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Reversible severe mitral regurgitation caused by systolic anterior motion of the mitral valve in the absence of left ventricular hypertrophy: A case report.

ABSTRACT: A 67-year-old woman with exertional dyspnea was referred to our hospital. Transthoracic echocardiography revealed severe mitral regurgitation and significant left ventricular (LV) outflow tract obstruction due to prominent systolic anterior motion (SAM) of the mitral valve without LV hypertrophy. Oral bisoprolol remarkably attenuated SAM. Two- or three-dimensional echocardiographic analysis demonstrated the elongation of anterior and posterior mitral leaflets and interventricular septum (IVS) bulging due to narrow aorto-mitral angle. In the present case, elongation of mitral leaflet and hyperkinetic motion of left ventricle, and IVS bulging due to narrow aorto-mitral angle possibly play important roles in the development of SAM. <Learning objective: Mitral regurgitation due to systolic anterior motion (SAM) can be dramatically improved by beta-blocker therapy. Although the precise mechanism of SAM has not been fully elucidated, structural changes of mitral apparatus (elongation of mitral leaflet and papillary muscle displacement), and structural or functional features of left ventricle (hyperkinetic motion, small ventricle, interventricular septum bulging, narrow aorto-mitral angle) possibly play important roles in the development of SAM.>.

SUBMITTER: Kim K

PROVIDER: S-EPMC6262098 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Background and objectiveThe prevalence of hypertrophic cardiomyopathy (HCM) is estimated to be 1 in 200 to 500 individuals, with systolic anterior motion (SAM) of the mitral valve (MV) and left ventricular outflow tract (LVOT) obstruction present in 60% to 70%. In this narrative review, we aim to elucidate the pathophysiology of SAM-septal contact and LVOT obstruction in HCM by presenting a detailed review on the anatomy of the MV apparatus in HCM, examining the various existing theories pertaining to the SAM phenomenon as supported by cardiac imaging, and providing a critical assessment of management strategies for SAM in HCM.MethodsA literature review was performed using PubMed, EMBASE, Ovid, and the Cochrane Library, of all scientific articles published through December 2021. A focus was placed on descriptive studies, reports correlating echocardiographic findings with pathologic diagnosis, and outcomes studies.Key content and findingsThe pathophysiology of SAM involves the complex interplay between HCM morphology, MV apparatus anatomic abnormalities, and labile hemodynamic derangements. Echocardiography and cardiac magnetic resonance (CMR) vector flow mapping have identified drag forces, as opposed to the "Venturi effect", as the main hydraulic forces responsible for SAM. The degree of mitral regurgitation with SAM is variable, and its severity is correlated with degree of LVOT obstruction and outcomes. First line therapy for the amelioration of SAM and LVOT obstruction is medical therapy with beta-blockers, non-dihydropyridine calcium-channel blockers, and disopyramide, in conjunction with lifestyle modifications. In refractory cases septal reduction therapy is performed, which may be combined with a 'resect-plicate-release' procedure, anterior mitral leaflet extension, surgical edge-to-edge MV repair, anterior mitral leaflet retention plasty, or secondary chordal cutting.ConclusionsRecent scientific advances in the field of HCM have allowed for a maturation of our understanding of the SAM phenomenon. Cardiac imaging plays a critical role in its diagnosis, treatment, and surveillance, and in our ability to apply the appropriate therapeutic regimens. The increasing prevalence of HCM places an emphasis on continued basic and clinical research to further improve outcomes for this challenging population.

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Reversible severe mitral regurgitation caused by systolic anterior motion of the mitral valve in the absence of left ventricular hypertrophy: A case report.

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