Methods Thirty-one stable, African-American outpatients with SCD (mean age 32±8 yrs) prospectively underwent CMR (Philips 1.5 Tesla) and TTE (Philips iE33). Retrospectivelygated cines of left ventricular (LV) 2-, 3-, and 4-chamber, and short axis cine stack were obtained using SSFP (temporal resolution 25-40ms). Late gadolinium enhancement (LGE) images of the same views were obtained 10-20 minutes after infusion of Gd-DTPA (0.15 mmol/kg) using phase sensitive inversion recovery (TR 4.5 ms, TE 2.2ms, TI 250-300 ms, flip angle 30°, PSIR flip angle 5°). Single short-axis, mid-ventricular myocardial T2* slice and coronal, hepatic T2* slice were acquired with a single breath-hold, at six echo-times (2.3 to 14 msec) using a gradient echo sequence. Tissue T2* signal intensity was measured in LV septum and liver at two separate echo times and T2*= ΔTE/ln (SITE2/ SITE1) where ΔTE represents time difference between the two echo times and ITE1 and ITE2 represent signal intensity at echo time one and two. Myocardial and hepatic T2* were abnormal if <20ms and <18ms, respectively. CMR LV volumes, ejection fraction (EF), and mass were calculated using method of disks and indexed for body surface area. The presence or absence of LGE was determined. Diastolic dysfunction (DD) was identified based on echocardiographic measurements including tissue Doppler (age adjusted E/A ratio) and left atrial volumes.
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