Why Do I Keep Having Chest Pain?
A 46-year-old gentleman with a past medical history significant for hypertension, hyperlipidemia, type 2 diabetes mellitus and obesity presented to an outside hospital emergency department (ED) with chief complaints of sharp, episodic, 6/10 chest pain with no radiation and no exacerbating/relieving factors. He also endorsed that he had experienced flu-like symptoms 8 days ago that resolved in 3 days after taking over the counter anti-allergic medications. ED workup showed atrial fibrillation on his electrocardiogram (ECG). He was started on flecainide and rivaroxaban by an outpatient electrophysiologist. He presented to the ED again, 1week later, with worsening chest discomfort. He underwent an exercise stress test that could not be completed due to patient fatigue. A subsequent left heart catheterization did not show any significant occlusion. He continued to have episodes of chest pain and volume overload for which he was admitted to our hospital. Pulsed-wave Doppler spectrum of mitral inflow velocities on admission showed significant respiratory variation of peak E-wave velocity (26%) (Figure 1).
A fat-pad suppression sequence cardiac magnetic resonance imaging (CMR) at that point showed pericardial thickening (5 mm), edema, inflammation, and respirophasic septal shift as well as a new pericardial effusion for which he underwent echocardiographic guided pericardiocentesis (Figure 2, Video 1).
Pericardial fluid analysis was negative for infectious or malignant causes of effusion. His inflammatory markers including ESR and high-sensitivity CRP were markedly elevated at 32 mm/hr and 4.5 mg/L respectively. He was diagnosed with effusive constrictive inflammatory pericarditis and started on treatment with dual-anti-inflammatory therapy with ibuprofen 800 mg three times a day and colchicine 0.6 mg once a day (he experienced significant gastrointestinal discomfort on colchicine twice daily) as well as diuresis with Furosemide 40mg once day. His symptoms improved and he was discharged with instructions for periodic outpatient follow-up. As an outpatient, his symptoms of volume overload (bilateral pitting edema and abdominal ascites) remained well controlled with diuresis. Serial evaluation with fat-pad suppressed CMR showed improvement in constrictive physiology and he was tapered off all anti-inflammatory agents over the course of a year. However, he represented to the clinic with complaints of episodic chest discomfort. CMR findings showed reappearance of pericardial thickening, inflammation, and diastolic septal bounce consistent with constrictive physiology (Figure 3). He was re-initiated on anti-inflammatory therapy including anakinra. His symptoms remained well controlled on subsequent follow-up.
Which one of the following statements is true in this case?