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]