A 56-year-old male with obesity, hypertension, diabetes mellitus type 2, and dyslipidemia presented with nonexertional chest pain that wakes him up at night exacerbated by coughing and laying supine. There were no associated fever, dizziness syncope, and palpitation. He recalls symptoms of an upper respiratory tract infection which have resolved a few weeks earlier. Our patient is an office worker with no additional risk factors as smoking, chest trauma, recent travel, significant outdoor exposure, and family history of malignancy.
On evaluation, blood pressure was 144/68 mmhg, HR was 101 bpm, RR was 24 cpm, and the patient was afebrile. Eye and oral examination showed no suspicious lesions. There was no skin rash and synovitis. Cardiovascular examination was negative for jugular venous distention and hepatojugular reflex. Precordium was mildly tender, point of maximal impulse was adynamic and nondisplaced, and there was no palpable ventricular heave. On auscultation, S1 and S2 sounds were muffled; a precordial rub was appreciated over the left sternal border and is heard throughout the cardiac cycle. The remainder of the physical examination was unremarkable.
Electrocardiography showed nonspecific ST-T wave changes and no PR abnormalities. Troponin values were normal. A transthoracic echocardiogram demonstrated a mildly thickened pericardium with no pericardial effusion. Global ventricular wall motion was normal. Results of the initial laboratory investigation are outlined in Table 1. This shows leukocytosis with lymphopenia and monocytosis, elevated ESR, and normal renal function. The patient was then started on a course of Ibuprofen and Prednisone for suspected viral pericarditis.
During his 4-week follow-up, the patient reported some improvement of the chest discomfort but now endorses decreased exercise tolerance, exertional dyspnea, and worsening fatigue. D-Dimer was obtained and was slightly elevated, 0.47 (reference: 0.27-0.40 mcg/ml). Computed tomography of the chest demonstrated no pulmonary artery embolism. The pericardium was markedly thickened, along with a small amount of nonloculated pericardial effusion. Visualized were multiple enlarged mediastinal and subcarinal lymph nodes and a 1.2 cm pulmonary nodule in the left lower lobe (Figure 1). Taking his risk factors into account, his symptoms were now concerning for coronary ischemia. Myocardial Perfusion Scanning revealed a moderately intense area of reversible defect consistent with ischemia and infarction of the inferior wall. There were no features of hemodynamic collapse. Subsequent Coronary Angiography confirmed severe three-vessel coronary artery disease (mid-LAD 80%, 1st Diagonal 90% ostial lesion, 2nd Diagonal 80%, and RCA 100% with collaterals). Left ventriculogram showed hypokinesis of the basal inferior myocardium with an estimated EF of 50%.
The patient underwent urgent Coronary Artery Bypass Grafting (CABG). Intraoperatively, upon violating the pericardial sac, it was immediately evident that he had extensive nodular adhesions on the visceral and parietal pericardium. Gram stain and cultures for bacteria and acid fast bacilli were negative. Histopathology demonstrated a necrotizing granulomatous inflammation that stained positive for fungal elements within the central necrotic tissue. No malignant cells were identified (Figure 2). Screening for sarcoidosis, tuberculosis, and HIV infection was negative. Further serologic testing confirms H. capsulatum infection (Table 1). His postoperative course remained unremarkable. Treatment with Itraconazole was initiated with instructions to complete a 6-month course and a follow-up chest CT scan to monitor progression of the visualized solitary pulmonary nodule.