ABSTRACT
The purpose of the study is to investigate the variation in Hounsfield unit (HU) values calculated using dual-energy computed tomography (DECT) scanners. A tissue characterization phantom inserting 16 reference materials were scanned three times using DECT scanners [dual-layer CT (DLCT), dual-source CT (DSCT), and fast kilovoltage switching CT (FKSCT)] changing scanning conditions. The single-energy CT images (120 or 140 kVp), and virtual monochromatic images at 70 keV (VMI70) and 140 keV (VMI140) were reconstructed, and the HU values of each reference material were measured. The difference in HU values was larger when the phantom was scanned using the half dose with wrapping with rubber (strong beam-hardening effect) compared with the full dose without the rubber (reference condition), and the difference was larger as the electron density increased. For SECT, the difference in HU values against the reference condition measured by the DSCT (3.2 ± 5.0 HU) was significantly smaller (p < 0.05) than that using DLCT with 120 kVp (22.4 ± 23.8 HU), DLCT with 140 kVp (11.4 ± 12.8 HU), and FKSCT (13.4 ± 14.3 HU). The respective difference in HU values in the VMI70 and VMI140 measured using the DSCT (10.8 ± 17.1 and 3.5 ± 4.1 HU) and FKSCT (11.5 ± 21.8 and 5.5 ± 10.4 HU) were significantly smaller than those measured using the DLCT120 (23.1 ± 27.5 and 12.4 ± 9.4 HU) and DLCT140 (22.3 ± 28.6 and 13.1 ± 11.4 HU). The HU values and the susceptibility to beam-hardening effects varied widely depending on the DECT scanners.
Subject(s)
Phantoms, Imaging , Tomography, X-Ray Computed , Tomography, X-Ray Computed/methods , Image Processing, Computer-Assisted/methods , Radiation DosageABSTRACT
BACKGROUND: Abnormalities of the endocardial subvalvular apparatus (SVA), which includes the papillary muscles directly attached to the mitral leaflet and left ventricular apical-basal muscle bundles, are occasionally identified in hypertrophic cardiomyopathy (HCM). Their associations with left ventricular outflow tract (LVOT) obstruction are unknown. METHODS: We retrospectively reviewed cardiac computed tomography image data sets of 107 consecutive patients with HCM [56 obstructive (HOCM) and 51 non-obstructive (HNOCM)] as well as 53 controls. We evaluated anomalies of the SVA, measured the cross-sectional area of the SVA at the level of the LVOT, and subsequently assessed its correlation with the LVOT pressure gradient with and without medication. RESULTS: The area of the SVA was greater in HOCM than in HNOCM patients and in the control group (2.5 ± 1.3 cm(2), 1.4 ± 0.8 cm(2), and 0.9 ± 0.6 cm(2), respectively; p < 0.0001). Anomalies in the SVA were more often observed in the HOCM group than in the HNOCM patients and controls (abnormal papillary muscles, 14%, 8%, and 0%, respectively; P = 0.010; LV apical-basal muscle bundles, 73%, 65%, and 45%, respectively; P = 0.0094). Among HOCM patients, logistic regression analysis demonstrated that an SVA area of 2.2 cm(2) was an independent risk factor of residual severe LVOT obstruction (≥50 mmHg) after medication (odds ratio, 10.1; 95% confidence interval, 2.05-49.80). CONCLUSION: An increased area of the endocardial subvalvular apparatus could be an independent risk factor for clinically relevant LVOT obstruction refractory to medication.