Myocardial contractility by strain echocardiography: Comparison with physiological measurements in an in vitro model

Strain echocardiography (SE) provides the rate and extent of myocardial segment shortening and lengthening. Thus we hypothesized that SE will noninvasively provide estimates of shortening velocity (SV) and length change (δL). We compared SE-derived strain rate (SR) and strain (ε) to force/length transducer-derived SV and percent 8L in isolated muscle strips at multiple load levels and under varying conditions. Electrically stimulated contractions in left ventricular muscle strips (n = 20) were simultaneously recorded with a force/length transducer (to measure SV and percent 8L) and an ultrasound transducer (to measure SR and ε). Measurements were made at baseline, after inotropic stimulation, and during hypoxia at multiple load clamp levels (simulating multiple levels of afterload). Despite a difference in absolute numbers, there was a close correlation between SR and SV at baseline (R² = 0.95), with dobutamine treatment (R² = 0.99), and during hypoxia (R² = 0.99). SR was load dependent at baseline (r = 0.98), with dobutamine treatment (r = 0.99), and during hypoxia (r = 0.92). Similarly, there was a close correlation between ε and δL at baseline (R² = 0.99), with dobutamine treatment (R² = 0.96), and during hypoxia (R² = 0.87). Percent ε was load dependent at baseline (r = 0.98), with dobutamine treatment (r = 0.98), and during hypoxia (r = 0.94). Bland-Altman analysis revealed a systematic overestimation of SV by SE-derived SR at baseline and with dobutamine treatment. There was no bias with SR measurements during hypoxia or with ε measurements. SE closely tracks standard physiological parameters of regional contractile function, such as SV and δL, under conditions of varying afterload.