Left ventricular strain and peak systolic velocity: responses to controlled changes in load and contractility, explored in a porcine model

Abstract

Background: Tissue velocity echocardiography is increasingly used to evaluate global and regional cardiac function. Previous studies have suggested that the quantitative measurements obtained during ejection are reliable indices of contractility, though their load-sensitivity has been studied in different settings, but still remains a matter of controversy. We sought to characterize the effects of acute load change (both preload and afterload) and change in inotropic state on peak systolic velocity and strain as a measure of LV contractility.

Methods: Thirteen anesthetized juvenile pigs were studied, using direct measurement of left ventricular pressure and volume and transthoracic echocardiography. Transient inflation of a vena cava balloon catheter produced controlled load alterations. At least eight consecutive beats in the sequence were analyzed with tissue velocity echocardiography during the load alteration and analyzed for change in peak systolic velocities and strain during same contractile status with a controlled load alteration. Two pharmacological inotropic interventions were also included to generate several myocardial contractile conditions in each animal.

Results: Peak systolic velocities reflected the drug-induced changes in contractility in both radial and longitudinal axis. During the acute load change, the peak systolic velocities remain stable when derived from signal in the longitudinal axis and from the radial axis. The peak systolic velocity parameter demonstrated no strong relation to either load or inotropic intervention, that is, it remained unchanged when load was systematically and progressively varied (peak systolic velocity, longitudinal axis, control group beat 1-5.72 ± 1.36 with beat 8-6.49 ± 1.28 cm/sec, 95% confidence interval), with the single exception of the negative inotropic intervention group where peak systolic velocity decreased a small amount during load reduction (beat 1-3.98 ± 0.92 with beat 8-2.72 ± 0.89 cm/sec). Systolic strain, however, showed a clear degree of load-dependence.

Conclusions: Peak systolic velocity appears to be load-independent as tested by beat-to-beat load reduction, while peak systolic strain appears to be load-dependent in this model. Peak systolic velocity, in a controlled experimental model where successive beats during load alteration are assessed, has a strong relation to contractility. Peak systolic velocity, but not peak strain rate, is largely independent of load, in this model. More study is needed to confirm this finding in the clinical setting.

Figure 1

A representative pressure-volume measurement sequence during controlled load reduction by transient vena cava balloon occlusion is shown. This demonstrates that there are progressive beat-by-beat reductions in both pre- and post-systolic volumes and pressures, indicating systematic and progressive reduction in preload and afterload. The volumes and pressures for this measurement sequence are within the normal operating ranges for the heart and circulation.

Figure 2

End-diastolic and end-systolic volumes for the load alteration sequences are shown here, grouped by beat in the sequence. All the first beats are grouped together, all the second beats, etc. The change in load, as demonstrated by volumes for the sequences collected during experimental alteration in inotropic status, is clearly shown. These load ranges correspond to the grouped tissue velocity and strain measures in later figures. Data are presented as mean ± SEM, n = 13. Filled diamond = Control; Open triangle = Adrenaline; Open square = Beta-blockade. EDV = end diastolic volume; ESV = end systolic volume. # p < 0.05 with repeated measures ANOVA.

Figure 3

Peak systolic velocity (PSV) showed no change in PSV value during progressive load reduction for 5 of these 6 groups, and the decrease in PSV for the longitudinal axis measurement in the negative inotropy group was small. Data are presented as mean ± SEM, n = 13. Filled diamond = Radial projection; Open square = Longitudinal projection. # p < 0.05 with Repeated Measures ANOVA.

Figure 4

Systolic Strain. Systolic strain increased during load reduction in half the group, and notably for the negative inotropy groups. Data are presented as mean ± SEM, n = 13. Filled diamond = Radial projection; Open square = Longitudinal projection. # p < 0.05 with Repeated Measures ANOVA.

Figure 5

Tissue velocities, radial axis. This representative example shows the tissue velocities from the inferior/posterior left ventricular base, with aortic valve opening (AVO) and aortic valve closure (AVC) marked. Isovolumic contraction (IVC) and the peak systolic velocity (PSV) are also shown. Isovolumic relaxation (IVR) is sometimes a subtle finding, and early diastolic velocity (E’) and late diastolic velocity (A’) are marked. E’ was often difficult to identify during the whole preload reduction sequence, as load decreased. b. Tissue velocities from apical 4 chamber image, septal base region, signal from multiple beats during vena cava occlusion and adrenaline intervention. PSV coincides with the maximal velocities, which remain relative constant throughout the load reduction (see also progressively changing E’ and A’, which move to a fusion curve during the last beats in the sequence. The goal in signal acquisition (septum) was to be as close to the septal annulus as possible, though as illustrated here, occasionally, signal quality dictated that interrogation was performed a small distance from the annulus. This was accepted since the main findings involve relative changes from beat-to-beat over the load reduction sequence. c. Strain in the apical 4 chamber view. The values at zero represent zero deformation during diastole, and the peak systolic strain starts at values of approximately −45% (long axis shortening). In the radial axis, peak systolic strain is positive, starting from a diastolic zero deformation, since the ventricular wall thickens.