Systolic Anterior Motion of the Mitral Valve in the Presence of Annular Calcification.
Autor: | Friend EJ; Heart and Vascular Institute, Einstein Medical Center Philadelphia, Thomas Jefferson University, Philadelphia, Pennsylvania., Wiener PC; Division of Cardiovascular Medicine, Washington University School of Medicine, St. Louis, Missouri., Murthy KS; Heart and Vascular Institute, Einstein Medical Center Philadelphia, Thomas Jefferson University, Philadelphia, Pennsylvania., Peterson E; Heart and Vascular Institute, Einstein Medical Center Philadelphia, Thomas Jefferson University, Philadelphia, Pennsylvania., Al-Sudani H; Department of Medicine, Einstein Medical Center Montgomery, Thomas Jefferson University, East Norriton, Pennsylvania., Pressman GS; Heart and Vascular Institute, Einstein Medical Center Philadelphia, Thomas Jefferson University, Philadelphia, Pennsylvania. Electronic address: Gregg.Pressman@Jefferson.edu. |
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Jazyk: | angličtina |
Zdroj: | Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography [J Am Soc Echocardiogr] 2023 Apr; Vol. 36 (4), pp. 421-427. Date of Electronic Publication: 2022 Dec 16. |
DOI: | 10.1016/j.echo.2022.12.011 |
Abstrakt: | Background: Mitral annular calcification (MAC) has been reported as a possible cause of systolic anterior motion (SAM) of the mitral valve and dynamic left ventricular outflow tract (LVOT) obstruction. While morphologic features predisposing to SAM in other clinical settings have been described, patients with MAC+SAM have not been systematically investigated. We hypothesized that bulky calcium deposits in the mitral annulus could displace the valve toward the septum, thus promoting development of SAM. Methods: We studied 30 patients with severe MAC who had SAM with septal contact. Three comparator groups (matched for age and sex) were developed: 30 controls without MAC or SAM, 30 with severe MAC but no SAM, and 30 with SAM but no MAC. Results: Significant differences were found across groups for mitral valve coaptation point-septal distance (CSD), anterior mitral leaflet (AML) length, left ventricular diastolic dimension, and ejection fraction. Comparing all MAC subjects (n = 60) with controls, CSD was less (20.5 ± 4.1 vs 23.2 ± 3.7 mm, P = .003) and ejection fraction was higher (67.7% ± 7.8% vs 60.9% ± 6.4%, P < .0001) in MAC patients. Within MAC subjects AML was longer (21.9 ± 3.0 vs 17.4 ± 2.2 mm, P < .0001) and CSD was smaller (18.0 ± 2.7 vs 23.1 ± 3.6 mm, P < .0001) when SAM was present despite similar height of the calcium bar in the 2 MAC groups (12.4 ± 2.9 vs 11.1 ± 3.1 mm, P = .11). Regression analysis confirmed AML length and CSD as independent predictors of SAM. MAC+SAM patients also had more echocardiographic risk factors for SAM (acute aortomitral angle, small LVOT, long AML, small CSD, and presence of a septal bump) than MAC/no-SAM patients (3.4 ± 0.9 vs 1.8 ± 1.0, P < .0001). Conclusions: Bulky MAC appears to contribute to dynamic LVOT obstruction when it accumulates in such a way that the mitral valve is displaced anteriorly toward the septum. However, other features are also associated with SAM in these patients, particularly a long AML. A combination of morphologic features and favorable hemodynamics may be needed for SAM to develop in patients with severe MAC. (Copyright © 2022 American Society of Echocardiography. Published by Elsevier Inc. All rights reserved.) |
Databáze: | MEDLINE |
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