A 34-year-old woman was admitted because of headache, blurred vision, apraxia and abnormal feeling in the right arm. Examination revealed finger petechiae. Infection parameters were low. Magnetic resonance imaging of the brain showed multiple cortical and white matter lesions. Echocardiography showed vegetations on the aortic valve, severe aortic regurgitation and left ventricular volume overload (figure 1).
Figure 1 .
Parasternal short-axis view of the aortic valve with vegetations on the valve margins (left panel). Parasternal long-axis view showing large vegetation on aortic valve and dilated left ventricle (right panel).
Because of the severe regurgitation, the highly mobile vegetation and cerebral embolisation, early aortic valve replacement was performed as well as mitral valve replacement because extensive small vegetations were seen on the mitral valve apparatus at inspection. There was no growth in cultures of blood and specimens from the removed valves. Pathological examination of the removed aortic valve showed a mass of fibrin without inflammatory reaction (figure 2).
Figure 2 .
Macroscopic view of aortic valve leaflet with large vegetation (left panel). Microscopic view of aortic valve surface (upper part) with large vegetation (lower part) consisting mainly of fibrin, platelets and foam cells (right panel).
In the postoperative phase lymphadenopathy appeared in the neck. Poorly differentiated caecal adenocarcinoma was revealed as the primary tumour. Non-bacterial thrombotic endocarditis (NBTE) in the setting of metastatic adenocarcinoma was diagnosed. Despite treatment with chemotherapy, progression of disease was marked and the patient died six months later. In 1924, Libman and Sacks were the first to describe valvular vegetations without bacteria.1 Since then, the terms marantic endocarditis2 and NBTE3 have been used for describing bacteria-free vegetations mainly seen in neoplastic diseases and autoimmune disorders. NBTE is usually diagnosed post-mortem3,4 Underlying disease-associated hypercoagulability and damage to the valvular endothelium seem to be prominent pathophysiological factors.2,5 As treatment of NBTE is different from infective endocarditis, recognition of this distinct clinical entity is important.3
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References
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