Objective: The aim of this study was to evaluate the effect of volume overload on left ventricular myocardial contractility using strain and strain rate imaging. We could analyze the possible mechanisms of their dependence on loading conditions and provide objective evidence for accurate selection of surgical operation.Methods1 The subjects included 44 patients with LV volume overload (patient group, male 29 and female 15 with a mean age of 30.5?4.8 years) and 45 age- and gender- matched normal volunteers (control group, male 26 and female 19 with a mean age of 30.8?3.7 years). In the patient group, 21 patients were treated with surgery and echocardiography follow-up was done 3 months after operation.2 A color Doppler ultrasonic system (GE Vivid 7) and 2-5MHz transducer equipped with Echo Pac workstation, tissue velocity imaging (TVI) and strain rate imaging (SRI) analysis software was used.3 All echocardiography studies were performed with the subjects lying in the lateral decubitus position in connectionwith electrocardiogram. Real-time 2D TVI data were recorded with 3 continuous beats in 3 standard apical views: 4-chamber, 2-chamber, and long-axis view at a high frame rate of ^100 frames/s. The TVI data were stored in hardware for off-line analysis in Echo Pac.4 Then the machine was shift to SRI condition and froze in the end-diastole (at the ECG R-peak). Analysis was performed in mid-septal and mid-lateral walls in the apical 4-chamber view, in mid-inferior and mid-anterior walls in the apical 2-chamber view, and in mid-posterior and mid-anteroseptal walls in the apical long-axis view (sample volume is 10mm). We obtained all the walls SR curves (figure 1), and recorded the peak systolic strain rate (PSSR) in every cardiac cycles, the wall's PSSR were averaged over 3 consecutive cardiac cycles. Strain curve was obtained by integrating the mean strain rate values over time, it's only one negative peak (figure 2), and we can obtain the peak systolic strain (PSS) value.5 Left ventricular end-diastole volume (LVEDV) was obtained by two-plane Simpson method and LVEDV index (LVEDVI) was obtained by normalized LVEDV with surface body area. According to normal range of LVEDVI from control group and the American Heart Association's standard about LV significant augmentation, we divided the patients to three groups: LVEDVI normal group (LVEDVI^60ml/m2, male 5 and female 5 with a mean age of 31.22?1.05 years); LVEDVIaugmentation group (LVEDVI were between in 60 and 80 ml/m2, male 6 and female 4 with a mean age of 31. 4?18. 81 years); LVEDVI significant augmentation group (LVEDVI^ 80 ml/m2, male 18 and female 6 with a mean age of 29.79?4.73 years). The above data were also achieved in control group and the patients after surgery 3 months. Results1 The LV mean PSSR value and PSS value were obtained by averaging the left ventricle's six walls PSSR value and PSS value because no significant difference was found in the six walls data (table 1).2 LVEDVI normal group and LVEDVI significant augmentation group in LV mean PSSR value and PSS value compared to control group were no significant difference (P>0.05). But the LVEDVI augmentation group was significantly higher in LV mean PSSR value and PSS value than in control group, LVEDVI normal group and LVEDVI significant augmentation group (P<0.05). LVEDVI normal group and LVEDVI significant augmentation group were no significant difference in LV mean PSSR value and PSS value (table 2).3 LV mean PSSR value in LVEDVI normal group and LVEDVI correlation was positive significant (r=0.8, PO.05). LV mean PSSR value in LVEDVI augmentation group and LVEDVI correlation was no significant (r=0.46, P>0.05). LV mean PSSR value in LVEDVI significant augmentation groupand LVEDVI correlation was negative significant (r=-0.72, PO.01). The LV mean PSSR value and LVEDVI correlation can see their scatter-plot chart. We found when LVEDVI^ 80ml/m2, LV mean PSSR value was increasing with...
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