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Noninvasive Cardiac Imaging in Patients With Hypertrophic Cardiomyopathy

Department of Cardiology, The Methodist DeBakey Heart Center, The Methodist Hospital, Houston, Texas.

View larger version (68K): [in this window] [in a new window] [Download PPT slide]   Figure 1 (A) Asymmetric septal hypertrophy; (B) concentric hypertrophy; (C) apical hypertrophy.

View larger version (92K): [in this window] [in a new window] [Download PPT slide]   Figure 2 (Upper left) Mitral left ventricular (LV) inflow; (upper right) pulmonary venous flow; (lower left) tissue Doppler velocities at lateral side of mitral annulus; (lower right) tricuspid regurgitation (TR) jet by continuous wave (CW) Doppler. Mitral inflow is pseudonormal (E/A ratio of 1), and systolic/diastolic (S/D) velocity (and time velocity integral) ratio >1 in the pulmonary veins. However, atrial reversal (Ar) velocity in pulmonary venous flow is increased both in amplitude and duration, indicating increased LV end diastolic pressure. The early diastolic (Ea) velocity is reduced and Ea/ late diastolic (Aa) velocity ratio is <1, indicating abnormal LV relaxation. The E/Ea ratio is increased to 12.5, indicating increased LV pre-A pressure. Peak TR velocity = 2.8 m/s, indicating an RV and pulmonary artery (PA) systolic pressure of at least 31 mm Hg.

View larger version (57K): [in this window] [in a new window] [Download PPT slide]   Figure 3 (Left) Flail segment of posterior mitral leaflet. (Right) Color Doppler with eccentric mitral regurgitation jet directed antero-medially. LA = left atrium.

View larger version (67K): [in this window] [in a new window] [Download PPT slide]   Figure 4 (Left) Transesophageal echocardiography of left ventricular outflow tract showing sub-valvular membrane (arrow). (Right) Continuous wave signal of abnormal flow. Note the early peaking with a gradient of almost 100 mm Hg and the presence of aortic regurgitation. Both are unexpected with dynamic obstruction. AV = aortic valve; LA = left atrium; LV = left ventricle.

View larger version (50K): [in this window] [in a new window] [Download PPT slide]   Figure 5 (Left) Apical long-axis view after opacification of septal base with radiographic contrast in the course of alcohol septal ablation. (Right) Color Doppler showing the site of flow acceleration in relation to the opacified septal base.

View larger version (100K): [in this window] [in a new window] [Download PPT slide]   Figure 6 Septal and lateral base function by Doppler strain–time curves, after alcohol injection. Systolic compression is present in the lateral wall, but the base of the septum is dysfunctional. The arrow points to post-systolic compression, which is not uncommon in hypertrophic cardiomyopathy and seems related to abnormal loading conditions and possibly ischemia.

View larger version (51K): [in this window] [in a new window] [Download PPT slide]   Figure 7 (A) Parasternal long- and short-axis views and tissue Doppler (TD) velocities at lateral and septal side of mitral annulus, from a 20-year-old subject carrying a known mutation for hypertrophic cardiomyopathy. Left ventricular hypertrophy is absent, but systolic (Sa) and early diastolic (Ea) velocities are reduced for age. (B) After 2 years, asymmetric septal hypertrophy developed and TD annular velocities remain reduced. AO = aorta; Aa = late diastolic velocity; LA = left atrium; LV = left ventricle; RV = right ventricle.

View larger version (97K): [in this window] [in a new window] [Download PPT slide]   Figure 8 Single-photon emission computed tomography perfusion imaging from a hypertrophic cardiomyopathy patient. Septal thickness is increased as is the count activity (hot spot) in the septum relative to lateral wall. The computer analysis software registered a fixed perfusion defect (scar) in the lateral and apical regions upon normalization to the septum. HLA = horizontal long axis; PDS = perfusion defect size; SA = short axis; VLA = vertical long axis.

View larger version (81K): [in this window] [in a new window] [Download PPT slide]   Figure 9 End-diastolic (left) and end-systolic (right) frames with the grid laid across the image. Notice the increased anteroseptal thickness and the reduced stripe deformation in that area.

View larger version (130K): [in this window] [in a new window] [Download PPT slide]   Figure 10 (A) In vivo end diastolic images, (B) in vivo gadolinium-enhanced images, (C) corresponding sections from explanted heart, and (D) staining with sirius red for collagen. Areas of gadolinium enhancement correspond to unstained pale myocardium and red-stained collagen. A representative area is marked by the arrow. Reproduced with permission from Moon et al. (72).