Left atrial volume and function of uremic patients
Chronic renal failure is associated with a high incidence of morphological and functional changes in the heart. Cardiac insufficiency is a severe complication of uremia and a major cause of death of uremic patients. Therefore, assessment of heart function at an early stage is a key imperative in patients with uremia, which can guide timely treatment and prolong the patients' survival time. At present, research on patients with uremia at home and abroad is largely limited to the structure and function of the left ventricle [8]. LV diastolic dysfunction is a main manifestation of early cardiac changes in patients with uremia. Several factors such as electrolyte disturbances, renal hypertension and hypervolemia may induce LV stiffness and decrease in compliance. In addition, LV diastolic dysfunction increases left atrial load. To compensate for ventricular dysfunction and to maintain cardiac output, left atrium increases ejection by increasing both atrial pressure and atrial volume. Studies on hypertension and obesity have demonstrated that the changes in LA structure and function occur in the early stage of cardiac insufficiency [3, 9]. Therefore, evaluation of LA function in uremic patients may help in early detection of abnormal LV diastolic function before LV remodeling. In a study by Vaturi et al., LA function was shown to be related to the exercise capacity in patients with normal LV function [10]. Kokubu et al showed that LA strain rate decreases in patients with hypertension prior to the onset of LA enlargement or LV hypertrophy [3].
The left atrium plays many roles in the cardiac cycle. Firstly, the left atrium acts as a reservoir which receives blood from the pulmonary veins during ventricular diastole and systole. Secondly, left atrium acts as a conduit when blood is sucked into the left ventricle passively during early diastole. Finally, active contraction of left atrium in late diastole reflects the booster pump function [6, 11]. It is widely accepted that LAVmax, LAPEF and LAAEF represent the reservoir function, conduit function and booster pump function [12].
In this study, we observed that left ventricle systolic (LVEF) and diastolic (E/e) dysfunction in uremic patients deteriorated with progression of the NYHA functional class (Table 1). The increased pressure in LV end-diastole augmented the left atrial afterload. As a compensatory mechanism, the reservoir function of left atrium enhanced, which was reflected by the gradual increase in LAVmax in our study. Myocardial stiffness caused by uremia reduces the LV active suction capacity [13]. The decrease in LAPEF indicated that LA conduit function declined synchronously with the cardiac function. The increased residual blood in LA activated the Frank-Starling mechanism, as observed by the increased booster pump function in NYHA class II patients [14]. However, the effect of this compensatory mechanism gradually diminished with deterioration of cardiac function, which was reflected in the reduced LAAEF in NYHA class III and IV patients.
It is particularly noteworthy that, compared with the control group, increased LAV was detected in uremic patients with normal cardiac function (NYHA class I) at an early stage, although LAEF had not changed at this time. Previous studies have shown that left atrial enlargement is closely related to the occurrence of adverse cardiovascular events such as atrial fibrillation, ischemic stroke, heart failure, and can be used as an independent predictor of patient death [15, 16]. Aquaro et al. showed that left atrial remodeling can sensitively reflect left ventricular diastolic dysfunction [17].
Left atrial strain rate in uremic patients
Previous studies have shown that apart from conventional Doppler echocardiography, two dimensional STI can also be used to assess LA structure and function [18, 19]. The STI can track motional speckle consisting of 20–40 pixels in high frame rate two-dimensional images. Using this new, reliable technique to track speckles on the myocardium, we can obtain the strain rate, which reflects myocardial deformation. Strain refers to the ability of the myocardium to deform, that is, the percentage change in the length of the myocardium from its original length. 2D-STI allows for a more objective and accurate assessment of atrial function as it can distinguish LA motion from that of mitral annulus and ventricle [20]. STI offers an advantage over conventional echocardiography as it can discern subtle changes in the LA wall. Inaba et al. proposed that SRs reflect the reservoir function, while SRe reflects conduit function and SRa reflect the booster pump function on strain rate curve [21]. Changes in LA function in uremic patients can be objectively reflected in the strain rate curve of the left atrium.
In this study, we observed a steady decrease in SRs with progression from NYHA class I to NYHA class IV, which indicates that the stretchability of the atrial wall decreased with enlargement of left atrium. In addition, compared with the control group, we found abnormal SRs in uremic patients with NYHA functional class I. Synchronously, left ventricular stiffness led to ventricular diastolic dysfunction; therefore, SRe, the parameter that represents conduit function, also showed a significant decrease in uremic patients with poor cardiac function. SRa first increased and then decreased, which is consistent with the initial compensatory increase in active systolic function of left atrium followed by its weakening due to cardiac decompensation. Some studies have shown that abnormal myocardial deformation is related to myocardial fibrosis [22, 23].
Correlation between LA function and LA strain rate
Results of correlation analyses showed a strong correlation between LAVmax and SRs, between LAPEF and SRe, and between LAAEF and SRa (correlation coefficient r=-0.878, 0.862, 0.756, respectively). Strain rate is defined as the deformation of myocardium per unit time. The ability of myocardial deformation is an essential factor that influences cardiac systole and diastole. Moreover, the volume and emptying fraction of the left atrium are also affected by preload and afterload. The interaction of cardiac load (external factor) with myocardial motion (an internal factor) affects the volume and function of left atrium [24]. In short, there is a close relationship between LA function and LA strain rate.
Study Limitations
There were some inherent limitations in this study, including: First, this study focused only on uremic patients with normal sinus rhythm. Left atrial function and strain rate in patients with arrhythmia are yet to be explored. Second, Qlab software used to analyze the LS was originally designed for assessment of left ventricle. However, its use for evaluation of left artial strain has also been validated.