From the Guidelines

Mitral regurgitation (MR) typically increases left ventricular ejection fraction (LVEF) in the early stages of the disease.

In chronic, severe, primary MR, the pure volume overload on the left ventricle (LV) results in eccentric hypertrophy and LV dilation, which augments LV ejection fraction (EF), making it typically supranormal 1.
The increased preload, combined with low-to-normal afterload, contributes to the increased LVEF 1.
However, as the LV dilates, LV wall stress increases, and incipient and irreversible myocardial dysfunction may occur with longstanding LV volume overload 1.
It is essential to note that EF is a load-dependent measure of LV systolic function, and it can be preserved even as myocardial contractile function begins to decline 1.

Current clinical practice guidelines recommend surgical intervention in asymptomatic patients with primary MR and LVEF <60% or LV end-systolic dimension >40 mm 1.
The presence of any degree of secondary MR is associated with worsened prognosis in patients with ischemic or nonischemic cardiomyopathy 1.
In patients with severe MR, the LVEF may be supranormal due to the low-impedance ejection pathway, making the assessment of LV muscle contractility difficult 1.
LV systolic dysfunction in subjects with MR is defined as LV ejection fraction <60% or LVESD >40 mm 1.

From the Research

Mitral regurgitation (MR) is generally believed to create a systolic 'unloading' effect, which can increase the left ventricular ejection fraction (LVEF) 2.
However, studies have shown that chronic MR is not associated with an unloading effect, and calculated values for circumferential and meridional wall stress were found to be normal or high in patients with chronic MR 2.
In patients with decompensated MR, systolic wall stress tends to increase after mitral valve replacement (MVR), which can contribute to a postoperative decline in myocardial fibre shortening and a lower LVEF 2.
In contrast, patients with compensated MR exhibit a decline in systolic wall stress after MVR, but the valve replacement can still cause a postoperative decline in fibre shortening and LVEF 2.
Other studies have found that LVEF may not adequately detect a reduction in left ventricular systolic performance resulting from chronic MR, due to ventricular unloading into the low-impedance left atrium 3.
Additionally, LVEF was found to be normal in MR patients, despite an increase in left ventricular end-systolic volume index, and LV end-systolic pressure-volume and stress-volume ratios in MR patients were lower than in controls 3.

Speckle-tracking global longitudinal strain (GLS) has been shown to detect further impairment in left ventricular systolic function in patients with severe secondary MR, even when LVEF is comparable to patients without MR 4.
Patients with severe MR had significantly lower forward ejection fraction and more impaired GLS compared to patients with no or mild MR, despite similar LVEF 4.
The presence of severe secondary MR was significantly associated with worse LV GLS, suggesting that GLS may be a more sensitive measure of left ventricular systolic function than LVEF in patients with MR 4.
Another study found that contractile function is impaired in some patients with long-term MR and a normal LVEF, and that an earlier consideration of mitral valve surgery may be warranted to preserve contractile function in these patients 5.
The study also found that LVEF can decrease after MVR, even in patients with compensated MR, and that this decrease is not solely due to increased systolic loading 5.