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First-Pass MR Imaging in the Assessment of Perfusion Impairment in Patients with Hypertrophic Cardiomyopathy and the Asp175Asn Mutation of the -Tropomyosin Gene¹

¹ From the Depts of Clin Radiology (P.S., H.M., H.J.A.), Medicine (K.P., P.J., M.L., J.K.), and Clin Physiology and Nuclear Medicine (M.H.S., J.T.K., E.V., T.L.), Kuopio Univ Hosp, Puijonlaaksontie 2, 70210 Kuopio, Finland; Niuvanniemi Hosp, Kuopio, Finland (J.T.K.); Dept of Radiology, Turku Univ, Turku, Finland (P.N.); and Dept of Radiology, Helsinki Univ Central Hosp, Helsinki, Finland (K.L., H.J.A.). From the 2000 RSNA scientific assembly. Received Nov 25, 2001; revision requested Feb 5, 2002; revision received Apr 8; accepted Jun 24. Supported by Kuopio Univ Hosp Research Grants 5063502 and 410K29, Helsinki Univ Central Hospital Research Fund Grant TYH0220, the Radiological Society of Finland, Orion Research Funds, the Ida Montin Foundation, and the Instrumentarium Science Foundation. Address correspondence to P.S. (e-mail: petri.sipola@kuh.fi).

View larger version (124K): [in a new window]   Figure 1. End-diastolic cine MR images (60/4.8, 20° flip angle, 10-mm section thickness, 219 x 250-mm field of view, and 110 x 256 matrix) (upper row) and turbo fast low-angle shot first-pass MR images (4.5/2.2/300, 8° flip angle, 10-mm section thickness, 250 x 250-mm field of view, and 128 x 128 matrix) (lower row). Anatomic features were evaluated on the end-diastolic cine MR images, and perfusion was evaluated on the turbo fast low-angle shot first-pass MR images. A in upper row shows location of anterior (AFW), lateral (LFW), and posterior (PFW) free walls and anterior (AS) and posterior (PS) septa on MR cine image. A in lower row shows location of corresponding segments on first-pass MR image. B in upper row shows measurement of LV wall thickness (white lines) on MR cine image. B in lower row shows corresponding regions of interest on first-pass MR image for the plotting of SI versus time curves. At the apical level, LV wall thickness was measured in the middle of septal and free wall segments (white lines on C in upper row), whereas the regions of interest covered the whole segments (white lines on C in lower row).

View larger version (28K): [in a new window]   Figure 2. Graph depicts data obtained in a 48-year-old man with the Asp175Asn substitution of the TPM1 gene but no hypertrophy at MR imaging. Time is displayed along the x axis, and myocardial SI is displayed along the y axis. The curved lines show the fitted power curves. The dashed line indicates SI change rate during at-rest imaging. The continuous line indicates SI change rate during adenosine stress MR imaging. During rest, the SI change rate (calculated as SI increaserest divided by trest) was 1.9 AU, and during stress, the SI change rate (calculated as SI increasestress divided by tstress) was 2.3 AU, resulting in an FPR value (calculated as SI change ratestress divided by SI change raterest) of 1.2.

View larger version (20K): [in a new window]   Figure 3. Scatterplot depicts the negative correlation between global FPR and maximal LV wall thickness in 17 patients with the Asp175Asn mutation of the TPM1 gene. Arrows indicate two patients with HCM who had moderate coronary artery disease.

View larger version (97K): [in a new window]   Figure 4. Images in a 22-year-old man with the Asp175Asn mutation of the TPM1 gene and extensive LV hypertrophy. Upper row: In a series of short-axis MR images of the LV at the papillary muscle level obtained during a breath hold with the patient at rest and during the first pass of 0.05 mmol/kg of gadopentetate dimeglumine with a turbo fast low-angle shot sequence (4.5/2.2/300, 8° flip angle, 10-mm section thickness, 250 x 250-mm field of view, and 128 x 128 matrix), the delay time for the arrival of the contrast agent in the LV blood is displayed in each image. There were no signs of impaired first-pass enhancement in this patient at rest. Lower row: A series of short-axis first-pass MR images of the same section obtained during adenosine stress shows that first-pass enhancement is widely impaired. The poorest enhancement was observed in the hypertrophied (25-mm) posterior septum (arrow), in which the FPR was 0.2.

View larger version (29K): [in a new window]   Figure 5. Scatterplot depicts the correlation between segmental FPR and LV wall thickness in 17 subjects with the Asp175Asn substitution of the TPM1 gene. Segmental FPR correlated inversely with segmental LV wall thickness (r = -0.389, P < .001).