Mechanism of mitral regurgitation in the acute phase of inferior wall myocardial infarction: reduced closing force as a consequence of left ventricular systolic dysfunction in the presence of tethering as a determinant of mitral regurgitation

Abstract

BACKGROUND: To delineate the mechanism of mitral regurgitation (MR) in the acute phase of inferior wall myocardial infarction (MI).

METHODS AND RESULTS: In 97 patients (age 59 ± 12 years) with acute inferior wall MI, the severity of MR, left ventricular (LV) geometric changes and function within 1.7 ± 1.3 days after MI by echocardiography was retrospectively evaluated. Infarct size was measured within 3.9 ± 1.7 days by cardiac magnetic resonance. Mild MR was present in 16 (16.5%) and moderate MR in 12 (12.4%) of 97 patients. There were no significant differences in mitral annular area, sphericity and distances between papillary muscle tips and the contralateral mitral annulus. However, patients with moderate MR had significantly larger LV end-systolic volume, tenting area and infarct size. There was a graded relationship between the severity of MR and LV ejection fraction. In a multivariable regression analysis, LV ejection fraction and tenting area were found to be independent predictors of the severity of MR (r(2)=0.180, P=0.001).

CONCLUSIONS: MR was associated with LV systolic dysfunction, increase in end-systolic LV volume and tethering of mitral leaflet, suggesting reduced closing force as a consequence of LV systolic dysfunction in the presence of leaflet tethering would play a more pivotal role in the development of MR.