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.