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.