The Bicuspid Aortic Valve (BAV) is the most common congenital anomaly in adults, with a global incidence of 1.3%. Despite being well documented, BAV presents significant clinical challenges due to its phenotypic heterogeneity, diverse clinical manifestations, and variable outcomes. Pathophysiologically, BAV differs from tricuspid valves in calcification patterns and hemodynamic effects, leading to increased shear stress and aortic root dilatation, while it is influenced by genetic and hemodynamic factors. This is why therapeutically, BAV presents challenges for both surgical and transcatheter interventions, with surgical approaches being traditionally preferred, especially when aortopathy is present. However, transcatheter aortic valve implantation (TAVI) has emerged as a viable option, with studies showing comparable outcomes to surgery in selected patients, while advancements in TAVI and a better understanding of BAV’s genetic and pathophysiological nuances are expanding treatment options. The choice between mechanical and bioprosthetic valves also presents considerations, particularly regarding long-term durability and the need for anticoagulation. Future research should focus on long-term registries and genetic studies to refine therapeutic strategies and improve patient outcomes. This review aims to evaluate current approaches in the surgical and interventional management of BAV, focusing on its anatomy, pathogenesis, pathophysiology, and therapeutic strategies.

Suicide left ventricle after transcatheter aortic valve replacement is a well described phenomenon associated with increased morbidity and mortality. Prompt actions should be implemented to prevent this situation, and the alarm signs should be recognized. We present a case report of successful recognition, prevention and treatment of this complication. (Level of Difficulty: Intermediate.)

Transcatheter aortic valve implantation (TAVI) has emerged as a revolutionary therapeutic modality for the management of severe aortic stenosis (AS), particularly in patients who are at high or prohibitive risk for surgical aortic valve replacement (SAVR). Over the past decade, extensive clinical evidence has expanded the indications for TAVI to include intermediate- and low-risk populations, which usually represent a population of younger age, in which the most common complications of TAVI, including paravalvular leak (PVL) and pacemaker implantation, should be avoided. This review focuses on the incidence and predictors of PVL in various types of TAVI implantation, its clinical implication, and the prevention strategies to tackle this complication.

Left ventricular diastolic dysfunction (LVDD) is characterized by impaired ventricular relaxation and increased chamber stiffness during diastole, resulting in increased left ventricular filling pressures. It represents a highly prevalent yet frequently underdiagnosed cardiac condition with significant clinical implications, serving as a major contributor to heart failure with preserved ejection fraction (HFpEF), particularly among elderly individuals and those with hypertension, diabetes mellitus, obesity, or coronary artery disease. Multiple studies have identified the progression of LVDD as a marker of adverse prognosis, associated with increased morbidity and mortality, highlighting the importance of early recognition and targeted therapeutic strategies to improve diastolic function and clinical outcomes. This review summarizes the pathophysiology, current diagnostic strategies, and treatment options for LVDD, emphasizing its importance in clinical practice.

Background: Endothelial dysfunction and inflammation are associated with the progression of coronary artery disease (CAD) and the pathophysiology of acute coronary syndrome (ACS). We examined the prognostic role of endothelial function and pro-inflammatory cytokines in patients admitted with ACS. Methods: The study population consisted of 864 subjects. From 663 subjects who presented with chest pain, ACS was diagnosed in 460. We additionally recruited 201 consecutive patients with stable CAD. Endothelial function was assessed using flow-mediated dilatation (FMD). Tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) levels were measured via ELISA. Subjects with ACS were followed up for major adverse cardiovascular events (MACE), defined as cardiovascular death, cardiac arrest, myocardial infarction, stroke, nonfatal stroke, other arterial thrombotic events, and hospitalization due to cardiovascular conditions. Results: There was a stepwise impairment in FMD, logTNF-α, and logIL-6 in patients with chest pain of non-epicardial CAD etiology compared to patients with stable CAD and those with ACS (p < 0.001 for all). Moreover, patients who presented with chest pain had increased odds of ACS in accordance with the increasing levels of TNF-α, IL-6, and impaired FMD (p < 0.05 for all). Interestingly, from all these markers, in patients with ACS, we found that only TNF-α levels above 5.19 pg/mL had a 2.5-times-increased risk of MACE compared to patients with TNF-α levels below 5.19 pg/mL, independently of other confounders. Conclusions: In the current study, we found that patients who presented with ACS had impaired endothelial function and increased levels of IL-6 and TNF-α.