LA strain in ESRD
LV diastolic dysfunction generated volume and pressure overload, which
can result in LA dilation and increased pressure in ESRD patients on
regular HD, may lead to a sustained elevation in LV filling pressure.
Mitral E/A and E/e’ ratio used to evaluate LV diastolic dysfunction by
classical echocardiographers. However, they appeared late and showed
variations, depending on loading situations and other conditions, such
as heart rate, mitral regurgitation and so on. In addition, E/e’ may be
elevated in ESRD due to extracellular volume expansion.[2]
Similar to LV function, LA strain can evaluate early subclinical
functional changes in ESRD. LA volume and pressure overload lead to
myocardial fibrosis and compliance reduction, and then lead to left
atrial remodeling and left atrial systolic function reduction, affecting
the reduction of myocardial strain. Our research was concordant with
other studies. The difference is the method of calculating strain.
Previous studies have reported that LA strain analysis using speckle
tracking echocardiography is useful for assessing LA function [14].
3D-STI technology can track the motion track of myocardial ”spot” in 3D
space and construct 3D images of myocardial motion, including
longitudinal strain, circumferential strain and radial strain, but the
analysis of different phases is insufficient. At present, LA strain
calculation is based upon the length of different lines in each
anatomical direction during the three phases by 4D-LAQ.In addition, 4D
LAQ have brought new insights into particular situations, which
displayed LA myocardial volume and strain with high sensitivity and
repeatability.
The muscle fibers of LA are predominantly arranged in 2 layers: the deep
layer and the shallow layer. The shallow layer runs along the transverse
diameter. The deep layer contains two kinds of myocardium, longitudinal
and circular, which constitute the 3D spatial structure and complex
motion of the atrium. The LA strain parameters in this study are
longitudinal and circumferential strain with deep myocardial involvement
only, which undertakes the most of work and is related to the vendor.
During the cardiac cycle in normal subjects, the volume contribution of
ventricular filling (75-80%) mainly comes from the reservoir and
conduit phase, while 20-25% comes from atrial contraction. However, the
composition of these three phases has also been redistributed when
myocardial damage in ESRD. Reservoir function: In ESRD, the reduction of
LV relaxation and untwisting/reverse rotation possibly leads to elevated
LV filling pressure and LA pressure [15], resulting in impairment of
LA compliance and relaxation. In our study, the LA longitudinal and
circumferential strain during reservoir phase significantly decreased in
ESRD. Moreover, the longitudinal strain revealed a strong connection
with LV filling by multivariate analysis. Conduit function: The
progressive worsening of LV diastolic delay and compliance reduction, LA
remodeling, and diastolic function worsening leads to the reduction in
the conduit phase. In our study, the LA longitudinal and circumferential
strain during conduit phase showed decrease significantly in ESRD.
Moreover, the circumferential strain reveals a strong connection with LV
filling by multivariate analysis. Contraction function: The volume
contribution of LA contraction at first compensates for the decrease in
the early diastolic and diastasis phase. Lon-term exposure to
accelerated volume and pressure will eventually affect the function of
LA pump. Compared with the control group, our findings show that LA
longitudinal strain during the contraction phase in ESRD was reduced
while circumferential strain showed no significant change.
When LV diastolic function is impaired early/mild, the conduit flow is
reduced while flow increases during the reservoir and pump phase
[16]. With progressive worsening of diastolic function, three phases
volume increases. The reason may be that RAAS system is activated to
increase myocardial contractility, which is responsible for the
compensation and maintenance of adequate ventricular filling through
Frank-Starling mechanism. With the worsening of LA enlargement and LV
diastolic dysfunction, LA strain during the three phases decreased due
to the LA and LV now acting as one chamber [15]. In our study, the
early damage of LA strain occurred during the reservoir and conduit
phase, and contraction damage may be associated with abnormal systolic
function. In conclusion, the change of LA strain is earlier than LA
dimension and volume; that is, the change of function is earlier than
the structuration. Moreover, LASr and LAScd-c may be associated with LV
diastolic filling pressure, which is an echocardiographic marker of LV
dysfunction.