Objectives: The aim of this work was to characterize patterns of late gadolinium enhancement (LGE) by cardiovascular magnetic resonance imaging in a hemodialysis population at high risk for cardiovascular events.
Background: The prevalence and distribution of LGE and its relationship to left ventricular mass (LVM) and function in this population is unknown.
Methods: Chronic hemodialysis patients at high risk for cardiovascular events-age >50 years, diabetes, or known cardiovascular disease-were enrolled prior to concerns regarding nephrogenic systemic fibrosis. Cardiovascular magnetic resonance imaging was performed in 24 patients (age, 59 +/- 11 years; dialysis, 45 +/- 38 months) and included steady-state free precession cine imaging and late gadolinium-enhanced, phase-sensitive, inversion-recovery gradient echo images. Left ventricular mass, volumes, and function were calculated and indexed to body surface area. A 16-segment analysis was performed to calculate percentage of LGE, LV wall thickness, and percentage of wall thickening.
Results: Left ventricular ejection fraction was 48 +/- 15%, and the LV mass index was 100 +/- 52 g/m(2). Late gadolinium enhancement was observed in 79% (19 of 24) of patients in 3 distinct patterns: infarct-related (32%, 6 of 19), diffuse (37%, 7 of 19), and focal noninfarct (37%, 7 of 19). Late gadolinium enhancement constituted 15 +/- 18% of the LVM and correlated with LVM (r = 0.44, p = 0.03). A significant, inverse relationship existed between segmental LGE and the percentage of wall thickening (p > 0.0001). Excluding infarct-related segments, as end-diastolic wall thickness increased, so did LGE (p < 0.0001), and as LGE increased, the percentage of wall thickening decreased (p = 0.0012). After 23 +/- 3 months of follow-up, 1 patient had developed nephrogenic systemic fibrosis. Seven of the patients (29%) had developed a hard cardiovascular event, 5 of 19 (26%) with LGE and 2 of 5 (40%) without.
Conclusions: Late gadolinium enhancement is prevalent in the hemodialysis population and its extent is related to LVM. Most cases of LGE are not infarct-related and are associated with hypertrophied, dysfunctional LV segments. Non-infarct-related LGE may signify fibrosis from LV hypertrophy and/or an infiltrative process. Further studies in this patient population will not be possible due to the risk of nephrogenic systemic fibrosis.