Fig 2 Left ventricular (LV) interventricular septal wall thickne

Fig. 2 Left ventricular (LV) interventricular septal wall thickness and LV posterior wall thickness were 15 mm and 10 mm on parasternal long axis view at diastolic phase and papillary muscle was hypertrophied (arrow) (A). Color Doppler of 2D echocardiography … Fig. 3 One hundred and five degree color compared view of transesophageal echocardiography shows the linear mobile subaortic Selleck LY2835219 membrane on basal Inhibitors,research,lifescience,medical interventricular septum (arrow). The subaortic membrane disturbs

the forward flow toward ascending aorta. Fig. 4 (A) Double pressure tracing was performed using radial sheath and coronary catheter in left ventricle. (B) Aortic pressure curve was recorded at the ascending aorta level. There is notch on systolic phase of pressure curve (arrow). (C) Aortic pressure … Discussion Subaortic membrane is a rare congenital heart disease and one of the pathologies of the ventricular hypertrophy in adults but never recognized in early infancy.1),2) It is thought that underlying genetic predisposition Inhibitors,research,lifescience,medical and various geometric and anatomical variations

of LVOT leading to flow turbulence result in the subaortic membrane.3) The echocardiographic assessment of the severity and the cause of LVOT obstruction is a very important in terms of its impact on the clinical outcome.4) Differential diagnosis between subaortic membrane Inhibitors,research,lifescience,medical and obstructive HCMP could be difficult. As subaortic membrane is infrequent cause of LVOT obstruction in adulthood, HCMP and dynamic LVOT obstruction would mask the presence of the subaortic membrane and cause a false diagnosis as obstructive HCMP.5) Although most of subaortic stenosis is usually a fixed lesion such as fibrous

ridge rather than mobile membrane,3),6) Inhibitors,research,lifescience,medical flail subaortic membrane diagnosed with TTE was also documented.7) Unlike this report, we initially misdiagnosed the patient as having obstructive HCMP by TTE. Obstructive HCMP usually has the following characteristics: LVOT obstruction, SAM of the anterior Inhibitors,research,lifescience,medical leaflet of the mitral valve or chordae, and mitral regurgitation.8) However, our patient showed increased pressure gradient between LV and aorta but no definite SAM of anterior mitral valve leaflet or chordae and mitral regurgitation on TTE; detect subaortic membrane Edoxaban on TEE. Thus, it is clear that not all cases of LVOT obstruction are due to septal hypertrophy. TEE is more useful than TTE in visualizing perivalvular structures and would help to confirm the presence of unusual causes for severe LVOT obstruction and left ventricular hypertrophy, such as subvalvular or supravalvular stenosis; cardiac catheterization would aid to find the hemodynamic impact of the pathologic lesions. In conclusion, meticulous evaluation including TEE and cardiac catheterization would be necessary to confirm various causes for the LVOT obstruction, especially undetected subaortic membrane on TTE.

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