## 1 Introduction  
Valuvalar disorders of the heart are a prominent contributor to cardiovascular disease, impacting around 2-3 million individuals in the United States only [1]. Approximately 0.2% of the United States population is afflicted with hypertrophic cardiomyopathy (HCM), the predominant form of genetic heart disease [2, 3]. This condition increases the susceptibility to heart failure, stroke, and many types of abnormal heart rhythms, including sudden cardiac death. HCM is a hereditary condition characterized by abnormal thickening of the heart muscle. Notably, more than two-thirds of HCM patients have an obstruction [4]. Hypertrophic Obstructive Cardiomyopathy (HOCM) is a significant cause of sudden cardiac deaths in young individuals, including highly skilled athletes, and affects both genders [5]. In most cases, the condition arises from an irregular enlargement of the interventricular septum, which leads to a narrowing that may impede or reduce the blood flow from the left ventricle (LV) to the aorta (Ao) [2, 4, 6]. Moreover, roughly 60% to 70% of these instances are characterized by the presence of systolic anterior motion (SAM) of the mitral valve (MV) and obstruction of the left ventricular outflow tract (LVOT) [7]. In addition to the thickening of the interventricular septum, the LVOT might experience a reduction in size either during or after cardiac valve surgeries. For example, therapies targeting mitral regurgitation (MR) may entail replacing the natural MV leaflet with either a metallic prosthetic valve or bioprostheses. These substitutions have the capacity to extend into the LVOT, potentially resulting in blockage [8]. In many cases, open MV surgery and the use of cardiopulmonary bypass are not viable due to a heightened surgical risk. Consequently, transcatheter MV implantation (TMVI) has emerged as an innovative alternative strategy for treating MR. TMVI is frequently performed in patients with irreparable MV disease, with a particular emphasis on preserving the intact mitral subvalvular apparatus [8]. Prior TMVI, all patients receive a contrast-dyed cardiac computed tomography (CT) scan to assess the LVOT and MV annulus. The obstruction of blood flow in the LVOT after TMVI can be caused by many reasons [9]. An example of a contributing component is the aorto-mirtal-annular (AMA) angle, which denotes the angle created by the aortic and mitral valves. The angle influences the degree and orientation of the artificial mitral valve's projection into the outflow tract [10]. Individuals diagnosed with HCM may increase the likelihood of encountering issues related to the Left Ventricular Outflow Tract (LVOT), which involve the thickening of the wall that separates the ventricles, a condition known as interventricular septal hypertrophy [11]. Additionally, having a smaller left ventricular chamber is considered a risk factor, as a bigger left ventricular cavity is normally more suitable for accommodating an artificial prosthetic MV [12]. Preserving the anterior mitral leaflet (AML) after TMVI might result in the narrowing of the LVOT [13; 14]. Flow obstruction at LVOT may occur because of struts from the artificial valve protruding into the LVOT, or due to the AML being excessively elongated and protruding into the outflow tract. Placing a transcatheter heart valve into the native MV necessitates the AML planes to be in an open position, which may possibly obstruct the LVOT. The displacement of the AML towards the septum is more pronounced in specific situations, such as when the AMA planes are sharply angled, the septum between the ventricles bulges into the LVOT, and the AML is elongated. This shift can cause a considerable blockage in the LVOT, especially during TMVI. Moreover, after TMVI, a very enlarged AML may protrude forward into a narrowed LVOT, resembling situations seen in hypertrophic cardiomyopathy.