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.