Immune Checkpoint Inhibitor–Related Myopericarditis with Constrictive Physiology: Diagnostic Value of Cardiac MRI

Presenting Author(s)

• 

  Eugenia Pomeraantz, MD

  Cardiologist specialized in advanced cardiovascular imaging
  Hospital Italiano de Buenos Aires
  1425, Ciudad Autonoma de Buenos Aires, Argentina

Primary Author(s)

• 

  Eugenia Pomeraantz, MD

  Cardiologist specialized in advanced cardiovascular imaging
  Hospital Italiano de Buenos Aires
  1425, Ciudad Autonoma de Buenos Aires, Argentina

Co-Author(s)

• 

  Santiago del castillo, MD

  Cardiologist
  Hospital Italiano de Buenos Aires
  Buenos Aires, Ciudad Autonoma de Buenos Aires, Argentina
• LF

  Lucia Fileni, MD

  Cardiologist specialized in advanced cardiovascular imaging
  Hospital Italiano de Buenos Aires, Argentina
• RA

  Ramiro Antunez, MD

  Cardiologist specialized in advanced cardiovascular imaging
  Hospital Italiano de Buenos Aires, Argentina
• 

  Sebastian Tonso, MD

  Medical associated
  Hospital Italiano de Buenos Aires
  Buenos Aires, Ciudad Autonoma de Buenos Aires, Argentina
• MG

  Mariela Fernanda Gago, MD

  Cardiologist specialized in advanced cardiovascular imaging
  Hospital Italiano de Buenos Aires, Argentina
• MF

  Mariano L. Falconi, MD

  Staff of Cardiovascular Imaging
  Hospital Italiano de Buenos Aires
  BUENOS AIRES, Ciudad Autonoma de Buenos Aires, Argentina
• PD

  Perez de Arenaza Diego, MD

  Cardiologist
  Hospital Italiano de Buenos Aires
  Capital federal, Buenos Aires, Argentina

Description of Clinical Presentation: We report the case of a 38-year-old male, former smoker, with no previous cardiac history, recently diagnosed with stage III C squamous cell lung carcinoma and started on dual immune checkpoint inhibitor (ICI) therapy with nivolumab and ipilimumab.

Three months later (fifth cycle of treatment), he presented with dyspnea and cough. Laboratory tests revealed elevated cardiac biomarkers (hs-TnT: 19 pg/mL (ULN 15); NT-pro-BNP: 235 pg/mL), inflammatory markers (CRP: 125 mg/dL; ESR: 41 mm), and transaminases. EKG showed sinus tachycardia. Abdominopelvic CT angiography demonstrated free fluid in the perihepatic, perisplenic and pelvic regions, mild right pleural and severe pericardial effusion. Echocardiography confirmed cardiac tamponade. Pericardiocentesis was performed, yielding 1500 mL of serohematic exudate; cultures were negative and cytology showed no atypical cells. He improved clinically and was discharged with analgesic therapy. Immunotherapy was resumed, but 3 weeks later he presented again with chest pain, worsened in the supine position and fever.

Diagnostic Techniques and Their Most Important Findings: On admission EKG showed diffuse T-wave inversion. Laboratory tests revealed normal values of hs-TnT (13 pg/m), greater elevation than before of NT-proBNP (553 pg/mL), and of inflammatory biomarkers (ESR 64 mm, CRP 221 mg/L), with normal WBC count (8645/mm³).

Echocardiography demonstrated mildly reduced systolic function (LVEF 48%), pericardial thickening with a mildly effusion, and constrictive physiology (septal bounce, dilated IVC). Cardiac magnetic resonance (CMR) was performed, showing preserved biventricular function (LVEF 63%, RVEF 57%), septal bounce (more evident in free-breathing sequences), subepicardial late gadolinium enhancement (LGE) at the infero-apical and latero-apical segments. Both pericardial layers were thickened (up to 7 mm) with inflammatory features, including edema on fat-suppressed T2-weighted STIR sequences, elevated T2 mapping (80 ms) and T1 mapping (1382 ms), and extensive pericardial LGE - findings consistent with acute inflammatory pericarditis with constrictive physiology and mild myocarditis.

A diagnosis of severe ICI-related myopericarditis was made. Immunotherapy was discontinued, and treatment with high-dose prednisone, colchicine, and ibuprofen led to rapid clinical and laboratory improvement (CRP 8.2 mg/L, ESR 6 mm). At three months, echocardiography still showed signs of constriction. Follow-up CMR confirmed persistent septal bounce and extensive pericardial LGE, with partial improvement in mapping values, consistent with chronic constrictive pericarditis with residual inflammation. The patient remains clinically stable under multidisciplinary follow-up.

Learning Points from this Case: This case underscores the critical role of multimodality imaging—particularly CMR—in diagnosing and monitoring ICI-related pericardial disease, excluding metastatic cardiac involvement, and guiding immunosuppressive therapy within a multidisciplinary approach.

Figure 1. CMR findings: A) and B) extensive pericardial late gadolinium enhancement on PSIR sequences in the four-chamber and mid-ventricular short-axis views, respectively. C) and D) elevated pericardial T1 mapping values (1382 ms) in the four-chamber and mid-ventricular short-axis views, respectively. E) elevated pericardial T2 mapping values (80 ms) in the mid-ventricular short-axis view. Findings are consistent with acute inflammatory pericarditis with constrictive physiology and mild myocarditis.
Figure 2. CMR findings at 3-month follow-up. Compared with the initial study, there is persistent pericardial enhancement on PSIR sequences 10 minutes after gadolinium infusion: A) four-chamber view and B) mid-ventricular short-axis view. Partial improvement is observed in pericardial mapping values — T1 mapping (1000 ms): C) four-chamber view and D) mid-ventricular short-axis view; T2 mapping (60 ms): E) mid-ventricular short-axis view. Findings are consistent with chronic constrictive pericarditis with residual inflammation.