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Managing The Mitral Valve In HCM Surgery: Tips And Tricks
Sara Ranchordás1, Miguel Abecasis1, Eduard Quintana2
1Cardiac Surgery, Hospital Santa Cruz, ULSLO, Carnaxide, Portugal.
Insights
Mitral regurgitation in hypertrophic cardiomyopathy is often caused by systolic anterior motion (SAM) of the mitral valve (MV). Other structural issues may also contribute, requiring tailored surgical approaches for effective treatment.
Area of Science:
- Cardiology
- Cardiac Surgery
- Echocardiography
Background:
- Mitral regurgitation (MR) in hypertrophic cardiomyopathy (HCM) patients is primarily attributed to systolic anterior motion (SAM) of the mitral valve (MV).
- Additional structural abnormalities, including mitral leaflet elongation, papillary muscle anomalies, and mitral-aortic discontinuity, can contribute to MR in HCM.
- Intraoperative echocardiography is crucial for assessing MV function and regurgitant jets to identify all contributing mechanisms of MR.
Purpose of the Study:
- To elucidate the diverse mechanisms of mitral regurgitation in hypertrophic cardiomyopathy patients.
- To highlight the importance of comprehensive echocardiographic evaluation for identifying concomitant causes of MR beyond SAM.
- To discuss surgical strategies for addressing SAM and associated mitral valve abnormalities in HCM.
Main Methods:
- Review of echocardiographic findings in HCM patients with mitral regurgitation.
- Analysis of intraoperative echocardiographic assessments to identify SAM and other structural causes of MR.
- Evaluation of surgical techniques employed for correction of SAM and mitral valve disease.
Main Results:
- Systolic anterior motion (SAM) is the predominant cause of MR in HCM, but other factors like leaflet abnormalities and mitral-aortic discontinuity can coexist.
- Preoperative identification of concomitant MR mechanisms is possible through structural detection or pharmacological provocation.
- Surgical interventions may include myectomy, mitral valve repair (e.g., AML plasty, papillary muscle reorientation, edge-to-edge repair), or replacement, depending on the specific pathology.
Conclusions:
- Effective management of MR in HCM requires a thorough understanding of all contributing mechanisms, not solely SAM.
- Tailored surgical approaches, addressing both SAM and intrinsic mitral valve disease, are essential for optimal outcomes.
- Postoperative echocardiography, including provocative testing, confirms the elimination of SAM, LVOT obstruction, and resolution of MR.
Abstract:
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.
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