Endocardial linear infarct exclusion technique for non-ischaemic functional mitral regurgitation caused by cardiac sarcoidosis: a case report

心内膜线性梗死排除术治疗由心脏结节病引起的非缺血性功能性二尖瓣反流:病例报告

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Abstract

INTRODUCTION: Damage to the posterior wall of the left ventricle (LV) can cause tethering mitral regurgitation (MR). We present a patient with non-ischaemic tethering MR and congestive heart failure due to cardiac sarcoidosis who was treated using an endocardial linear infarct exclusion technique. CASE PRESENTATION: A 63-year-old woman with a history of uveitis presented to our hospital complaining of dyspnoea. Echocardiography revealed dyskinesis of the posterolateral wall of the LV and severe tethering MR (regurgitation volume: 92 mL). The LV ejection fraction was reduced to 45%. Cardiac catheterization revealed no stenosis. Magnetic resonance imaging with late gadolinium enhancement revealed a contrast effect and thinning of the posteriolateral wall. The abnormal accumulation was also observed with fluorodeoxyglucose-positron emission tomography. Together, these findings indicated cardiac sarcoidosis, and we determined that cardiac sarcoidosis had resulted in aneurysm development in the posterior wall of the LV, subsequent advanced tethering at the posterior mitral valve cusp, and severe functional MR. The patient underwent an endocardial linear infarct exclusion technique (ELIET), mitral annuloplasty, tricuspid annuloplasty, and the full MAZE procedure. Histopathological analysis of the posterior wall myocardium revealed marked thinning of the endocardium, replacement fibrosis, lymphocyte infiltration, and epithelialization. These findings were consistent with sarcoidosis. The patient's condition improved to New York Heart Association (NYHA) Class I, and cardiac events were rare at 6 months after surgery. DISCUSSION: Endocardial linear infarct exclusion technique is useful for treating tethering MR. To our knowledge, this is the first reported case of successful treatment using ELIET for non-ischaemic tethering MR caused by cardiac sarcoidosis.

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