ABSTRACT
Magnetic resonance tagging (MRI) can be used to study intramyocardial trains in human in vivo. We wished to determine whether patients with severe mitral regurgitation demonstrate subtle myocardial contractile dysfunction despite normal left ventricular (LV) ejection fraction (EF) and how, mitral valve repair (MVR) may preserve EF in such patients. MRI was performed on seven patients with severe mitral regurgitation (mean age +/- SD, 65+/-13 years) and normal EF day 1 (range, 0-8 days) before (Pre) and week 8+/-3 after (Post) MVR and on nine normal volunteers (mean age, 32+/-4). LV mass index (LVMI), end-diastolic and end systolic volume, mass/volume ratio, EF, and sphericity index were measured Pre and Post. Two-dimensional strain analysis of MR tagged images was performed and expressed as L1 (greatest systolic lengthening, radial in normal subjects), L2 (greatest systolic shortening, circumferential in normals), and beta (angular deviation of L1 from the radial direction). LVMI fell from 142+/-38 g/m2 Pre to 117+/-44 g/m2 Post (p < or = 0.008) as did LV end-diastolic volume (117+/-26 to 69+/-12 ml, p < or = 0.003), whereas EF remained unchanged (59+/-7% at both time points). LV mass/volume ratio increasedfrom 2.2+/-0.3 g/ml Pre to 3.1+/-0.4 g/ml Post (p < or = 0.02) and sphericity index fell from 0.86+/-0.10 to 0.71+/-0.13 (p = 0.02). In the short axis, L1 was greater in patients with mitral regurgitation than normal subjects (19+/-9% vs 16+/-6%, p < or = 0.003) and tended to increase further after MVR (21+/-8%, p < or = 0.06 vs. Pre). Beta was abnormal in mitral regurgitation (19+/-8 vs. 12+/-8 degrees in control subjects, p < 0.0001) and remained abnormal after MVR (19+/-9 degrees). L2 in the short axis was depressed in mitral regurgitation compared with control subjects (12+/-6% vs. 21+/-6%, p < or = 0.001) and was further depressed after MVR (9+/-7%, p < 0.001 vs. Pre). As detected by MRI, regional myocardial strains are abnormal in severe mitral regurgitation despite normal EF, characterized by increased short-axis systolic lengthening that is abnormally directed and by reduced shortening. After MVR, the further increase in short-axis lengthening may preserve EF despite its abnormal direction and a fall in shortening. The increase in short-axis lengthening may be due in part to the reduction in LV sphericity after MVR.
