circumflex occlusion, first Trop I was negative and peak 7,000.

Disharge ECG had persisting Q wave in III with small reperfusion T wave inversion, and tall T waves anteriorly from posterior T wave inversion:

Case 4: myocarditis diagnosed after angiogram ruled out inferoposterolateral OMI

• H: normal sinus
• E: normal conduction
• A: normal axis
• R: normal R wave progression
• T: normal voltages
• S: inferolateral concave STE, II>III, without reciprocal STD in aVL and with ST/T>25% in V6. But there’s also ST depression V2

Impression: r/o inferoposterolateral OMI. Treated with aspirin and ticagrelor and stat cardiology consult. When first troponin I returned at 2,000ng/L (normal <26) the cath lab was activated: normal coronaries but trop peaked at 8,000 and echo revealed mild hypokinesis to basal and inferolateral walls, corresponding to ECG changes. Diagnosed with myocarditis and treated with NSAIDS and colchicine.

Discharge ECG had resolution of ST changes and development of T wave inversion:

Case 5: pericarditis secondary to aortic dissection

• H: normal sinus rhythm
• E: normal conduction
• A: physiological left axis
• R: normal R wave progression
• T: normal voltages
• S: inferolateral concave ST elevation, II>III, PR depression, ST/T>25% in lateral leads

Impression: ECG compatible with pericarditis but patient is a 75 year old with acute chest/back pain. Treated with aspirin, serial troponin rose from 30ng/L (normal<26) to 60, leading to consideration of myocarditis. But back pain increased, and CT chest revealed type A aortic dissection with small pericardial effusion.

Case 6: pericarditis secondary to infective endocarditis

• H: normal sinus rhythm
• E: normal conduction
• A: normal axis
• R: early R wave progression
• T: tall voltages
• S: inferolateral concave ST elevation with more prominent Q waves, STE II>III, reciprocal STD in aVR only

Impression: history suggests infectious cause and ECG compatible with pericarditis except for Q waves, raising concern for myocarditis vs acute coronary occlusion. Cath lab was activated: normal coronaries and negative troponin, so patient diagnosed with acute pericarditis and discharged on colchicine. But immunosuppression and fever are risk factors for complications. Patient returned a week later with ongoing symptoms, ECG still showing inferolateral concave ST elevation II>III, but now troponin 600:

Admitted for myocarditis but echo found mitral valve vegetation in addition to pericardial effusion, and blood cultures were positive. Diagnosed with infective endocarditis and treated with IV antibiotics. Discharge ECG revealed progression of pericarditis changes, with resolution of inferolateral ST elevation and development of T wave inversion.

Case 7: pericarditis diagnosed after other causes and complications excluded

• H: normal sinus rhythm
• E: normal conduction
• A: normal axis
• R: early R wave progression
• T: normal voltages
• S: diffuse concave ST elevation, STE II>III with no reciprocal change in aVL, TP downsloping and PR depression, with reciprocal ST depression and PR elevation in aVR

Impression: ECG compatible with pericarditis, but in a patient with risk factors for other conditions and pericarditis complications. Patient treated with aspirin and referred to cardiology. Serial troponins were negative, CT chest was negative for PE or dissection, echo was normal, CRP was elevated, infectious workup was negative. Patient diagnosed with pericarditis.

Case 8: pericarditis diagnosed after other causes and complications excluded

• H: normal sinus rhythm
• E: normal conduction
• A: normal axis
• R: normal R wave progression
• T: normal voltage
• S: mild inferolateral concave ST elevation without reciprocal change in aVL and with reciprocal STD in aVR only; no hyperacute T waves and high ST/T ratio

Impression: ECG compatible with pericarditis but in 50yo with pleuritic chest pain. Serial troponins were negative, D-dimer was positive but CT chest was negative for PE. Echo was normal, CRP was elevated, and patient was diagnosed with acute pericarditis.

Case 9: early repolarization

• H: normal sinus rhythm
• E: normal conduction
• A: borderline right axis
• R: normal R wave progression
• T: normal voltages
• S: inferolateral concave ST elevation, proportional to tall R wave, associated with J wave and small ST/T ratio, similar to previous. The negative T wave in aVL is concordant to the QRS complex, and the minimal ST depression is reciprocal to the normal variant ST elevation

Impression: early repolarization. Patient repeatedly diagnosed with pericarditis and treated for months with colchicine, nsaids and steroids, despite atypical history, no effusion on echo and inflammatory markers repeatedly negative. Eventually diagnosed with benign chest pain, removing the label of “pericarditis.”

Take home points for pericarditis – a diagnosis of exclusion

Pericarditis is a diagnosis of exclusion requiring 3 steps

1. Exclude more serious causes of chest pain, eg wraparound LAD occlusion, inferior OMI
2. Exclude complications of pericarditis, eg myocarditis, large pericardial effusion
3. Exclude normal variant ST elevation presenting with benign chest pain

References for ECG Cases 27 Acute Pericarditis – A Diagnosis of Exclusion

1. Adler Y, Charron P, Imazio M, et al. 2015 ESC guidelines for the diagnosis and management of pericardial diseases: the Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC). Eur Heart J 2015 Nov 7;36(42):2921-2964.
2. El-Menyar A, Zubaid M, Sulaiman K, et al. Atypical presentation of acute coronary syndrome: a significant independent predictor of in-hospital mortality. J of Cardiol 2011 Mar;57(2): 165-171.
3. Witting MD, Hu KM, Westreich AA, et al. Evaluation of Spodick’s sign and other electrocardiographic findings as indicators of STEMI and pericarditis. J of Emerg Med 2020;58(4):562-569.
4. Bischof JE, Worrall C, Thompson P, et al. ST depression in lead aVL differentiates inferior ST-elevation myocardial infarction from pericarditis. Am J of Emerg Med 2016;34:149-154.
5. Mattu A, Tabas JA, Brady WJ, eds. Electrocardiography in Emergency, Acute, and Critical Care, second edition. American College of Emergency Physicians, 2019, p 141, 179.
6. Bhardwaj R, Berzingi C, Miller C, et al. Differential diagnosis of acute pericarditis from normal variant early repolarization and left ventricular hypertrophy with early repolarization: an electrocardiographic study. Am J of Med Sci 2013 Jan;345(1): 28-32.