Indices of Remodeling
IMR is a common complication of the
LV global or local pathological remodeling caused by acute and chronic
coronary artery diseases[2].
It often represents the pathological
result of increased tethering forces and decreased MV coaptation, which
finally leads to IMR[33]. IMR is common and
seriously affects the prognosis. Even mild IMR can have adverse effects
on survival. There is a strong grade relationship between IMR severity
and survival rate[34]. The full closure of the MV
leaflets is a balance between two opposing forces: the closing force of
the LV contraction and the tethering force of the chordae tendineae
(Figure 1 )[35]. IMR is in a
self-perpetuating cycle due to the imbalance caused by either a decrease
in the closing force or an increase in the tethering
force[36].
IMR occurs when the MV leaflets do not adequately cover the MV orifice
in systolic period. Two main mechanisms of IMR are generally accepted:
ischemic LV dysfunction and non-ischemic dilated cardiomyopathy. IMR
results from LV remodeling, which directly affects the spatial
relationship between LV and MV. This deformation finally affects the
leaflet coaptation and valve competency. The following mechanisms play
roles in the pathophysiology of IMR: 1. PM dysfunction: During systole,
PM contraction is important to keep the MV leaflets close in the LV. PM
ischemia can lead to hypokinesia and detectable
MR[37]. The anterolateral PM has a dual blood
supply, however, the posteromedial papillary muscle has a solitary blood
supply[38]. Because of the vascular anatomy of the
PM, the posterior PM is more susceptible to
ischemia[39]. 2. MA function: The MA enlargement
and flattening also contributes to the development of IMR. The abnormal
MA shape, and/or the loss of the saddle-shape, would result in increase
of the leaflet stress and abnormal leaflet
remodeling[40]. 3. Mechanical coordination of
systole: a loss of ventricular mechanical coordination after myocardial
infarction would decrease the closing forces during systole, which is
thought to be a factor in deteriorating IMR[41].
The disordered contraction of the LV
near the PM would increase the tethering
forces[42]. Dyssynchrony between atrial and
ventricular systole would generate diastolic
MR[43]. Due to the MR, the time required to reach
the maximal coaptation during acute ischemia is prolonged, which would
result in severe MR even during “early systole” and maximal
coaptation[44].
IMR is believed to initiate from LV remodeling caused by increased
diastolic wall stress and persistent increased end-systolic
volume[45]. The lateral and apical PM displacement
secondarily affects the MV coaptation, resulting in the valve
incompetence. In IMR, the tethering forces exerted by the chordae are
increased while the closing forces are reduced due to LV systolic
dysfunction. The PM displacement result from from a regional LV
remodeling or the global LV dilation after MI, so one or both PM can be
affected. When abnormal wall motion and local remodeling in a specific
region lead to adequate MV tethering to generate
IMR[46]. MV tethering is symmetric in the global
remodeling, while asymmetric tethering mainly occurs following localized
LV remodeling and mostly affects the posterior
PM[47].