A 49-year-old farm laborer was referred to our hospital with complete heart block, incidentally discovered when he presented with persistent left sciatica despite analgesic treatment. No personal or familial history except a smoking habit was reported. The sciatica did not require immediate surgical management according to the physicians' assessment after a spinal magnetic resonance imaging. Electrocardiogram (Figure 1) revealed complete atrioventricular block associated with atrial tachycardia. Thus, this patient was sent to our intensive care unit for cardiac investigation. Clinical history revealed New York Heart Association (NYHA) class II dyspnea, associated with clinical signs of global heart failure. Chest radiography demonstrated cardiomegaly and bilateral hilar overload. Transthoracic echocardiography (Figure 2(a), see Movie 1 Supplementary Material available online at doi:10.1155/2011/740928) revealed extensive localized thickening of the right ventricle, right atrium, interatrial septum, and basal to mid interventricular septum associated with a pericardial effusion. The infiltration extended around the root of the pulmonary artery and aorta (Figure 2(b), Movie 2). Left ventricular systolic function was slightly impaired (ejection fraction = 54%). Analysis of tissue Doppler indices showed elevated left ventricular filling pressures (E/E' ratio = 16.4). Blood sample tests found an isolated inflammatory syndrome: C-Reactive Protein raised to 50 mg/L. Nt-proBNP increased to 1150 pg/mL (N < 125 pg/mL). Serological tests for a bacterial, fungal, or immunological (including anti-nuclear antibodies, antineutrophil cytoplasmic antibodies, rheumatoid factor) cause were negative. QuantiFERON-TB Gold test was negative, and the angiotensin-converting enzyme level was normal. Cardiovascular magnetic resonance (CMR) imaging was performed to localize and characterize the nature of the tissue thickening. Four-chamber (Figure 3(c), Movie 3), apical short-axis, and long-axis (Movie 4) cine images were performed using steady-state free precession (SSFP) cine sequences. The right ventricular wall was akinetic, with preservation of apical contractility. Short-axis dark-blood T2-weighted (Figures 3(a) and 3(b)) sequences confirmed concentric thickening and oedema of the right ventricle. First-pass perfusion (Figure 3(d), Movie 5) showed enhancement of the right ventricular and interventricular septum infiltration consistent with an active inflammatory process. Delayed enhancement CMR (Figures 3(e) and 3(f)) sequences demonstrated widespread and heterogeneous enhancement of the right ventricle. Combined (18)F-fluoro-2-deoxyglucose positron emission tomography (FDG PET)/computed tomography (CT) was performed to look for primary malignant lesion (Figure 4) showing moderate FDG uptake involving mainly the right heart chambers of the heart. This whole body exam did not detect any extracardiac locations of FDG uptake. 
The patient was treated with diuretics, angiotensin-converting enzyme inhibitors, spironolactone, amiodarone, and adequate anticoagulation (INR 2.0-3.0) with warfarin associated with steroid therapy (prednisolone 1 mg/kg/day). Right ventricular myocardial biopsy and implantation of a dual-chamber epicardial pacemaker were performed via a sternal thoracotomy. Hematoxylin-eosin-saffron stained sections of the tissue sample showed a granulomatous reaction consisting of nodular cellular infiltrates (histiocytes associated with lymphocytic elements) with an abundant fibrotic reaction (Figures 5(a) and 5(b)). Immunohistochemistry revealed a prevalence of T lymphocytes (CD3 positive; Figure 5(c)) mixed with B lymphocytes (CD20 positive), histiocytes (CD68 positive; Figure 5(d)) and a few plasma cells (CD138 positive). Neither giant cells nor epithelioid cells were observed, thus rejecting the diagnoses of giant cell myocarditis and cardiac sarcoidosis. Vessels were not specifically concerned with the cellular infiltrates, so that a diagnosis of vasculitis was also excluded. Congo red and hematoxylin-eosin stained sections did not show amyloid deposits. Nested/reverse transcription-PCR did not detect any genomes of enterovirus, adenovirus, parvovirus B19, or human herpes virus type 6.
At followup twelve months later, the patient described NYHA class II dyspnea, with no clinical signs of heart failure. Echocardiography revealed persistent myocardial infiltration, although the pericardial effusion had resolved. The patient remained pacemaker dependent with underlying complete heart block, which is probably the consequence of infiltration of the cardiac conduction system with granulomatous tissue. Nt-proBNP had decreased to 550 pg/mL.