Subaortic stenosis, a heart disease characterised by a narrowing of the left ventricular outflow tract, is frequently caused by the presence of a subaortic membrane (SAM) located at the aortic valve inlet. This anatomical obstruction leads to significant haemodynamic alterations and leaflets fluttering, whose mechanisms are not yet fully understood. This research investigates, through computer simulations, the SAM's haemodynamic impact and the mechanism behind leaflets fluttering. A mono-physics fluid-structure interaction approach, based on the meshless smoothed particle hydrodynamics method, was employed. This approach represents both blood and structures with particles without defining interfaces, efficiently capturing large deformations and dynamic phenomena. Two common types of SAMs were investigated - a discrete thin SAM layer (flexible) and a thick fibromuscular ridge SAM (stiff) - and compared with a healthy aortic valve. Projected dynamic valve area (PDVA) was used as a reference parameter to quantify leaflet oscillation. While the PDVA in the healthy aortic valve stabilised at 283 mm2 without oscillation, both pathological cases exhibited self-sustained periodic fluctuations. In the presence of discrete thin SAM layer, the mean PDVA decreased by 3% compared to the healthy control. This reduction was more pronounced for thick fibromuscular ridge configurations, where the mean PDVA was 9% lower than the healthy case. Notably, stiffer SAM configurations more than doubled the oscillation amplitude (from 3.12 mm2 to 6.77 mm2) and increased the oscillation frequency by 8% relative to flexible membranes. Vortices dynamics was analysed, determining the phases of their formation, growth and migration. Through the analysis of velocity, vorticity, and shear stress maps, this study provides critical insights into the origin of fluttering and its influence over these key haemodynamic parameters. Findings demonstrate that the oscillatory leaflet motion is the result of vortices formation and shedding. The stiffness of the SAM significantly modulates the fluttering behaviour. While structural damage and haematological complications were not directly simulated, the identified oscillations represent haemodynamic conditions associated in literature with such pathologies. The observed alterations in wall shear stress magnitude and direction provide a physical basis for the mechanical environment that could contribute to endothelial cell dysfunction in the presence of SAM. Subvalvular aortic stenosis, also known as subaortic stenosis (SAS), is a significant form of left ventricular outflow tract (LVOT) obstruction characterized by fixed anatomical narrowing immediately below the aortic valve. Although valvular aortic stenosis remains the most common cause of LVOT obstruction, SAS represents a meaningful subset of congenital heart disease—particularly in infants, children, and young adults—and poses unique diagnostic, surgical, and long-term management challenges. The chronic pressure overload created by this fixed subvalvular obstruction promotes the development of concentric left ventricular hypertrophy (LVH), which, when untreated, increases the risk of myocardial ischemia, malignant arrhythmias, and ultimately congestive heart failure, adversely impacting long-term survival. As such, SAS requires ongoing surveillance and timely intervention to interrupt the progressive cascade of myocardial remodeling and its downstream complications. Anatomically, SAS manifests in 3 principal morphologic forms. The discrete membranous subtype, accounting for approximately 70% of cases, consists of a thin fibrous membrane attached to the upper interventricular septum and extending toward the anterior mitral leaflet, typically forming a crescent-shaped ridge (see Image. Discrete Subaortic Stenosis on Computed Tomography). A related but thicker variant, the fibromuscular ridge, produces similar hemodynamic consequences. Less commonly, tunnel-type SAS (<30%) presents as diffuse fibromuscular narrowing extending from the left ventricular (LV) cavity to the hypoplastic aortic annulus, often accompanied by septal thickening and requiring more extensive surgical approaches, such as the Konno procedure. Rarely, accessory mitral valve tissue may protrude into the LVOT, contributing to obstruction. Importantly, the distance between the obstructive membrane and the aortic valve is prognostic; distances of less than 5 mm are associated with increased risk of aortic valve injury and higher recurrence rates following resection. The natural history of SAS is one of gradual but persistent progression. Turbulent, high-velocity systolic flow is directed toward the structurally normal aortic valve cusps, leading over time to cusp thickening, fibrosis, and the development of secondary aortic regurgitation (AR), a hallmark of disease evolution. This combination of fixed subvalvular obstruction and progressive AR perpetuates substantial LV pressure overload, fueling further LVH and raising the risk of adverse cardiac outcomes. Early recognition and strategic intervention are therefore crucial to limiting the long-term consequences of sustained pressure burden and preventing irreversible ventricular remodeling.

Subvalvular aortic stenosis (SAS) is a relatively uncommon cause of left ventricular outflow tract (LVOT) obstruction, constituting only 8-20% of cases. Among the etiologies, subaortic membranes (SAoM) are the most prevalent, manifesting in various anatomical forms, including thin discrete membranes, fibromuscular ridges, and diffuse tunnel-like narrowings. While transthoracic echocardiography (TTE) is the primary diagnostic tool, it often presents challenges, particularly in cases where the membrane is not readily visible, and needs further imaging with transesophageal echocardiogram (TEE) or cardiac magnetic resonance imaging (CMR). This case series explores 2 diagnostically challenging instances of SAoM, highlighting the importance of multimodal imaging and the nuances of interpreting these findings. The first case is of a 19-year-old female with congenital aortic stenosis and ESRD presented with worsening dyspnea; initial TTE, TEE, and CMR failed to identify a subaortic membrane, but intra-procedural 3D TEE revealed an oval-shaped membrane, redirecting management from balloon angioplasty to surgical excision. The second is of a 62-year-old female with prior diagnosis of hypertrophic obstructive cardiomyopathy (HOCM) and progressive dyspnea was found on TEE to have a SAoM, contradicting her prior diagnosis; medical therapy was adjusted, and she was referred for surgery. These cases underscore the diagnostic challenges of SAoM, often evading detection on initial TTE and CMR, necessitating advanced techniques like 3D TEE. Misdiagnosis, as seen with HOCM, can lead to years of inappropriate treatment. In conclusion, accurate and early differentiation through expert interpretation of multimodal imaging, particularly TEE, is crucial for guiding proper management and avoiding unnecessary interventions.

