Discussion
As a subtype of CHD, TVD is more serious than single-vessel and
double-vessel disease, which has a higher incidence of cardiovascular
events and
mortality[10]. The
LVEF is the most common parameter to evaluate myocardial systolic
function[11], but
relevant studies have shown that the sensitivity of it is poor in
detecting mild myocardial dysfunction which can be is detected
quantitatively by measuring ventricular wall
deformation[12].
Speckle tracking is a new echocardiographic technique developed in
recent years. At present, 2D-STE has been widely used in clinical and
experimental
research[13,14].
But the limitation of 2D-STE is that the tracking of myocardial acoustic
spots is limited to the two-dimensional section, which makes it
untraceable when some of the spots move completely outside the
two-dimensional section. The
3D-STE overcomes
the‘out-of-plane’phenomenon of 2D-STE in
scanning[15,16].
It can quantitatively evaluate the deformation of regional myocardium in
all directions, and reflect motion and function of myocardium in
three-dimensional space more realistically and
accurately[17,18].
Crosby et al[19]study on local myocardial function using speckle tracking technology
shows that 3D-STE can accurately identify the myocardium with local
myocardial dysfunction.
In our study, the LV structure of the group B was no obvious difference,
and LVEF was also within the normal range compared with group A.
However, the group C had larger LV volume and lower LVEF than those in
other two groups. The left ventricular structure and LVEF can remain
normal in group B, because the motion of myocardium in the ischemic
region may be compensated by adjacent region myocardium. With the
deterioration of disease, insufficiency of myocardial blood supply can
cause ischemia, hypoxia and abnormal energy metabolism of myocardial
cell, and even the loss of myocardial cell, and which further develops
into diffuse myocardial fibrosis. Progressive aggravation of myocardial
load gives rise to LV dilatation and increase of myocardial oxygen
consumption which exacerbates the vicious cycle of myocardial overload
and LV dilation, eventually leading to heart
failure[20]. Kane
et al [21] have
shown that the decrease of LV diastolic function is earlier than that of
systolic function in patients with CHD. Our study evaluated LV diastolic
function in line with the guideline issued by the American society of
echocardiography in
2016[22], which
proved that the LV diastolic function was decreased in group B and group
C. This is consistent with the results of Rydberg et
al[23], indicating
that LV diastolic function is closely related to the degree of coronary
artery stenosis. Due to TVD, the myocardial blood and energy supply is
insufficient leading to the decrease of LV diastolic dysfunction, which
is earlier than the change of systolic dysfunction in group B. With the
aggravation of TVD, the degeneration and necrosis of the myocardium can
result in fibroplasia and scar formation. Ultimately, myocardial
compliance is reduced and ventricular diastolic function is impaired.
The myocardium of the LV is divided into three layers: the inner layer
of the right hand spiral, the middle layer of the ring spiral and the
outer layer of the left hand
spiral[24,25].
Due to the orientations of myocardial fibers are different, its movement
directions are also different. When the inner layer and outer layer
myocardial fibers contract, there is movement in the direction of the
long axis, and when the middle layer myocardium contracts, there is
movement in the direction of the short axis. GLS, GCS and GRS
respectively represent the myocardial deformation in the longitudinal,
circumferential and perpendicular directions of endocardium. In
addition, GAS is a new
parameter[26,27],
which is the integration of GLS and GCS, and it represents the area
change rate of endocardium. Longitudinal motion of myocardium is mainly
determined by the myocardium fibers in the inner layer, and
circumferential and radial motion are determined by the myocardium
fibers in the middle
layer[28,29].
Our study found that the GLS in groups B and C were obviously diminished
compared to control group, and the changes were statistically
significant. Blood supply to the endocardium comes from the vessels at
the end of the coronary artery and studies have shown that change of GLS
is dominated by the endocardial
myocardium[30]. So
the endocardium is more sensitive to ischemia and hypoxia when the
patients with TVD have myocardial ischemia, which means that GLS has
changed under normal conditions of
LVEF[31]. If
stenosis rate of TVD further aggravates leading to the overload of
cardiac and the enlargement of cardiac, the decrease of GLS is more
significant. In our study, it was found that the GCS in groups B and C
were obviously lower than that in control group(P<0.05). The
pericardial contraction of the short axis of the cardiac is mainly
caused by the movement of the middle layer, and the inner layer is also
involved. Generally, myocardial ischemia gradually expands from the
endocardium to the
epicardium[32], so
when myocardial ischemia and hypoxia occur, the inner layer and the
middle layer of myocardial segments are affected, resulting in reduction
of GCS. GRS represents the thickness of the ventricular wall and the
change of the LV volume from the LV short axis
view[33]. In our
study, the reduction of GRS in groups A and B were not statistically
significant. It might be because the radial movement is closely related
to the annular middle layer, and the had not completely involved the
middle layer of the myocardium in this study. Furthermore, the radial
thickening of ventricular wall is the result of the interaction of cross
fibers between different myocardial layers and the inner and outer
myocardium fibers perpendicular to fiber orientation. The strains of
endocardial and epicardial myocardium fibers are similar in the
orientation of parallel myocardial fibers, while it contributes less to
GRS in the orientation of perpendicular to myocardial fibers. In the
group C, GRS was obviously decreased compared with the other two groups.
It showed that the further development of the disease had affected the
middle layer, which was consistent with the research results of Winter
et al[34]. As a
specific indicator of 3D-STE, GAS is the integration of GLS of the
ventricular long axis and GCS of the ventricular short axis, so the
significant reduction of GAS can better assess the cardiac systolic
dysfunction in patients with TVD.
NT-proBNP is produced by the hydrolysis of proBNP which can produce BNP
at the time, and NT-proBNP may be more specific to cardiac activity than
BNP[35]. Studies
have confirmed BNP may be actively degraded in peripheral blood, so the
test of NT-proBNP is more
reliable[36].
NT-proBNP, as a polypeptide neurohormone, is mainly synthesized and
secreted by ventricular
myocytes[37]. In
recent years, more and more attention has been paid to the diagnostic
and prognostic of BNP in patients with different clinical types of
CHD[38-40]. Some
studies have showed the change of serum NT-proBNP closely related to
myocardial ischemia and hypoxia. When the systolic function of cardiac
is abnormal, the ventricular volume load increases and the ventricular
wall is pulled, causing the synthesis and release of
NT-proBNP[41]. Our
results showed the level of NT-proBNP was distinctly difference among
the three groups. NT-proBNP of group C was highest among of three
groups. It was due to the severe stenosis of the TVD result in ischemia
of cardiomyocytes and LV systolic dysfunction, which stimulates the
synthesized and secreted of NT-proBNP by ventricular myocytes. In group
C, the study demonstrated each 3D-STE strain parameter were negatively
correlated with NT-proBNP. And the correlation analysis also
demonstrated GLS was negatively correlated with NT-proBNP in group B.
Therefore, the level of serum NT-proBNP is consistent with the 3D-STE in
the evaluation of LV systolic function in patients with TVD.