LA deformation in ESRD
In accordance with previous studies, we found that LV dimension and wall thickness increased in ESRD compared to normal healthy groups, and hypertension was found in 81% of HD group. LV hypertrophy, diastolic dysfunction, and volume overload may lead to elevated LV filling pressure and LA afterload in patients with ESRD [10] Therefore, these alterations trigger a compensatory mechanism, which is characterized by dilating and the stretching of the atrial myocardium. This contributes to an enhanced LA emptying volume activation of the Frank-Starling mechanism, which is partially responsible for the maintenance of the stroke volume in ESRD patients. [4]
The dimension and volume of LA by 2D/3D echocardiography is significantly increased, while LAEF is decreased but in the normal range. The changes in the LA functional properties were accompanied by an increase in E/e’, ePCWP, PASP, and an decrease in E/A, velocities of the septal and lateral mitral annulus, peak A, which is an echocardiographic marker of LV dysfunction.
However, in the late stage of chronic renal diseases increases in the LA afterload results in LA remodeling, which is featured by increases in the LA wall thickness and focal collagen, as well as atrial myocardium fibrosis. LA remodeling is also associated with atrial interstitial fibrosis and cell hypertrophy, as well as impaired calcium uptake in the cardiomyocytes, which may contribute to the LA systolic and diastolic dysfunction [11][12][4] .With the deterioration of LA deformation, lung vessel compliance is reduced and vascular remodeling that can lead to right ventricular overload and dysfunction. [13]