A 63-year-old man presents to the emergency department because of chest pain that began 2 days ago. The patient describes the pain as sharp and substernal. It worsens with deep inspiration and when lying flat and improves when he sits forward. He reports associated fatigue and low-grade fevers over the past week. Six weeks ago, he was hospitalized for an anterior ST-elevation myocardial infarction and underwent successful percutaneous coronary intervention to the left anterior descending artery. Since discharge, he has been taking aspirin, clopidogrel, atorvastatin, metoprolol, and lisinopril as prescribed. Temperature is 38.1°C (100.6°F), blood pressure is 126/78 mm Hg, pulse is 96/min, and respiratory rate is 18/min. Oxygen saturation is 98% on room air. Cardiac examination reveals a scratching sound best heard along the left sternal border while the patient leans forward. Lung examination is normal.
Laboratory studies show the following:
ECG demonstrates diffuse ST-segment elevations and PR-segment depressions. Transthoracic echocardiography reveals a small circumferential pericardial effusion without tamponade physiology.
Which of the following is the most likely underlying mechanism of this patient’s condition?
The correct answer is:
A) Autoimmune inflammation directed against pericardial antigens exposed during myocardial injury
This patient has Dressler syndrome, a form of autoimmune pericarditis that develops weeks to months after myocardial infarction. The diagnosis is suggested by the timing following MI, pleuritic and positional chest pain, low-grade fever, elevated inflammatory markers, diffuse ST-segment elevations, PR-segment depressions, and a pericardial friction rub.
The syndrome is believed to result from an autoimmune response directed against cardiac and pericardial antigens released during myocardial necrosis. Rather than representing ongoing ischemia, the condition reflects immune-mediated inflammation of the pericardium. Patients typically present several weeks after infarction with fever, malaise, pleuritic chest pain, and evidence of pericardial inflammation.
A key Step 2 distinction is recognizing the difference between acute post-infarction pericarditis and Dressler syndrome. Acute pericarditis may occur within several days of a transmural infarction due to direct inflammation overlying the infarcted myocardium. Dressler syndrome occurs later and is mediated by an autoimmune process.
Treatment typically consists of anti-inflammatory therapy, most commonly aspirin. Prognosis is generally favorable.
Answer choice B: Bacterial infection of the pericardial space following coronary intervention, is incorrect.
Purulent pericarditis is uncommon and usually occurs in patients with bacteremia, thoracic surgery, trauma, or contiguous spread of infection. Patients are often significantly ill and may develop sepsis. The classic post-MI timing, diffuse ECG changes, and friction rub are much more consistent with Dressler syndrome.
Answer choice C: Extension of myocardial infarction due to recurrent coronary artery occlusion, is incorrect.
Recurrent infarction would typically present with ischemic chest pressure rather than pleuritic, positional pain. Rising cardiac biomarkers and ischemic ECG changes would be expected. This patient’s normal troponin level and diffuse ST-segment elevations favor pericarditis rather than recurrent infarction.
Answer choice D: Hemorrhagic pericarditis caused by dual antiplatelet therapy, is incorrect.
Although antithrombotic therapy can increase bleeding risk, it does not explain the characteristic constellation of fever, friction rub, elevated inflammatory markers, diffuse ST-segment elevation, and the classic timing several weeks after MI.
Answer choice E: Ventricular free wall rupture with slow accumulation of blood in the pericardium, is incorrect.
Free wall rupture generally occurs within the first week after transmural MI and typically presents with sudden hemodynamic collapse and cardiac tamponade. A stable patient presenting six weeks after MI with inflammatory symptoms and classic pericarditis findings is far more consistent with Dressler syndrome.
Key Learning Point
Dressler syndrome is an autoimmune pericarditis that occurs weeks to months after myocardial infarction. Patients present with fever, pleuritic positional chest pain, a pericardial friction rub, diffuse ST-segment elevation, and elevated inflammatory markers.
