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Corresponding author: Dr Robert Dennert, Department of Cardiology, Maastricht University Medical Center, P. Debyelaan 25, 6229 HX, Maastricht, The Netherlands. Tel.: +31-43-3882949; fax: +31-43-3882952.
A 54-year-old man with a history of type 1 diabetes mellitus and hyperthyroidism presented
with typical symptoms of pericarditis after an episode of flu-like symptoms. His electrocardiogram
revealed diffuse ST-T segment elevation not confined to an arterial territory. Plasmatic
levels of cardiac troponin remained within normal values. Treatment with nonsteroidal
anti-inflammatory drugs was initiated, but he presented with recurrent symptoms and
progressive dyspnea several weeks later. Further evaluation revealed a history of
frequent purulent nasal discharge. Urine analysis demonstrated microhematuria. Echocardiography
revealed a thickened pericardium without effusion, augmented respiratory variation
of mitral inflow (Fig. 1A), normal medial peak E′ velocities (Fig. 1B), and abnormal septal motion during diastole (septal bounce). Cardiac magnetic resonance
imaging showed marked pericardial thickening on cine, T1-, T2-weighted, and delayed
enhancement (DE) imaging (Fig. 1, D-F), with diastolic septal bounce on cine imaging (see Videos 1 and 2; view videos online) compatible with constriction.
On T2-weighted and DE imaging, the hyperintense visceral and parietal pericardium
were clearly discernable. Midwall linear hyperintensity in the basal inferolateral
segments complemented the diagnosis of acute perimyocarditis. Endomyocardial biopsies
did not show active myocarditis or granuloma formation on histology. Additional immunohistological
analysis revealed borderline leukocyte infiltration (13 CD45-positive inflammatory
cells per mm2; Fig. 1C) and an increased parvovirus-B19 viral load (319 copies per microgram DNA) in polymerase
chain reaction assay. A serology test showed the presence of perinuclear-antineutrophil
cytoplasmic antibody (ANCA) (titer: 1/128) confirmed with proteinase 3-capture enzyme-linked
immunosorbent assay and a marked increased soluble interleukin-2 (5587 pg/mL), consistent
with granulomatosis with polyangiitis (formerly known as Wegener granulomatosis).
Figure 1(A) Pulsed wave Doppler signal of mitral inflow with > 25% respiratory variation of
peak E velocity; (B) tissue Doppler signal with normal medial peak E′ velocities; (C) CD45 immunostaining shows borderline myocardial leukocyte infiltration (arrows); (D) thickened pericardium on diastolic still frame on cine; (E) T2-weighted black-blood turbo spin-echo with fat suppression; and (F) delayed enhancement (DE) images. Visceral (arrows) and parietal pericardium (arrows) show increased signal intensity on (E) T2-weighted and (F) DE images, with focal linear, midwall hyperintensity on the DE images, compatible
with acute perimyocarditis.
view videos online) compatible with constriction.
