Oki T, Fukuda N, Iuchi A, Tabata T, Yamada H, Fukuda K, Manabe K, Ito S
Second Department of Internal Medicine, Tokushima University School of Medicine, Japan.
Clin Cardiol. 1996 Aug;19(8):639-43. doi: 10.1002/clc.4960190811.
This study was undertaken to clarify the mechanisms of mitral regurgitation (MR) in dilated hearts.
In all, 68 patients with dilated heart and MR, including 26 patients with dilated cardiomyopathy (DCM), 24 with prior anterior myocardial infarction (A-MI), and 18 with prior posteroinferior myocardial infarction (I-MI), as well as 25 normal subjects were examined by transesophageal two-dimensional and color Doppler echocardiography.
The maximum area of the MR signal in the DCM group correlated positively with the anteroposterior diameter of the mitral annulus at late systole. Although the coaptation edge length of the anterior and posterior mitral leaflets appeared shorter in dilated hearts than in the hearts of controls, a significant difference did not exist. The length of the coaptation edge correlated negatively with the maximum area of the MR signal in all dilated hearts, and characteristic systolic displacement of the coaptation point of both mitral leaflets occurred. The MI groups demonstrated anterior and posterior displacement in the direction of the short axis of the left ventricle in the A-MI and I-MI groups, respectively. However, the DCM group demonstrated inferior displacement toward the long axis of the left ventricle; its magnitude correlated positively with the maximum area of the MR signal.
A major cause of MR in dilated hearts is mitral malcoaptation due to displacement of the coaptation point of the mitral leaflets along the long or short axis of the left ventricle. This is caused by left ventricular enlargement and/or asynergy of the left ventricular wall, rather than by a decrease in mitral coaptation edge length due to mitral annular dilation.
