P228 Mitral valve aneurysm in the context of post-infective endocarditis in hypertrophic cardiomyopathy: an issue of inflammation or pressure gradients?

Abstract

Mitral valve aneurysms (MVA) are uncommon and usually develop acutely in the setting of infective endocarditis (IE). We present a case report of a patient with a ruptured aneurysm of the mitral valve (MV) leaflet and obstructive hypertrophic cardiomyopathy (HCM), previously treated for IE. Echocardiography is essential for diagnosis, highlighting the importance of imaging for early identification and timely intervention. CASE REPORT 68-year-old male patient with type 2 diabetes mellitus and dyslipidemia was admitted to hospital with a 3-week history of malaise, fever and recent left-sided abdominal pain. No past relevant history. Physical examination revealed a grade II/VI systolic heart murmur at the cardiac apex, fever, abdominal tenderness in the left upper quadrant and purpuric lesions in the inferior limbs. Neutrophilia, CPR 211mg/L. Positive blood cultures for Staphylococcus aureus methicillin-sensitive. Spleen embolization, with no abcess on abdominal CT. Transthoracic (TTE) and transesophageal echocardiography (TEE) disclosed a highly mobile polypoid mass in the atrial side of the anterior MV leaflet, septal left ventricular hypertrophy and systolic anterior motion (SAM) of the MV. Mild mitral regurgitation (MR). No evidence of abcess, aneurysm or valve perforation. The diagnosis of IE was established and the patient completed 42 days of Flucloxaciline. Favorable clinical evolution, residual lesions on the MV. TTE and TEE were repeated on follow-up. Besides HCM and SAM of the MV, an aneurysm of the anterior leaflet of the MV was identified and two regurgitant jets: one due to incomplete coaptation of the leaflets; other through the perforated aneurysm. Mild global MR. A strategy of close follow-up was adopted. Beta blocker dose was increased. Maintenance of the characteristics of the aneurysm. DISCUSSION MVA are rare, with perforation and significant MR development as the most serious complications. They mostly develop in the acute setting of IE of the aortic valve (AV), due to the "jet lesion" from the regurgitant jet or direct extension of the infection. In this case, MVA developed as a late complication of IE of the MV. Previous infection and inflammation lead to increased susceptibility of the valve leaflet, with possible persistent chronic inflammation. In the setting of obstructive HCM, the lesioned endothelium is exposed to significant intraventricular pressure gradients, which have probably raised its propensity to bulge towards the atrium, resulting in aneurysm formation and perforation. Optimal approach to MVA has not been defined. If the setting of perforation with severe MR, surgery must be performed in order to avoid a fatal outcome. In small aneurysms with mild MR, a conservative approach seems reasonable. The purpose of this case is to highlight potential complications of IE, which should be actively investigated, with echocardiography playing a central role in the diagnosis and follow-up.