Subaortic stenosis (SAS) is characterized by a fibromuscular membrane located just below the aortic valve, causing fixed outflow tract obstruction. There is a paucity of studies evaluating this condition. This cohort study reviewed the contemporary characteristics and outcomes of SAS in adult patients in a single large referral center. We retrospectively studied adult patients with SAS evaluated at our center during 2011 to 2022. The primary outcome was all-cause mortality and heart failure hospitalizations during follow-up, with secondary end points including recurrence of SAS and repeat surgery after initial SAS surgery. Among 484 patients with SAS, key characteristics included mean age 55±18 years, 67.5% female, left ventricular outflow tract peak velocity 352±140 cm/s and gradient 57±40 mm Hg, left ventricular ejection fraction 60%±14%, 54.8% had prior SAS surgery, and 45.1% had surgery during follow-up. Over a median follow-up of 5.5 (1.5-12.3) years, 11.5% (n=56) died, 6.8% (n=33) had heart failure hospitalizations, 8.0% (n=39) experienced SAS recurrence, and 14 (5.9%) underwent repeat SAS surgery. Multivariable analyses identified older age per 10-years (hazard ratio [HR], 1.37 [95% CI, 1.12-1.68]) and baseline New York Heart Association class (HR, 2.48 [95% CI, 1.54-3.99]) to be statistically significantly associated with the primary end point; higher body mass index, New York Heart Association class, and peak left ventricular outflow tract gradient were also statistically significantly associated with SAS recurrence and redo surgery. Almost half of patients with SAS had surgery in the past or during follow-up, and a significant minority had mortality or morbidity events during follow-up. Identified prognosticators warrant further research to guide management.

Subaortic stenosis (SAS) is a common congenital heart disease that can cause significant morbidity and mortality if not treated promptly. Patients with heart valve disease are prone to complications after replacement surgery, and the existence of SAS can accelerates disease progression, so timely diagnosis and treatment are required. However, the effects of subaortic stenosis on mechanical heart valves (MHV) are unknown. This study aimed to investigate flow characteristics in the presence of subaortic stenosis and computationally quantify the effects on the hemodynamics of MHV. Through the numerical simulation method, the flow characteristics and related parameters in the presence of SAS can be more intuitively observed. Based on its structure, there are three types of SAS: Tunnel-type SAS (TSS); Fibromuscular annulus SAS (FSS); Discrete SAS (DSS). The first numerical simulation study on different types of SAS found that there are obvious differences among them. Among them, the tunnel-type SAS formed a separated vortex structure on the tunnel-type narrow surface, which exhibits higher wall shear force at a low obstacle percentage. However, discrete SAS showed obvious differences when there was a high percentage of obstacles, forming high peak flow, high wall shear stress, and a high-intensity complex vortex. The presence of all three types of SAS results in the formation of high-velocity jets and complex vortices in front of the MHV, leading to increased shear stress and stagnation time. These hemodynamic changes significantly increase the risk of MHV dysfunction and the development of complications. Despite differences between the three types of SAS, the resultant effects on MHV hemodynamics are consistent. Therefore, early surgical intervention is warranted in SAS patients with implanted MHV.

Discrete subaortic stenosis (DSS) is an obstruction of the left ventricular outflow tract (LVOT) due to the formation of a fibromuscular membrane upstream of the aortic valve. DSS is a major risk factor for aortic regurgitation (AR), which often persists after surgical resection of the membrane. While the etiology of DSS and secondary AR is largely unknown, the frequent association between DSS and aortoseptal angle (AoSA) abnormalities has supported the emergence of a mechanobiological pathway by which hemodynamic stress alterations on the septal wall could trigger a biological cascade leading to fibrosis and membrane formation. The resulting LVOT flow disturbances could activate the valve endothelium and contribute to AR. In an effort to assess this hypothetical mechano-etiology, this study aimed at isolating computationally the effects of AoSA abnormalities on septal wall shear stress (WSS), and the impact of DSS on LVOT hemodynamics. Two-dimensional computational fluid dynamics models featuring a normal AoSA (N-LV), a steep AoSA (S-LV), and a steep AoSA with a DSS lesion (DSS-LV) were designed to compute the flow in patient-specific left ventricles (LVs). Boundary conditions consisted of transient velocity profiles at the mitral inlet and LVOT outlet, and patient-specific LV wall motion. The deformation of the DSS lesion was computed using a two-way fluid-structure interaction modeling strategy. Turbulence was accounted for via implementation of the k-ω turbulence model. While the N-LV and S-LV models generated similar LVOT flow characteristics, the DSS-LV model resulted in an asymmetric LVOT jet-like structure, subaortic stenotic conditions (up to 2.4-fold increase in peak velocity, 45% reduction in effective jet diameter vs. N-LV/S-LV), increased vorticity (2.8-fold increase) and turbulence (5- and 3-order-of-magnitude increase in turbulent kinetic energy and Reynolds shear stress, respectively). The steep AoSA subjected the septal wall to a 23% and 69% overload in temporal shear magnitude and gradient, respectively, without any substantial change in oscillatory shear index. This study reveals the existence of WSS overloads on septal wall regions prone to DSS lesion formation in steep LVOTs, and the development of highly turbulent, stenotic and asymmetric flow in DSS LVOTs, which support a possible mechano etiology for DSS and secondary AR.