Patients with chronic heart failure and a reduced ejection fraction commonly show evidence of functional mitral regurgitation (MR), which may result from two distinct pathophysiological mechanisms. 1 First, MR can occur primarily as a result of enlargement of the left ventricle, which leads to mitral annular dilatation and the tethering of the valve leaflets by displaced papillary muscles. Second, MR can be caused by left ventricular (LV) dyssynchrony due to a localized electrical or mechanical disturbance that leads to uncoordinated support of the valve leaflets during systole. Although the degree of MR may be mild and of little consequence, one-third of patients with chronic heart failure manifest severe MR, which is related to either LV enlargement or LV dyssynchony. 2
Identifying patients with disproportionate functional mitral regurgitationThe two mechanisms leading to functional MR can be distinguished in the clinical setting. 3 When the principal reason for MR is LV enlargement, there is a predictable relationship between LV end-diastolic volume (LVEDV) and the effective regurgitant orifice area (EROA), assessed by Doppler echocardiography. An EROA of 0.1-0.2 cm 2 can be expected when the LVEDV is 150-200 mL, whereas an LVEDV of 250-300 mL generally leads to EROA of 0.3-0.4 cm 2 (i.e. severe MR). A patient who has severe MR in association with an LVEDV of 250-300 mL has a regurgitant lesion that is proportionate to the LVEDV, i.e. the MR can be explained entirely by LV enlargement. In contrast, when the EROA is of 0.3-0.4 cm 2 but the LVEDV is only 150-200 mL, the degree of MR is much greater than expected from the LV chamber size; i.e. the MR is disproportionate to LV dilatation, typically because it is related to LV dyssynchrony. Thus, distinguishing between proportionate and disproportionate MR allows