T. Kono et al., MECHANISM OF FUNCTIONAL MITRAL REGURGITATION DURING ACUTE MYOCARDIAL-ISCHEMIA, Journal of the American College of Cardiology, 19(5), 1992, pp. 1101-1105
The mechanism and temporal manifestation of functional mitral regurgit
ation after acute myocardial ischemia were examined in eight dogs. Reg
ional ischemia was produced by selective microembolization of the left
circumflex coronary artery. Mitral regurgitation and regional left ve
ntricular wall motion abnormalities were evaluated with use of Doppler
color flow mapping and two-dimensional echocardiography, respectively
. Measurements were made at baseline (before embolization) and were re
peated at 30 min and 3 weeks after embolization. Mitral regurgitation
developed in all dogs 30 min after embolization and completely subside
d 3 weeks later. There was no evidence of mitral valve prolapse, mitra
l anulus dilation or left ventricular segmental dyskinesia at any time
during the study. Regional wall motion analysis showed only hypokines
ia of the left ventricular segment overlying the papillary muscle at 3
0 min with subsequent normalization of the segment at 3 weeks. Mitral
regurgitation was accompanied by an increase of the end-systolic dista
nce between the mitral anulus plane and the point of coaptation of the
mitral leaflets. This distance was 0.5 +/- 0.1 cm at baseline, increa
sed to 0.9 +/- 0.1 cm 30 min after the embolization (p < 0.001) and re
turned to near baseline (0.6 +/- 0.1 cm) 3 weeks after the embolizatio
n. These data indicate that mitral valve prolapse, mitral anulus dilat
ion and regional left ventricular dyskinesia are not necessary conditi
ons for the development of functional mitral regurgitation after acute
myocardial ischemia. Instead, hypokinesia of the ventricular segment
overlying the papillary muscle and leading to retraction of the mitral
leaflets toward the apex appears to be a sufficient condition for inc
omplete leaflet coaptation.