Case Presentation: A 64-year-old man with a history of apical hypertrophic cardiomyopathy and nonobstructive coronary artery disease (CAD) presented with acute onset non-radiating exertional chest pain localized to the precordium. His symptoms had progressed to the point of occurring even at rest. On arrival, his vital signs included a blood pressure of 112/65 mm Hg, heart rate of 68 bpm, and oxygen saturation of 98% on room air. Electrocardiogram (ECG) showed T-wave inversions in the anterolateral leads, consistent with prior ECG findings, and high-sensitivity troponin T levels trended up from 491 to 643 (normal level ≤22 ng/L). The patient was initially started on aspirin, ticagrelor, high dose rosuvastatin, and a heparin drip and was monitored on telemetry. A transthoracic echocardiogram (TTE) revealed moderate pericardial effusion with features of tamponade physiology, including right ventricular compression and right atrial inversion. The patient underwent pericardiocentesis with drainage of 50 to 75 ml of serosanguineous fluid. Post-pericardiocentesis imaging revealed only minimal pericardial effusion and no further signs of tamponade. He subsequently underwent cardiac catheterization which did not show any significant obstructive CAD. However, the cytological analysis of the pericardial fluid showed findings consistent with an aggressive B-cell non-Hodgkin lymphoma, concerning for DLBCL with BCL-6 translocation by FISH. A PET/CT scan performed for further characterization of disease burden revealed no evidence of FDG-avid lymphadenopathy or lymphoma elsewhere. Given the positive cytological findings in the pericardial fluid, the patient was initiated on pola-R-CHP (polatuzumab vedotin, prednisone, rituximab, cyclophosphamide, and doxorubicin).
Discussion: Pericardial effusion, particularly one causing cardiac tamponade, is an unusual initial manifestation of DLBCL. While pericardial involvement can occur in advanced hematologic malignancies, its presence as an isolated finding at presentation is exceedingly rare. In this case, our patient presented with progressive exertional chest pain, ultimately leading to the identification of tamponade physiology. Initial management focused on standard anti-ischemic measures, underscoring the difficulty in distinguishing primary cardiac conditions from malignant etiologies in the absence of other disease indicators. DLBCL typically presents with lymphadenopathy, B symptoms, or extranodal disease, all of which were absent in this case. The lack of systemic or nodal involvement on PET/CT was even more unusual, and it was only the pericardial fluid cytology that was ultimately diagnostic.
Conclusions: This case highlights the importance of considering malignancy in the differential diagnosis of pericardial effusion, even in patients without classic manifestations. Early recognition and cytologic examination of pericardial fluid are essential for prompt diagnosis, as initiating timely targeted treatment can improve outcomes and prevent recurrent effusion and other complications.