A Preliminary Study On Left Atrial Function In Hypertension By Strain Rate Imaging

Objective: To explore the left atrial functional change in various hypertension classified by diastolic state in virtue of strain rate analyzing. Hence to interrogate the strain rate parameters indicated left atrial function change in different diastolic classification. By comparing strain rate parameters and traditional echocardiographic indices of left atrial function, discrepancies are expected to be found, and to discuss the meanings of the new parameters.Methods: 1 The study population is consisted of 54 hypertensive patients (54 men, 20 women) without other cardiac diseases and systemic disorders, and 15 age- and gender- matched normal volunteers (control group, 6 men, 9 women). All subjects were in sinus rhythm and showed no abnormalities on ECG. For all, grey-scale 2D echo images showed normal cardiac function on visual inspection. The hypertensives are further divided into 2 groups based on echocardiographic diastolic function classification: Group A, hypertensive with normal diastolic function; Group B, hypertensive with mildly impaired diastolic function. 2 The echocardiographic examinations were performed with a GE Vivid7 scanner equipped with a 3.4 MHz phased array transducer. For data acquisition, four complete cardiac cycles were collected and stored in a cine-loop format. Data were acquired with the subjects at rest, lying in the lateral supine position.General echocarduigraphic parameters were measured: end diastolic volume (EDV) and end systolic volume (ESV) and derived ejection fraction (EF) of the left ventricular; Blood pool pulsed Doppler recordings obtained from the mitral valve inflow were used to measure the following Doppler flow parameters: the peak velocity of E and A waves, the E/A ratio and the deceleration time of the E wave (DT). TDI spectral of the lateral mitral annulus were obtained, from which early diastolic mitral annulus velocity (E') were measured. The criterion of mildly impaired diastolic function was E/A<1. An E/E'<10 was used as the determinant of normal diastolic function in hypertensive with E/A≥1.From 2D echocardiography, in apical 4-chamber view, the Simpson method was used to calculate the following indices: (1) pre-atrial contraction LA volume (Vpre), (2) minimal LA volume (Vmin), (3) maximal LA volume (Vmax). All volume indices were adjusted by body surface area(BSA).For the assessment of the LA function two indicators derived from volumes were used: LA active emptying fraction (LAAEF)=(Vpre-Vmin)/Vpre; LA passive emptying fraction (LAPEF)=(Vmax-Vpre)/Vmax.Left Atrial Systolic Force(LASF) was calculated according to the equation LASF=0.5×ρ×MOA×A~2. Average diastolic mitral orifice area (MOA) was calculated by continuity equation with Doppler stroke volume at the aortic valve divided by time velocity integral at the mitral annulus. A is the peak velocity of the mitral valve A wave.ρis the density of the blood (1.06 g/cm3).LASF then were adjusted by BSA.The longitudinal strain rate (SR) and strain(ε) were measured in the posterior LA wall (from the apical 3-chamber view). The SR/εprofiles were extracted and analyzed using EchoPAC software. SR profile within the segment of the LA wall was obtained by manually tracking that segment during the cardiac cycle. The myocardialεprofiles were calculated by integrating the SR profiles over time and compensating for drifting over the cardiac cycle. The peak values for SR during the contractile and conduit phase and the peak value forεduring the contractile phase were measured.3 Results are reported as means±standard deviations or M(QR).The differentε/SR indicators for the longitudinal deformation of the LA wall were compared between the groups with ANOVA. Differences in continuous variables between 2 groups were assessed using the t-test or Mann-Whitney U test. Categorical variables were analyzed by the Chi-squared test. The Pearson correlation coefficient (r) was used to measure the strength of the association between the parameters. All data analysis was performed using statistical analysis software packages SPSS 12.Results: 1 All general parameters except blood pressure, E and A velocity, and DT were not different among the groups.2 All the volume indexes were not different between group A and the control group, while the indexes of the two groups were lower than group B (P<0.05).And the LASVi was similar with the volume indexes. LAAEF were higher in hypertensive groups than in control group (P<0.05), but similar in two hypertensive groups. In control group, LAPEF was highest, while group B the lowest, group A in the middle, the difference is significant (P<0.05), the result in LASFi was reversed (P<0.05).3 Though ESR in group A was inclined to decrease compared with control group, no difference was found (P>0.05).ASR in group A was inclined to increase compared with control group, no difference was found as well (P>0.05). In group B, both ESR and ASR were higher than other two groups (P<0.01). ASS was similar between group A and control group, but in group B it's higher than other two groups.4 In control group, ASR correlated with LASFi(r=0.604, P<0.05), ASS correlated with LASVi(r=0.796, P<0.01) and LAAEF(r=0.861, P<0.001).In contrast, when all participant are included, the strength of the associations between above parameters are weaker, but still significant. For ASR and LASFi, Pearson correlation coefficient was 0.525(P<0.001); LASVi and ASS, 0.65(P<0.001); LAAEF and ASS, 0.509(P<0.001).Conclusion: As indices of left atrial wall deformation, strain rate may reflect the myocardial contractility in certain context; while local strain associates closely with global volume change. SR/εimaging is a novel implement for assessing left atrial wall deformation, and can be adopted as a new way to interrogate left atrium function. Our results on left atrial functional change expressed by SR/εin hypertensive were consistent with previous reports. As indices of local deformation, SR/εare not completely agree with global function indices. These data may help in understanding left atrial physiology and hypertension pathophysiology.