Key result
Post-systolic shortening index was significantly higher in patients with hypertrophic cardiomyopathy (6.1%) and cardiac amyloidosis (6.8%) compared to healthy controls (2.1%), with significant measurement variations among software vendors in patients with increased wall thickness.
Why the study?
Post-systolic shortening index measurement variability among software vendors and its relationship with mechanical dyssynchrony and mechanical dispersion index remained unknown.
Does post-systolic shortening index (PSI) measured by echocardiography differ between patients with hypertrophied left ventricles and healthy controls, and does it vary by software vendor?
Cross-Sectional (n=70)
Single-blind
No
Does post-systolic shortening index (PSI) measured by echocardiography differ between patients with hypertrophied left ventricles and healthy controls, and does it vary by software vendor?
PSI is significantly elevated in patients with HCM and cardiac amyloidosis and correlates with mechanical dyssynchrony, but significant inter-vendor measurement variability necessitates vendor-specific thresholds.
Vendor variability in PSI measurement warrants caution in clinical interpretation of dyssynchrony; leaves open standardization needs for hypertrophic phenotypes.
BACKGROUND: 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. PSI measurement variability amongst software vendor and its relationship with mechanical dyssynchrony and mechanical dispersion index (MDI) remains unknown. We evaluated PSI by speckle-tracking echocardiography from several vendors in patients with increased left ventricular wall thickness, and associations with MDI. METHODS: This is a prospective cross-sectional study of 70 patients (36 hypertrophic cardiomyopathy [HCM], 18 cardiac amyloidosis and 16 healthy controls) undergoing clinically indicated echocardiography. 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. RESULTS: There was a significant difference in mean PSI among controls 2.1±0.6%, HCM 6.1±2.6% and cardiac amyloidosis 6.8±2.7% (p <0.001). 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). Furthermore, there were moderate correlations between PSI and both MDI (r = 0.77) and left ventricular global longitudinal strain (r = 0.69). CONCLUSION: 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. 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.
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Saijo et al. (2022) conducted a cross-sectional in Hypertrophic cardiomyopathy and cardiac amyloidosis (n=70). Pathological increase in left ventricular wall thickness (HCM or cardiac amyloidosis) vs. Healthy controls was evaluated on Mean post-systolic shortening index (PSI) (p=<0.001). Post-systolic shortening index was significantly higher in patients with hypertrophic cardiomyopathy (6.1%) and cardiac amyloidosis (6.8%) compared to healthy controls (2.1%), with significant measurement variations among software vendors in patients with increased wall thickness.
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