Ablation Induced Pericarditis: "A Deep Burn"
Our patient is a 61-year-old female with past medical history notable for atrial flutter and paroxysmal atrial fibrillation s/p cavotricuspid and pulmonary vein isolation with radiofrequency ablation (5 years prior to presentation), recurrent atrial fibrillation s/p redo pulmonary vein isolation with radiofrequency ablation at outside facility complicated by left atrial perforation with hemopericardium and tamponade. She underwent pericardial drain placement for this (3 months prior to presentation) which was complicated by pericarditis (2 months prior to presentation) s/p medical treatment, now presenting for admission with worsening chest pain, shortness of breath and fever for 1–2-week duration.
Prior to discharge from her recent ablation, she was started on indomethacin 50mg three times a day (TID) x7 days and discharged on apixaban 2.5mg twice a day (BID) (dose reduced given hemopericardium) with resolution of pericardial effusion s/p pericardiocentesis. Two months prior to presentation, she presented to an outside emergency department with pleuritic chest pain and was found to have a trace effusion with pericardial thickening on computed tomography (CT), and started on colchicine 0.6mg BID, ibuprofen 600mg TID, pantoprazole and sucralafate with concern for pericarditis. She completed a 2-week course of ibuprofen and continued her colchicine for a total of 7 weeks (with intermittent use of NSAIDs for chest pain) with improvement, but not resolution of chest discomfort prior to discontinuing both medications for gastrointestinal (GI) side effects (abdominal pain). She continued to have minimal, but tolerable chest discomfort for 1 additional week, prior to developing clinical fever, fatigue and worsening pleuritic chest pain. She presented to an outside clinic for further evaluation and was found to have a moderate sized pericardial effusion without tamponade physiology and was referred to our facility for further evaluation and management. Upon arrival to our outpatient clinic, she had been off colchicine and NSAIDs for about 2 weeks, was found to have a large pericardial effusion on echocardiogram. She reported continued chest pain with positional and pleuritic features, fever, and progressive fatigue. She was then admitted to our hospital for expedited evaluation and management of her symptoms and imaging findings.
Upon admission, vitals were notable for T 36.5C, heart rate (HR) 125bpm, blood pressure (BP) 119/61 mmHg, RR 16/min, SaO2 95% on room air and without pulsus parodoxus (< 10mmHg fall in SBP on inspiration). Physical exam was notable for a comfortable appearing female sitting upright in bed, with an irregularly irregular tachycardic rhythm without abnormal heart sounds, murmur, or rub. She was clear to auscultation bilaterally with warm, well perfused extremities. Labs on admission notable for elevated erythrocyte sedimentation rate (ESR) 46mm/hr (0-15mm/hr), and elevated ultra-sensitive CRP 17.8mg/L (< 3.1mg/L). An electrocardiogram (ECG) was obtained and notable for atrial fibrillation with rapid ventricular rate (RVR), low voltage and electrical alternans (Figure 1: A, red arrows). Her transthoracic echocardiogram demonstrated a large circumferential pericardial effusion measuring 2.1cm along the inferolateral left ventricle (Figure 1: B). A cardiac magnetic resonance imaging (MRI) was obtained and notable for a moderate to large circumferential pericardial effusion, mostly located lateral to the left ventricle, with no apparent pericardial thickening. There was no diastolic septal bounce, but subtle respirophasic septal shift. There was no diastolic restraint or conical deformity of the ventricles. This constellation of findings was not consistent with the presence of constrictive physiology. There was circumferential late gadolinium enhancement (LGE) of the pericardium seen on fat suppressed imaging, indicative of inflammation (Figure 1: C). Cardiac MRI also demonstrated circumferential pericardial enhancement on T2 short-tau inversion recovery (STIR) sequencing, which indicates pericardial edema consistent with acute inflammation (Figure 1: D).
- Continued symptoms of positional and pleuritic chest pain
- Elevated inflammatory markers present
- Echo with a large effusion without tamponade physiology
- Cardiac MRI with active pericardial inflammation (circumferential pericardial LGE; pericardial edema) without constrictive physiology
A management decision was made, her symptoms improved, and repeat echocardiogram 5 days later was notable for complete resolution of her pericardial effusion.
Given this patient's clinical course, what is the next best step after obtaining the above imaging?