Confusable diagnoses · PANCE / PANRE

Acute Pericarditis vs Myocarditis

Acute Pericarditis and Myocarditis are easy to mix up on the boards. Here's a side-by-side comparison — presentation, workup, imaging, and first-line treatment — drawn from our full outlines.

Acute Pericarditis vs Myocarditis at a glance

  • Acute Pericarditis: Inflammation of the pericardium — pleuritic chest pain improved by leaning forward, friction rub, diffuse ST elevation with PR depression.
  • Myocarditis: Inflammation of the myocardium, most often viral, presenting as new-onset HF, chest pain, or arrhythmia in a previously healthy patient.

Try two board-style questions on Acute Pericarditis vs Myocarditis

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Question 1CardiovascularEasy
A 32-year-old woman with systemic lupus erythematosus (SLE) develops pleuritic chest pain. An ECG shows diffuse saddle-shaped ST elevation with PR depression. Echocardiography reveals a small pericardial effusion without wall motion abnormalities. Which of the following is the most likely cardiac diagnosis?
  • APericarditis
  • BLibman-Sacks endocarditis
  • CMyocarditis
  • DAccelerated atherosclerosis
Reveal answer & full explanation
Correct answer: A — Pericarditis
  • APericarditis✓
  • BLibman-Sacks endocarditis
  • CMyocarditis
  • DAccelerated atherosclerosis

Why Pericarditis is correct

  • Pericarditis is the most common cardiac manifestation of SLE
  • Diffuse, saddle-shaped (concave-up) ST elevation with PR depression across multiple leads is the classic ECG signature of acute pericarditis, and the pleuritic chest pain and small pericardial effusion fit
  • The absence of wall motion abnormality argues against myocardial involvement

Why the others are wrong

  • Libman-Sacks endocarditis — sterile verrucous valvular vegetations (often mitral) linked to antiphospholipid antibodies; it does not produce diffuse ST elevation or PR depression (buzzword-matching the SLE–heart association)
  • Myocarditis — would be expected to cause wall motion abnormalities and troponin elevation rather than the diffuse ST/PR pattern; the normal wall motion here refutes it (confused-with-pericarditis)
  • Accelerated atherosclerosis — a chronic long-term cardiovascular risk in SLE, not an explanation for this acute pleuritic, diffusely distributed ECG presentation (anchoring on SLE's vascular risk)
Question 2CardiovascularMedium
A 24-year-old man presents with 3 days of pleuritic chest pain and dyspnea, two weeks after a flu-like illness with fever and sore throat. He has no cardiac risk factors. Troponin I is markedly elevated and ECG shows diffuse ST-segment changes. Coronary angiography reveals unobstructed coronary arteries, and cardiac MRI shows subepicardial late gadolinium enhancement with T2 edema. Endomyocardial biopsy shows a dense infiltrate of small mononuclear cells with focal myocyte dropout. Which of the following best explains the findings?
  • ACatecholamine-driven microvascular dysfunction
  • BCoronary vasospasm causing transient ischemia
  • CAntigen-driven immune-mediated myocyte injury
  • DEosinophilic hypersensitivity reaction to a drug
Reveal answer & full explanation
Correct answer: C — Antigen-driven immune-mediated myocyte injury
  • ACatecholamine-driven microvascular dysfunction
  • BCoronary vasospasm causing transient ischemia
  • CAntigen-driven immune-mediated myocyte injury✓
  • DEosinophilic hypersensitivity reaction to a drug

Why Antigen-driven immune-mediated myocyte injury is correct

  • This is viral (lymphocytic) myocarditis: a recent viral antigen triggers a multi-phase response of initial direct myocyte damage from viral replication followed by innate and adaptive immune activation, with infiltration of lymphocytes and macrophages that often produces maximal myocardial injury.
  • The biopsy finding of a dense small mononuclear (lymphocytic) infiltrate with focal myocyte dropout (Dallas criteria) and the subepicardial, non-coronary distribution of late gadolinium enhancement on MRI reflect this inflammatory, immune-mediated process rather than an ischemic one.

