PURPOSE: To evaluate cardiac MRI (CMR) in the diagnosis of cardiac amyloidosis by comparing the T2 relaxation times of left ventricular myocardium in a pilot patient group to a normal range established in healthy controls. MATERIALS AND METHODS: Forty-nine patients with suspected amyloidosis-related cardiomyopathy underwent comprehensive CMR examination, which included assessment of myocardial T2 relaxation times, ventricular function, resting myocardial perfusion, and late gadolinium enhancement (LGE) imaging. T2-weighted basal, mid, and apical left ventricular slices were acquired in each patient using a multislice T2 magnetization preparation spiral sequence. Slice averaged T2 relaxation times were subsequently calculated offline and compared to the previously established normal range. RESULTS: Twelve of the 49 patients were confirmed to have cardiac amyloidosis by biopsy. There was no difference in mean T2 relaxation times between the amyloid cases and normal controls (51.3 +/- 8.1 vs. 52.1 +/- 3.1 msec, P = 0.63). Eleven of the 12 amyloid patients had abnormal findings by CMR, eight having LGE involving either ventricles or atria and four demonstrating resting subendocardial perfusion defects. CONCLUSION: CMR is a potentially valuable tool in the diagnosis of cardiac amyloidosis. However, calculation of myocardial T2 relaxation times does not appear useful in distinguishing areas of amyloid deposition from normal myocardium.
PURPOSE: To evaluate cardiac MRI (CMR) in the diagnosis of cardiac amyloidosis by comparing the T2 relaxation times of left ventricular myocardium in a pilot patient group to a normal range established in healthy controls. MATERIALS AND METHODS: Forty-nine patients with suspected amyloidosis-related cardiomyopathy underwent comprehensive CMR examination, which included assessment of myocardial T2 relaxation times, ventricular function, resting myocardial perfusion, and late gadolinium enhancement (LGE) imaging. T2-weighted basal, mid, and apical left ventricular slices were acquired in each patient using a multislice T2 magnetization preparation spiral sequence. Slice averaged T2 relaxation times were subsequently calculated offline and compared to the previously established normal range. RESULTS: Twelve of the 49 patients were confirmed to have cardiac amyloidosis by biopsy. There was no difference in mean T2 relaxation times between the amyloid cases and normal controls (51.3 +/- 8.1 vs. 52.1 +/- 3.1 msec, P = 0.63). Eleven of the 12 amyloid patients had abnormal findings by CMR, eight having LGE involving either ventricles or atria and four demonstrating resting subendocardial perfusion defects. CONCLUSION: CMR is a potentially valuable tool in the diagnosis of cardiac amyloidosis. However, calculation of myocardial T2 relaxation times does not appear useful in distinguishing areas of amyloid deposition from normal myocardium.
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