In patients with heart failure (HF) and left ventricular (LV) dilation, adverse LV remodeling
causes tethering of mitral valve (MV) preventing sufficient coaptation of normal leaflets and
resulting in functional MR. Because secondary functional MR usually develops as a result of
LV dysfunction, guideline-directed medical therapy for HF forms the mainstay of therapy.
However, beta blockers, angiotensin-converting-enzyme (ACE) inhibitors, and angiotensin
receptor blockers (ARB) fail to reverse adverse LV remodeling and functional MR, and the
morbidity and mortality of patients with functional MR remain high despite standard medical
therapy. Randomized trials to explore cardiovascular (CV) benefit of the sodium-glucose
co-transporter-2 (SGLT2) inhibitor have been performed and showed a significant reduction on
the risk of CV death or hospitalization for HF. However, its effect on cardiac structure and
function was not evaluated and further mechanistic studies are needed to interpret beneficial
clinical effects of the SGLT2 inhibitors. Based on studies demonstrating SGLT2 inhibitors'
favorable effects on LV modeling, investigators hypothesize that SGLT2 inhibitor,
ertugliflozin, is effective on improving MR in patients with functional MR secondary to LV
dysfunction and try to examine this hypothesis in a multicenter, double-blind, randomized
comparison study using echocardiography.