Why the others are wrong

  • Coronary vasospasm causing transient ischemia — vasospastic angina produces recurrent rest pain with transient ST elevation that resolves between episodes, and any resulting injury follows a coronary distribution; it does not generate subepicardial late gadolinium enhancement or a mononuclear myocardial infiltrate.
  • Catecholamine-driven microvascular dysfunction — the proposed mechanism of stress (Takotsubo) cardiomyopathy, which typically affects postmenopausal women after an emotional or physical stressor and shows transient apical ballooning, not a viral prodrome with biopsy-proven lymphocytic inflammation.
  • Eosinophilic hypersensitivity reaction to a drug — hypersensitivity myocarditis follows a new drug exposure and shows peripheral eosinophilia with an eosinophil-rich myocardial infiltrate, not the mononuclear infiltrate described here after a viral illness.

Cardiac MRI with Lake Louise criteria (edema plus late gadolinium enhancement) is the noninvasive diagnostic standard for myocarditis; endomyocardial biopsy is reserved for fulminant, refractory, or specific-treatment-changing cases.

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Side-by-side comparison

FeatureAcute PericarditisMyocarditis
At a glanceInflammation of the pericardium — pleuritic chest pain improved by leaning forward, friction rub, diffuse ST elevation with PR depression.Inflammation of the myocardium, most often viral, presenting as new-onset HF, chest pain, or arrhythmia in a previously healthy patient.
Classic presentationSharp, pleuritic, retrosternal or left precordial chest pain; Worse supine, better leaning forward; Radiation to trapezius ridge (highly specific — phrenic nerve); Low-grade fever, dyspnea, fatigue; Antecedent viral prodrome (URI, GI symptoms) common; Pericardial friction rub — three-component, scratchy, best at LLSB with patient…Young, previously healthy patient with new HF or chest pain after a recent flu-like illness, troponin elevation, and unobstructed coronaries on angiography.; Recent viral prodrome (URI, gastroenteritis) days to weeks prior; Chest pain (can mimic MI), dyspnea, palpitations; Acute decompensated heart failure: orthopnea, fatigue,…
Workup / key labsClassic 2015 ESC criteria (still the most widely taught): ≥2 of 4: (1) sharp pleuritic pain improved leaning forward, (2) pericardial friction rub, (3) new widespread ST elevation or PR depression, (4) new/worsening pericardial effusion. Supporting features: elevated CRP/ESR, evidence of pericardial inflammation on CT or CMR. The 2025…Troponin I or T (elevated, may be persistently elevated); BNP/NT-proBNP; CRP, ESR (often elevated); CBC with differential (eosinophilia suggests eosinophilic myocarditis or hypersensitivity); Viral PCR panel (limited yield; not routinely required for diagnosis); Targeted testing if suspected: Lyme serologies, HIV, ANA, rheumatoid…
Imaging12-lead ECG — diffuse concave ST elevation with PR segment depression (PR elevation in aVR is reciprocal — early sign); Echocardiography — assess for pericardial effusion and ventricular function (rule out tamponade and myocarditis); CXR — typically normal; cardiomegaly only with large effusion; Cardiac MRI — late gadolinium enhancement…12-lead ECG: sinus tachycardia, nonspecific ST/T changes, low voltage, conduction blocks, ventricular ectopy or VT; CXR: may show cardiomegaly and pulmonary edema; Transthoracic echo: global or regional LV dysfunction, wall thickening from edema, pericardial effusion; Cardiac MRI: late gadolinium enhancement (typically subepicardial,…
First-line treatmentNSAIDs — ibuprofen 600-800 mg PO TID × 1-2 weeks then taper, OR aspirin 750-1000 mg PO TID (preferred post-MI pericarditis); Colchicine 0.5 mg PO BID (0.5 mg daily if <70 kg) × 3 months — added to NSAID for FIRST episode reduces recurrence (COPE / ICAP trials); Proton pump inhibitor while on high-dose NSAIDs; Activity restriction until…Supportive care: hospitalization for telemetry monitoring; restrict competitive exercise for 3-6 months; avoid NSAIDs when LV dysfunction or HF is present (unlike pericarditis, they worsen HF and may increase myocardial injury); Guideline-directed medical therapy for HFrEF: ACEi/ARB or sacubitril/valsartan, evidence-based beta-blocker…

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