Cardiac magnetic resonance imaging in the evaluation of patients with hypertrophic cardiomyopathy

Figure 1.. CMR short axis diastolic cine-SSFP imaging of a 19-year-old male athlete, referred for suspected HCM. Once the crista supraventricularis (red arrow), moderating band (blue arrow) and false tendons (yellow arrow) were appropriately identified, it was corroborated that the septal thickness was only slightly increased (12 mm, white line).

Figure 2.. CMR imaging of different phenotypic expressions of HCM. A) Hypertrophic septal asymmetric cardiomyopathy. B) Asymmetric HCM with significant hypertrophy located exclusively in the inferior wall and in the lower portion of the interventricular septum. C) Asymmetric HCM with reversed septal contour. D) HCM with a focal hypertrophy in the basal segment of the anterior interventricular septum. E) Apical HCM. F) Diffuse HCM involving the anterior and inferior basal and middle walls. G) Asymmetric HCM with reversed septal contour. H) Mid-ventricular HCM with apical aneurism.

Figure 3.. Asymmetric septal HCM with obstruction of the left ventricular outflow tract. A) Black blood (spin echo) 3-chamber view. B) SSFP-cine 3-chamber view. C) Phase-contrast sequence demonstrating flow acceleration in the LVOT (orange coloured spectrum).

Figure 4.. 44 year-old female with asymmetric septal HCM, with reversed septal contour in a C-shape and extensive intramyocardial fibrosis.

Figure 5.. 64 year-old patient with asymmetric mid-ventricular HCM (2-chamber view).

Figure 6.. Hypertrophic septal asymmetric cardiomyopathy with apical obliteration and obliteration of the right ventricle (red arrows).

Figure 7.. Examples of LGE patterns (red arrows) of patients with HCM. A) Phenotype limited to the anterior interventricular septum, where a discrete patchy pattern of localized fibrosis is observed. B) Hypertrophy of the basal and medial segments with mesocardial fibrosis localized in the inferior wall. C) Diffuse involvement and significant mesocardial fibrosis in the areas of greater hypertrophy. In addition, important thinning and fibrosis in the apical level is observed. D) HCM with intense focal fibrosis at the level of the right ventricular insertion points in the interventricular septum. E) Almost transmural LGE at the level of the mid-anterior interventricular septum and very tenuous inferoseptal mesocardial enhancement. F) Marked mesocardial septal LGE and at the insertion points, as well as quasi-transmural mesocardial LGE in the lateral wall. G) Diffuse LGE in a patient with severe apical HCM, with an uneven distribution pattern. H) LGE with a subendocardial pattern in the inferolateral basal segment with wall thinning. Fibrosis is also observed in an apical aneurysm.

Figure 8.. Semi-automatic quantification of fibrosis using short-axis slices from base to apex, selecting 2 standard deviations of signal intensity to define LGE (pink zones). Fibrosis quantification: 32% of the total myocardial mass.

Figure 9.. Patient with asymmetric septal HCM. LGE and T1 mapping sequences were used to assess the presence of focal (arrows) and diffuse fibrosis. A) SSFP-cine-short axis view in contrast CMR. B) LGE-sequence-short axis view that shows the enhacement in the insertion points of the RV in IVS. C) T1 mapping sequence without contrast. T1 native in the focal fibrosis zone (white arrows) was 1240 ms (normal between 950 to 1050 ms). In the IVS but no focal fibrosis (gray arrow): 1126 ms and in non-hypertrophic zones: 1035 ms (blue arrow). D) T1 mapping sequence after contrast infusion. Shorter times in focal fibrosis zones.

Figure 10.. 46 year-old patient with obstructive HCM and apical implantation of the papillary muscles. A) Black blood (spin echo) 4-chamber view. B) SSFP-cine 4-chamber view. C) T1 mapping sequence showing the implant site of the tendinous cord. D) and E) Long axis and corresponding short axis view, in which the abnormal implantation of these muscle can be observed.

Figure 11.. LGE in a patient with end-stage mid-ventricular HCM. Left atrial fibrosis (red arrows) and fibrosis located in an apical aneurysm (green arrow) can be observed.

Figure 12.. Evaluation of longitudinal and transverse myocardial strain using feature tracking in a patient with HCM. A) Cine-SSFP 4-chamber view of a patient with predominantly septal hypertrophy (green arrow). B) Longitudinal strain obtained from cine-SSFP in 3-chamber, 2-chamber and 4-chamber views. Longitudinal strain is expressed in percentage as a negative value, the myocardial deformation is lower as the value approaches 0. Note the significant decrease in the septal deformation (green arrow). C) Transverse strain obtained from cine-SSFP in short axis basal, middle and apical slices. Transverse strain is expressed in percentage as a positive value, transverse myocardial deformation is lower as the value approaches 0. Note in this case also the significant decrease in septal deformation (green arrow).