Introduction
Functional (or secondary) mitral regurgitation (FMR) traditionally refers to the incompetency of a structurally normal mitral valve (MV) that derives from geometrical or electrical abnormalities of the left cardiac chambers, displacement of papillary muscles (PM), leaflet tethering (Carpentier type IIIb), and annular dilatation (Carpentier type I). 1,2 Unlike primary mitral regurgitation (MR), wherein components of the leaflets or apparatus are the source of the disease, FMR is more common and hemodynamically significant in patients after acute myocardial infarction (AMI) and in patients with all subgroups of systolic heart failure (HF)–be it with preserved, mid-range, or reduced ejection fraction (EF).1-5 This prevalence is expected to rise exponentially over the next few decades due to the aging population and the increasing survival of patients with ischemic heart disease or HF.2-4
Despite this prevalence and the consensus that FMR portends poor prognosis, only 5-22% of patients with isolated FMR undergo interventional treatment,5,6 and the optimal choice of treatment for FMR remains controversial within the cardiology and cardiac surgery community.7-9 Firstly, a large proportion of these FMR patients have multiple comorbidities and increased operative risks, with about 40-50% of patients responding favorably to guideline-directed medical therapy (GDMT) or cardiac resynchronization therapy (CRT) alone.2,3,5 Secondly, although surgical or transcatheter interventions targeting MV may improve symptoms and quality of life, a substantial mortality benefit has not been demonstrated.10-16 Thirdly, for surgical candidates with FMR, MV repair (usually with a down-sized annuloplasty ring) that enhances leaflet coaptation and preserves sub-annular apparatus has long been the preferred approach, this approach nevertheless has failed to achieve pre-specified benefits on cardiac geometry and long-term MV competency due in part to ongoing leaflet tethering caused by continued left ventricle (LV) remodeling, in spite of annular size reduction. Although mitral replacement could provide durable FMR correction results, it makes little sense to routinely replace “structurally normal” valves with artificial prostheses.17 Accordingly, the questions that have befuddled cardiac surgeons are: (1) If FMR is the consequence of LV dilatation and dysfunction, can surgical interventions that target the MV still be effective in certain patients? (2) How to select the right patients that would authentically benefit from surgical repair? and (3) What are the optimal surgical repairing techniques for these FMR patients?
Presenting an update of several recent studies on pathophysiology and mechanical interventions of FMR, this article aims to deepen our understandings of surgical strategies and outcomes of this challenging entity, and to provide insights in guiding the most appropriate surgical strategies for selective patients.