Objective: The mechanism of higher incidence of ischemic mitral regurgitation in patients with inferior compared with anterior myocardial infarction despite less global left ventricular remodeling and dysfunction is controversial. We hypothesized that inferior myocardial infarction causes left ventricular remodeling, which displaces posterior papillary muscle away from its normal position, leading to ischemic mitral regurgitation.
Methods: In 103 patients with prior myocardial infarction (61 anterior and 42 inferior) and 20 normal control subjects, we evaluated the grade of ischemic mitral regurgitation on the basis of the percentage of Doppler jet area, left ventricular end-diastolic and end-systolic volumes, midsystolic mitral annular area, and midsystolic leaflet-tethering distance between papillary muscle tips and the contralateral anterior mitral annulus, which were determined by means of quantitative echocardiography.
Results: Global left ventricular dilatation and dysfunction were significantly less pronounced in patients with inferior myocardial infarction (left ventricular end-systolic volume: 52 +/- 18 vs 60 +/- 24 mL, inferior vs anterior infarction, P<.05; left ventricular ejection fraction: 51% +/- 9% vs 42% +/- 7%, P <.0001). However, the percentage of mitral regurgitation jet area and the incidence of significant regurgitation (percentage of jet area of 10% or greater) was greater in inferior infarction (percentage of jet area: 10.1% +/- 7.5% vs 4.4% +/- 7.0%, P =.0002; incidence: 16/42 (38%) vs 6/61 (10%), P <.0001). The mitral annulus (area = 8.2 +/- 1.2 cm2 in control subjects) was similarly dilated in both inferior and anterior myocardial infarction (9.7 +/- 1.7 vs. 9.5 +/- 2.3 cm2, no significant difference), and the anterior papillary muscle-tethering distance (33.8 +/- 2.6 mm in control subjects) was also similarly and mildly increased in both groups (35.2 +/- 2.4 vs 35.2 +/- 2.8 mm, no significant difference). However, the posterior papillary muscle-tethering distance (33.3 +/- 2.3 mm in control subjects) was significantly greater in inferior compared with anterior myocardial infarction (38.3 +/- 4.1 vs 34.7 +/- 2.9 mm, P =.0001). Multiple stepwise regression analysis identified the increase in posterior papillary muscle-tethering distance divided by body surface area as an independent contributing factor to the percentage of mitral regurgitation jet area (r2 = 0.70, P <.0001).
Conclusions: It is suggested that the higher incidence and greater severity of ischemic mitral regurgitation in patients with inferior compared with anterior myocardial infarction can be related to more severe geometric changes in the mitral valve apparatus with greater displacement of posterior papillary muscle caused by localized inferior basal left ventricular remodeling, which results in therapeutic implications for potential benefit of procedures, such as infarct plication and leaflet or chordal elongation, to reduce leaflet tethering.