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A 51-year-old woman was diagnosed with critical aortic stenosis due to a bicuspid aortic valve (AV) and metastatic lung adenocarcinoma with epidermal growth factor receptor (EGFR) mutation at the same time (Panel A). Two weeks after AV replacement with a 21-mm Carpentier-Edwards Perimount pericardial bioprosthesis (Edwards Lifesciences, Irvine, CA, USA), she started gefitinib (Iressa®) at 250 mg daily, a selective inhibitor of the EGFR signal transduction pathway. Although the gefinitib therapy showed a favourable response, she started having progressive chest pain and dyspnoea at 6 months after the surgery. Serial transthoracic echocardiography showed progressive increases of the maximum and mean pressure gradients across the bioprosthetic AV to 75 and 45 mmHg (Panel B). Transoesophageal echocardiography showed nodular thickening of the leaflets and consequent severe aortic stenosis and mild aortic regurgitation (Panel C, D, E and F; see Supplementary data online, Video S1, S2, S3). Serum inflammatory and rheumatologic markers were all negative. There was no evidence of bacterial or fungal endocarditis. Because her symptoms were not relieved, a redo AVR was performed using a mechanical prosthetic valve. The removed bioprosthetic AV revealed multiple nodular lesions and unusual degeneration (Panel G). Histologically, there were vegetative dense fibrinous material deposits on the valve and focal acute inflammatory cell infiltrations (Panel H). In the superficial layers of both sides of the valve, there were large numbers of macrophage deposits (Panel I). This case is the first to show a potential link between EGFR inhibition and AV inflammation and degeneration in humans, although it is highly evident in EGFR-deficient mice.

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