Recurrent Pericarditis: Stick to the Guidelines
A 52-year-old pediatrician with a past medical history of hyperlipidemia and remote tobacco use presented with pleuritic chest pain related to a viral prodrome. The patient stated that the pain was "pressure-like," radiated up to his neck, and was worse when he was supine. During a local ED evaluation, his ECG was remarkable for diffuse ST-elevations and elevated C-Reactive Protein (CRP) level of 43mg/dL. A 2D echocardiogram was normal. He was diagnosed with acute pericarditis, and was given 125mg methylprednisolone with subsequent symptom resolution.
2 months later, the patient had a relapse of symptoms and diagnostic workup showed an elevated CRP level (222 mg/dL). He was diagnosed with recurrent pericarditis and was started on NSAIDS, colchicine, and prednisone 5mg. A rapid weaning of steroid therapy was unsuccessful as it led to recurrent pain and shortness of breath. A CT scan was remarkable for pericardial thickening with enhancement, a small pericardial effusion, and bilateral pleural effusions. Based on these results, prednisone increased to 10mg, however symptoms persisted. On a follow-up visit, prednisone was increased to 60mg, ibuprofen 800mg three times a day, and colchicine 0.6mg twice a day, with rapid improvement in symptoms.
The patient then presented for outpatient follow-up. His vital signs were stable and physical exam was unremarkable. There was no jugular venous distension, no pericardial rubs, or murmurs. His ECG is demonstrated as Figure 1, revealing normal sinus rhythm and non-specific ST-T wave changes. Laboratory evaluation was remarkable for a mildly elevated ultrasensitive CRP 11.5mg/L, ESR 14mm/hr and elevated liver function tests (ALT 197 AST 42).
Figure 1: ECG demonstrating normal sinus rhythm with normal PR segment and nonspecific ST segment and T wave changes.
There were no echocardiographic or MRI evidence of pericardial constriction (Figure 2). An echocardiogram and cardiac MRI revealed ejection fraction of 57% without significant pericardial effusion or valvular abnormalities. Delayed enhancement imaging was remarkable for circumferential pericardial enhancement on both fat saturated and fat suppressed imaging; consistent with active pericardial inflammation (Figure 3).
Figure 2: Tiles A and B represent 2D echo and SSFP MRI cine demonstrating normal biventricular size and systolic function. Tile C depicts mitral inflow pattern with E<A. Tile D demonstrates no significant respiratory variation in mitral inflow velocities.
Figure 3: Tile A is a fat-saturated delayed enhancement image depicting circumferential pericardial enhancement. Tiles B-C are fat-suppressed delayed enhancement images also depicting circumferential pericardial enhancement. The overall findings are consistent with active pericardial inflammation.
Which of the following is the next best step in management?