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  • Title: [MR imaging in cardiac amyloidosis--morphology, function and late enhancement].
    Author: Hosch W, Libicher M, Ley S, Heye T, Schnabel P, Dengler TJ, Katus HA, Kauffmann GW, Kauczor HU, Kristen AV.
    Journal: Rofo; 2008 Jul; 180(7):639-45. PubMed ID: 18561066.
    Abstract:
    PURPOSE: Since limited data is available using MR imaging in cardiac amyloidosis, the purpose of our study was to evaluate morphological and functional differences of the heart using cardiac MRI. MATERIALS AND METHODS: 19 consecutive patients (14 males, 5 females, mean age 59 +/- 6 years) with histologically proven cardiac amyloidosis were evaluated with MRI at 1.5 T. Results were compared with data of 10 healthy, age-matched control subjects (5 males, 5 females, mean age 60 +/- 6 years). Functional and morphological data including late enhancement (LE) was acquired. RESULTS: Compared to the control group, patients with cardiac amyloidosis had thickened atrial walls and dilated atriums. Both ventricles and the interventricular septum were thickened. The LV hypertrophy was focal in 11 / 19 (58 %) and global in 4 / 19 (21 %) of patients. A myocardial edema occurred in 2 / 19 patients with cardiac amyloidosis (11 %). An edema of the myocardium was visible in 2 / 19 (11 %) of patients. The LV ejection fraction was statistically significantly decreased. The prevalence of LE was 74 % (14 / 19 of patients). LE was detected predominantly in the LV anterior wall and in the interventricular septum. Within the segments LE was located predominantly in a subendocardial location. Between patients with and without LE no statistically significant differences of functional and morphological results were able to be established. CONCLUSION: There are three major outcomes of our assessment: 1. The LV hypertrophy is focal in the majority of patients with cardiac amyloidosis. 2. No statistically significant differences can be established in regard to the functional and morphological features between patients with and without LE. 3. Myocardial edema is a possible feature in cardiac amyloidosis.
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