J Cardiovasc Ultrasound.  2008 Mar;16(1):1-8. 10.4250/jcu.2008.16.1.1.

Mechanism of Ischemic Mitral Regurgitation

• Otsuji Y
• Levine RA
• Takeuchi M
• Sakata R
• Tei C

• KMID: 1486603
• DOI: http://doi.org/10.4250/jcu.2008.16.1.1

Abstract

No abstract available.

Keyword

Mitral regurgitation

MeSH Terms

Mitral Valve Insufficiency

Figure

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  Fig. 1 Apical displacement of the mitral leaflets in patients with Ischemic mitral regurgitation (MR). Normal mitral leaflets close at the annular level (yellow arrows). However, leaflets in patients with ischemic MR cannot reach the annular level and coapt at an apically displaced position (pink arrows).

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  Fig. 2 Two superimposing and opposing forces on the leaflets to determine its closing position. Reduced closing force and augmented tethering force may result in apically displaced leaflets and mitral regurgitation (MR).

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  Fig. 3 Practical method to measure papillary muscle (PM) tethering distance. In the apical 4- and 2-chamber views, distances between PM tip and the contralateral anterior annulus express outward displacement of the lateral and medial PM relative to the anterior annulus, respectively.

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  Fig. 4 Potential mechanism for the higher incidence of ischemic mitral regurgitation in inferior versus anterior myocardial infarction (MI). Although, global LV remodeling in anterior MI may involve broader LV without causing major alterations in the mitral valve complex. In contrast, LV remodeling in response to inferior MI may involve less globally but may cause local and major alterations in the mitral valve complex.

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  Fig. 5 Phasic changes in the degree of ischemic mitral regurgitation (MR) during systole. MR is minimal in mid-systole (white arrows) with maximal closing pressure, suggesting that reduced closing force augment MR in early and late systole (pink arrows).

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  Fig. 6 Initial proposal of papillary muscle (PM) dysfunction to cause ischemic mitral regurgitation (MR). PM dysfunction with reduced PM longitudinal shortening may induce leaflet prolapse and ischemic MR.

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  Fig.7 Two superimposing and opposing effects of papillary muscle (PM) dysfunction. Associated effects of PM dysfunction by remodeling of the adjacent wall may augment tethering and mitral regurgitation (MR). In contrast, direct effects of PM dysfunction reduced PM longitudinal shortening may reduce tethering and ischemic MR.

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  Fig. 8 Two representative patients with the same degree of mitral annular dilatation (pink arrows) and considerably different degrees of functional mitral regurgitation (MR). The left panel shows that annular dilatation in a patient with lone atrial fibrillation (Af) without left ventricular (LV) dilatation fails to cause leaflet tenting and significant MR. The right panel shows that the same degree of mitral annular dilatation in a patient with dilated cardiomyopathy (DCM) is associated with apically displaced leaflets and significant MR.

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  Fig. 9 Potential mechanism of beneficial surgical ring annuloplasty on ischemic mitral regurgitation (MR) despite that the surgery does not relieve tethering. The middle panel shows that development of the ischemic MR may be related to the consumption of physiological coaptation between the anterior and posterior leaflets. Surgical ring annuloplasty can potentially shift the posterior annulus and leaflet anteriorly so that the coaptation can be restored without rattenuating the tethering.

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  Fig. 10 Regional difference in tethering. Although apical displacement of leaflets involve whole anterior and posterior leaflets, the displacement is regionally augmented in the middle portion of the anterior leaflet (arrows).

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  Fig. 11 A patient with recurrent functional mitral regurgitation (MR) following mitral annuloplasty and aortic valve replacement. The mitral annuli are connected with a white line. The LV is dilated, the anterior leaflet is tethered (white arrow), and the posterior leaflet is extremely tethered (yellow arrow), resulting in more posterior coaptation (pink arrow) than posterior annulus (thinner yellow arrow).

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