Incomplete mitral leaflet closure in patients with papillary muscle dysfunction.

Abstract

SUMMARY Clinical acceptance of an association between papillary muscle dysfunction and mitral regurgitation is widespread, despite the lack of objective support. To evaluate a possible association, we performed echocardiographic examinations on 22 patients with prior myocardial infarction and clinical evidence of papillary muscle dysfunction, 40 patients with prior myocardial infarction and no clinical evidence of papillary muscle dysfunction, and 20 normal subjects. There was a unique pattern of incomplete mitral leaflet closure ina high percentage (91%) of infarct patients with mitral regurgitation. In these patients, one or both leaflets we3e effectively arrested within the cavity of the left ventricle during ventricular systole. Dyskinetic wall motion in the region immediately surrounding one of the papillary muscles was present in 23 of 24 patients (96%) with demonstrated incomplete closure. This study provides the first objective evidence that de novo mitral regurgitation in patients with prior myocardial infarction is due to dyskinesis involving the left ventricular myocardium beneath one of the papillary muscles, producing increased tension on the mitral leaflets and preventing normal closure.MITRAL INSUFFICIENCY has been recognized for many years to result from disorders of the mitral leaflets, chordae tendineae, annulus and related structures.'-' In 1963, Burch and colleagues directed attention to the possible etiologic role of papillary muscle dysfunction in producing mitral valve incompetence.4" They suggested two mechanisms by which this might occur. First, ischemia or fibrosis of a papillary muscle might prevent normal contraction. This would weaken systolic support for the valve leaflets and result in leaflet eversion or prolapse into the left atrium. Alternatively, ischemia or infarction of the left ventricular myocardium at the base of a papillary muscle might produce dyskinesis in this region. This would pull the papillary muscle away from the valve orifice, increasing tension on the leaflets and preventing complete closure.Angiographic studies have shown the occurrence of mitral valve prolapse in association with ischemic disease involving a papillary muscle, supporting the occurrence of the first of these two phenomena.6 7 Angiography is poorly suited to demonstrate displacement of a leaflet downward into the cavity of the ventricle. As a result, the alternative mechanism, leaflet arrest with resultant malapposition and valvular incompetence, has not been shown to occur.Cross-sectional echocardiography is a noninvasive method of assessing mitral leaflet motion through the cardiac cycle in multiple tomographic planes. As motion in patients with clinical papillary muscle dysfunction. The purposes of this study were (1) to determine whether abnormal leaflet motion or closure patterns could be observed by the cross-sectional echocardiogram in patients with clinical evidence of papillary muscle dysfunction, and (2) if abnormal motion did occur, how it related to the mechanisms proposed for leafl...

Geometric Distortions of the Mitral Valvular-Ventricular Complex in Chronic Ischemic Mitral Regurgitation

“…Previous clinical [15][16][17] and experimental 8,18,19 studies have described the role of papillary muscle displacement in the development in CIMR. Other investigators have used echocardiography to link both total and laterally-directed papillary muscle displacement to apical restriction of the mitral leaflets.…”

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“…The degree of MR did not differ between treatment groups (ERV mean MR grade 1.4Ϯ0.9 versus IMS 1.3Ϯ0.9). Apical displacement of mitral leaflet coaptation, also known as incomplete mitral leaflet closure pattern, 16 was noted in 40% of those with grade 2ϩ to 4ϩ MR.…”

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