PURPOSE: To perform myocardial T1 mapping pre- and post-gadolinium (Gd) administration and determine the volume of distribution of Gd (VdGd ) in patients with cardiac amyloidosis to assess extracellular space expansion from amyloid protein deposition. MATERIALS AND METHODS: T1 mapping was performed before contrast and 20 minutes following bolus administration of 0.15 mmol/kg of gadopentetate dimeglumine (Magnevist) in five subjects with cardiac amyloidosis and in eight healthy volunteers using previously validated 3-5 Modified Look-Locker Inversion (MOLLI) pulse sequence. The partition coefficient (λ) and VdGd were determined and compared between groups. RESULTS: Before contrast the T1 of the blood and myocardium are longer in amyloidosis as compared to controls (1665 vs. 1509 msec; P = 0.03 and 1144 vs. 963 msec; P < 0.001, respectively). Postcontrast blood T1 was also significantly longer in amyloidosis (486 vs. 408 msec; P = 0.003) with a trend towards shorter T1 in the myocardium (503 vs. 544 msec; P = 0.15). The VdGd was 83% higher in amyloidosis than in controls (0.51 vs. 0.28; P = 0.005). CONCLUSION: Myocardial VdGd is markedly increased in cardiac amyloidosis, reflecting the increased extracellular space occupied by amyloid proteins. The precontrast T1 of blood and myocardium are increased in amyloidosis extending diagnostic utility in patients who cannot receive Gd.
PURPOSE: To perform myocardial T1 mapping pre- and post-gadolinium (Gd) administration and determine the volume of distribution of Gd (VdGd ) in patients with cardiac amyloidosis to assess extracellular space expansion from amyloid protein deposition. MATERIALS AND METHODS: T1 mapping was performed before contrast and 20 minutes following bolus administration of 0.15 mmol/kg of gadopentetate dimeglumine (Magnevist) in five subjects with cardiac amyloidosis and in eight healthy volunteers using previously validated 3-5 Modified Look-Locker Inversion (MOLLI) pulse sequence. The partition coefficient (λ) and VdGd were determined and compared between groups. RESULTS: Before contrast the T1 of the blood and myocardium are longer in amyloidosis as compared to controls (1665 vs. 1509 msec; P = 0.03 and 1144 vs. 963 msec; P < 0.001, respectively). Postcontrast blood T1 was also significantly longer in amyloidosis (486 vs. 408 msec; P = 0.003) with a trend towards shorter T1 in the myocardium (503 vs. 544 msec; P = 0.15). The VdGd was 83% higher in amyloidosis than in controls (0.51 vs. 0.28; P = 0.005). CONCLUSION: Myocardial VdGd is markedly increased in cardiac amyloidosis, reflecting the increased extracellular space occupied by amyloid proteins. The precontrast T1 of blood and myocardium are increased in amyloidosis extending diagnostic utility in patients who cannot receive Gd.
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