![]() ![]() Two segmental strains peaking before end systole and having zero post systolic shortening are marked by blue arrows, while two segmental strains peaking after end systole and thus exhibiting post systolic shortening are marked by red arrows. Panel B shows four segmental strain curves dispersed in time and displayed as dashed lines, with their point-by-point average represented as a full black line. Time to peak interval, used to calculate mechanical dispersion index, and is represented by a broken arrow. If no regional post systolic strain present, its post-systolic strain index is 0. From these values, segmental post systolic strain index is calculated as: 100% × (maximum post-systolic strain–end-systole strain)/maximum post-systolic strain. Panel A shows a single time-delayed segmental strain curve with values of peak end-systole strain (global) and maximum post-systolic strain marked by arrows. Schematic representation of Strain curves demonstrating (a) method of calculation of segmental post-systolic shortening index and time to peak strain and (b) relationship between global mechanical dispersion index and post systolic strain index. ![]() However, there were significant variations in PSI measurements by software vendor especially in patients with pathological increase in LV wall thickness, suggesting that separate vendor-specific thresholds for abnormal PSI are required. PSI was greater in HCM and cardiac amyloidosis patients than controls, and a valuable tool for dyssynchrony evaluation, with moderate correlations to MDI and strain. Furthermore, there were moderate correlations between PSI and both MDI (r = 0.77) and left ventricular global longitudinal strain (r = 0.69). Variations between software vendors were significant in patients with pathologic increases in LV wall thickness (for HCM p = 0.03, for amyloidosis p = 0.008), but not in controls (p = 0.11). There was a significant difference in mean PSI among controls 2.1☐.6%, HCM 6.1☒.6% and cardiac amyloidosis 6.8☒.7% (p <0.001). PSI was measured using QLAB/aCMQ (Philips), QLAB/LV auto-trace (Philips), EchoPAC (GE), Velocity Vector Imaging (Siemens), and EchoInsight (EPSILON) software packages, and calculated as 100%×(post systolic strain-end-systole strain)/post systolic strain. This is a prospective cross-sectional study of 70 patients (36 hypertrophic cardiomyopathy, 18 cardiac amyloidosis and 16 healthy controls) undergoing clinically indicated echocardiography. We evaluated PSI by speckle-tracking echocardiography from several vendors in patients with increased left ventricular wall thickness, and associations with MDI. PSI measurement variability amongst software vendor and its relationship with mechanical dyssynchrony and mechanical dispersion index (MDI) remains unknown. Post-systolic shortening index (PSI) is defined as myocardial shortening that occurs after aortic valve closure, and is an emerging measure of regional LV contractile dysfunction. ![]()
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