This study evaluates if MR-relaxometry of myocardial tissue reveals significant differences in cardiac amyloidosis (CA) compared with patients with systemic amyloidosis but without cardiac involvement (NCA) and a healthy control group. Therefore, we measured T1 and T2 relaxation times (RT) of the left ventricular myocardium with magnetic resonance imaging at 1.5 T.
Nineteen consecutive patients (14 males, 5 females; mean age, 59 ± 6.1 years) with histologically proven CA were evaluated. T1-RT and T2-RT were measured by using a saturation-recovery TurboFLASH sequence and a HASTE sequence, respectively. Additionally, morphologic and functional data were acquired. Results were compared with patients with systemic amyloidosis but without cardiac involvement (NCA; 5 males, 4 females, 48.9 ± 15.4 years) and 10 healthy, age-matched control subjects (5 males, 5 females, 60.4 ± 6.4 years).
MR-relaxometry revealed a significant elevation of T1-RT of the left ventricular myocardium in CA-patients compared with that in NCA-patients and the age-matched control group [mean ± SD (95% CI) 1340 ± 81 (1303–1376) msec, 1213 ± 79 (1160–1266) msec, 1146 ± 71 (1096–1196) msec, respectively; CA vs. control, P < 0.0001; CA vs. NCA:, P < 0.0003; NCA vs. control, P = 0.07].
T2-RT showed a marginal but significant increase in CA-patients compared with NCA-patients and the control group [mean ± SD (95% CI) 81 ± 12 (76–86) msec, 71 ± 11 (64–79) msec, 72 ± 9 (65–79) msec, respectively; CA vs. control, P = 0.04; CA vs. NCA, P = 0.04; NCA vs. control, P = 0.91].
T1-RT was best suited to discriminate between the groups as shown by logistic regression. A cut-off value of ≥1273 milliseconds for T1-RT was defined using receiver–operator characteristics-analysis to establish the diagnosis of CA with a high sensitivity (84%) and specificity (>89%).
Measurement of T1 and T2 RT is a novel approach for noninvasive evaluation of CA. MR-relaxometry might improve diagnostic reliability of magnetic resonance imaging for evaluation of cardiac involvement in systemic amyloidosis.
From the *Department of Radiology, University Hospital Heidelberg, Heidelberg, Germany; †Departments of Medical Physics and ‡Radiology, German Cancer Research Center, Heidelberg, Germany; §Department of Radiology, University Hospital Cologne, Cologne, Germany; ¶Departments of Haematology and Oncology; and ∥Departments of Cardiology, Angiology, and Respiratory, Medical University Heidelberg, Heidelberg, Germany.
Received October 22, 2006, and accepted for publication, after revision, March 9, 2007.
Reprints: Waldemar Hosch, MD, Department of Radiology, University Hospital Heidelberg, Im Neuenheimer Feld 110, 69120 Heidelberg, Germany. E-mail: firstname.lastname@example.org.