Managing The Mitral Valve In Hcm Surgery: Tips And Tricks

• Author(s): Ranchordás, Sara ; Abecasis, Miguel ; Quintana, Eduard
• Date: 2025
• Origin: Portuguese Journal of Cardiac Thoracic and Vascular Surgery
• Subject(s): Hypertrophic Cardiomyopathy; systolic anterior motion; mitral regurgitation; septal myectomy
• Document Type: Journal article
• Language: English

Description

Mitral regurgitation (MR) in hypertrophic cardiomyopathy (HCM) patients is mainly due to systolic anterior motion (SAM) of the mitral valve (MV). However, other mechanisms contributing to mitral regurgitation may coexist as a result of further structural abnormalities. SAM might occur because of the increased septal thickness alone or due to simultaneous MV or subvalvular apparatus anomalies, such as mitral leaflet elongation, papillary muscle body anomalies, accessory papillary muscles or additional papillary muscle heads. Additionally, anomalous mitral chordae or the recently described mitral-aortic discontinuity (leading to a longer anterior mitral leaflet (AML)) can contribute to abnormal physiology. A closed aortomitral angle may also contribute. During intraoperative echocardiographic assessment, it is important to thoroughly evaluate the MV and the regurgitant jet to understand the mechanism(s) that cause MR in HCM patients. Although myectomy alone is frequently enough to correct SAM, concomitant MV procedures may be needed, especially when the septum is thin (<16-18 mm) and/or there is intrinsic MV disease. Detection of concomitant regurgitation mechanisms beyond SAM can eventually be identified preoperatively, either by direct structural detection (valve prolapse), by pharmacological palliation of SAM with vasopressors and negative inotropic agents or suspected by identification of anteriorly and centrally directed regurgitant mitral jets. Surgical techniques that can be employed to contribute to SAM elimination include plication/extension/retention plasty of the AML, resection/release/reorientation of papillary muscles, division of anomalous chordae, edge-to-edge repair, or, at times, prosthetic MV replacement. If there is structural MV disease concomitant to HCM, appropriately tailored techniques to address the MV may be used. Transoesophageal echocardiography at the end of the procedure should demonstrate elimination of SAM, resolution of LVOT obstruction, and appropriate coaptation of the MV leaflets and nearly resolution of MR. Provocation with inotropes can be used to ensure no latent obstruction persists.