A 75-year old man with hypertension, but otherwise healthy, was referred to our Cardiology department for a tentative diagnosis of congestive heart failure. Symptoms included fatigue, progressive dyspnea, position-dependent chest pain and pitting edema of the lower extremities. The symptoms had developed over a two-month period with worsening of symptoms seven days prior to admission. On admission his blood pressure was 136/65 mmHg, heart rate 90/min and a core temperature of 37.8   Celsius. Electrocardiography showed low voltage in the extremity leads, but no signs of arrhythmia or ischemia. Chest radiograph revealed ectasia cordis and left sided pleural effusion. Blood chemistry showed C-reactive protein 51 mg/L with a normal white blood cell count. Transthoracic echocardiography revealed concentric pericardial effusion measuring 16 mm, elevated central venous pressure, normal chamber dimensions and wall thickness, no valve disease and normal left ventricular systolic and diastolic function (Fig. 1A).
The patient was tentatively diagnosed with viral pericarditis and parapneumonic effusion and received oral amoxicillin/clavulanic acid, furosemide and ibuprofen as an outpatient. However the patient's condition deteriorated over the following months. Throughout the clinical course, the predominant symptoms remained: asthenia, intermittent chest pain and symptoms of heart failure with dyspnea and pitting edema of the lower limbs.
Diagnostic approach for evaluation of pericarditis included testing for tuberculosis as well as other infectious causes and rheumatic and autoimmune diseases.
Intensified diuretic therapy and pleurocentesis resulted in only transient alleviation of the symptoms. The patient showed signs of progressive heart failure with increasing dyspnoea, excessive edema of the lower extremities and he developed drug resistant atrial fibrillation. Repeat echocardiography showed thickening of the pericardium at four millimeters, pericardial effusion, and signs of the heart being incased in a non-pliable pericardium. Computed tomography (CT) scan revealed thickening of the pericardium, pericardial - and pleural effusions, but no other abnormalities (Fig. 1B, C). Invasive evaluation with simultaneous right - and left-heart catheterization showed an equalization of the end-diastolic pressures at 18 mmHg and pressure tracings showed the classic "Dip-plateau" or "Square-root" filling pattern. Both measurements are distinctive hallmarks of constrictive pericarditis.
Subtotal pericardiectomy through a median sternotomy was performed. Both the parietal and visceral pericardium showed significant thickening and fibrosis, and the visceral pericardium adhered completely to the myocardium. Postoperatively, the patient recovered rapidly with relief of symptoms. Bilateral cardiac catheterization revealed normalization of end-diastolic pressures and a marked improvement in cardiac output and cardiac index.
Gross examination of the pericardium showed severe fibrosis and thickening, approximately nine millimeters. Microscopic examination showed chronic inflammation and intense pericardial fibrosis. Tissue samples from both the parietal and visceral pericardium were cultured; C. acnes was recovered from two samples. No other infectious agents were recovered. Polymerase chain reaction (PCR) for Mycobacterium tuberculosis was negative. Antimicrobial susceptibility testing revealed that is was susceptible to penicillin.
The patient was treated with intravenous penicillin G for four weeks, followed by 12 weeks with oral amoxicillin/clavulanic acid. Six months after surgery the patient remained free of infection, showing continued improvement in overall cardiac function, and a complete remission of both pericardial - and pleural effusions as well as atrial fibrillation.