A 65-year-old man is admitted to the hospital with an acute ST-segment elevation myocardial infarction. The patient undergoes coronary angiography with stent placement in the left circumflex artery, and he is started on therapy with a beta blocker and antiplatelet agents. On day 3 of hospitalization he experiences chest pain. The pain, described as sharp and radiating to his neck and shoulders, is exacerbated by coughing and swallowing. He has no shortness of breath, lightheadedness, or abdominal pain. Temperature is 37.5 C (99.5 F), blood pressure is 130/80 mm Hg, pulse is 90/min and regular, and respirations are 20/min. The lungs are clear on auscultation. There is no peripheral edema. Which of the following is the most likely cause of this patient's chest pain?
Acute pericarditis | |
Etiology |
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Clinical features |
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SLE = systemic lupus erythematosus. | |
The sharp and pleuritic nature of this patient's new chest pain suggests pericardial involvement. The exacerbation with swallowing indicates that the posterior pericardium may be involved, and the radiation into the neck suggests involvement of the inferior pericardium, which is adjacent to phrenic nerve afferents supplying the diaphragm. The patient's low-grade fever indicates that this is an inflammatory process.
A fibrinous or serofibrinous pericarditis, known as peri-infarction pericarditis (PIP), develops in about 10%-20% of patients between 2 and 4 days following a transmural myocardial infarction (MI). This pericarditis is a reaction to necrosis of the myocardium near the epicardial surface; delayed treatment presentation increases the risk of PIP due to higher levels of necrosis. Inflammation of the visceral and parietal pericardium is usually localized to the areas overlying the necrotic myocardial segment. The condition is generally short-lived and resolves with several days of supportive care; sometimes therapy with high-dose aspirin is needed.
(Choice A) Dressler syndrome (postcardiac injury syndrome) is an autoimmune-mediated pericarditis that is likely provoked by antigens exposed or created by infarction and necrosis of the cardiac muscle. It is less common and has later onset than PIP, typically occurring a week to a few months after an MI. The pericardium is often diffusely affected in Dressler syndrome.
(Choice B) Viral pericarditis usually follows an antecedent upper respiratory infection. However, a viral cause for this patient's pericarditis is less likely than PIP as a direct complication of his transmural infarction.
(Choices D and E) Recurrent thrombosis of the recently stented vessel or thrombosis of another coronary vessel would be expected to cause similar pain to the patient's original, anginal type of pain. The pain of myocardial ischemia is not typically sharp or pleuritic, but rather constant, substernal, and "crushing."
Educational objective:
In contrast to angina, the chest pain of pericarditis is sharp and pleuritic and may be exacerbated by swallowing or coughing. Peri-infarction pericarditis (PIP) occurs between 2 and 4 days following a transmural myocardial infarction (MI). PIP is an inflammatory reaction to cardiac muscle necrosis that occurs in the adjacent pericardium.