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A 45-year-old mildly overweight man recovering from an anterior wall myocardial infarction develops sharp, sudden-onset pain in the left side of his chest.  The pain is worse with coughing and improves when sitting up and leaning forward.  The patient came to the emergency department 3 days earlier with substernal chest pain and diaphoresis for 10 hours.  He underwent coronary angiography with stent placement to the left anterior descending artery.  The patient has had no dyspnea, palpitations, or extremity swelling since admission to the hospital.  His medical history is significant for diabetes mellitus type 2.  Blood pressure is 120/78 mm Hg, and pulse is 60/min.  There is no change in blood pressure on deep inspiration.  The patient seems mildly restless, especially in the supine position.  His breathing is fast and shallow.  The lungs are clear on auscultation.  ECG is shown in the exhibit.  Which of the following is the most likely diagnosis for this patient?

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Explanation:

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This patient most likely has peri-infarction pericarditis (PIP).  In contrast with postcardiac injury (Dressler) syndrome, which is an immune-mediated pericarditis that typically occurs several weeks following myocardial infarction (MI), PIP results from local inflammation and typically occurs <4 days following MI.  Patients usually experience pleuritic chest pain that improves with sitting up and often radiates posteriorly to the trapezius ridges (lower portions of the bilateral scapulae).  Cardiac auscultation should reveal a pericardial friction rub, and ECG commonly shows diffuse ST-segment elevation.  Pericardial effusion is often seen on echocardiography.

Patients with delayed coronary reperfusion following ST-elevation MI (eg, >3 hours from symptom onset) are at increased risk of developing PIP.  Treatment is usually supportive; anti-inflammatory agents (eg, nonsteroidal anti-inflammatory drugs, corticosteroids) are typically avoided due to impairment of collagen deposition and possible increased risk of post-MI mechanical complications (eg, ventricular wall rupture).

(Choice B)  Acute stent thrombosis leads to coronary reocclusion.  Nonpleuritic chest pain and localized (rather than diffuse) ST-segment elevation in the anterior precordial leads (corresponding to left anterior descending artery occlusion) would be expected.

(Choice C)  Aortic dissection presents with sudden onset of sharp, tearing chest pain radiating to the back.  Pleuritic chest pain is not typical.

(Choice D)  Hospital-acquired pneumonia typically presents with fever, dyspnea, pleuritic chest pain, and pulmonary infiltrates.  Diffuse ST elevation on ECG is not expected.

(Choices E and F)  Rupture of the interventricular septum leads to biventricular failure, and papillary muscle rupture leads to severe mitral valve regurgitation.  Both complications typically occur 3-5 days after MI and lead to cardiogenic shock.  Clear lungs and the absence of hypotension make either complication extremely unlikely.

(Choice G)  Patients with acute pulmonary embolism typically have dyspnea, pleuritic chest pain, and sinus tachycardia.  ECG may show nonspecific ST-segment and T-wave changes, but diffuse ST elevation is not typical.

(Choice H)  Ventricular aneurysm is a late complication (weeks to months) of MI.  ECG should reveal persistent localized ST-segment elevation and deep Q waves in the leads corresponding to the previous MI.

(Choice I)  Rupture of the left ventricular free wall can occur <2 weeks after MI and lead to pericardial tamponade (hemopericardium).  This patient's normal blood pressure and absence of pulsus paradoxus (decrease in systolic blood pressure >10 mm Hg with inspiration) make tamponade extremely unlikely.

Educational objective:
Patients with peri-infarction pericarditis typically have pleuritic chest pain, a pericardial friction rub, and diffuse ST-segment elevations on ECG <4 days following myocardial infarction.  Treatment is usually supportive.