Rheumatic mitral stenosis remains a significant cause of cardiovascular morbidity in young adults worldwide, yet its diagnosis can be challenging when clinical presentation overlaps with concurrent infections. We present a case of a woman in her 30s who presented with dyspnoea, fever, and haemoptysis, initially attributed to community-acquired pneumonia with concurrent viral and bacterial infection. She received appropriate treatment and was discharged; however, her symptoms persisted, and she developed alveolar haemorrhage, prompting further investigations, which ultimately revealed severe mitral stenosis secondary to rheumatic heart disease. This case underscores the diagnostic complexity of mitral stenosis in the setting of overlapping pulmonary infections and highlights the critical importance of maintaining a broad differential diagnosis and pursuing thorough cardiac assessment in patients with unexplained haemoptysis.

Rheumatic heart disease predominantly affects left-sided cardiac valves. Quadrivalvular involvement with clinically significant pulmonary valve stenosis is exceedingly rare, and evidence regarding minimally invasive management strategies in such complex cases is limited.

Background: Hypoplastic left heart syndrome (HLHS) is defined as "a spectrum of congenital cardiovascular malformations with normally aligned great arteries without a common atrioventricular junction, characterized by underdevelopment of the left heart with significant hypoplasia of the left ventricle including atresia, stenosis, or hypoplasia of the aortic or mitral valve, or both valves, and hypoplasia of the ascending aorta and aortic arch". Without treatment, HLHS is usually lethal in the neonate. Many hypotheses have been advanced to explain the etiology of HLHS; however, no single theory appears to fully explain the phenotypic variability seen in HLHS. Furthermore, many of these theories offer no explanations regarding the precipitating events which lead to the development of HLHS. Objective: This review considers and critically evaluates the strengths and weaknesses of the leading theories proposed to explain the pathogenesis of HLHS-including hemodynamic disturbances, primary myocardial structural defects, valvar malformations, and genetic or epigenetic alterations that may provoke developmental and anatomic abnormalities. After presenting each model, we propose a novel, comprehensive, and data-driven framework which may assist researchers in developing models for the pathogenesis of the various subtypes of HLHS. Methods: Key findings from human fetal imaging, histopathology, genetic studies, and animal models were considered, as well as the hypothetical contribution of each in observed HLHS phenotypes. The rationales for these findings as causal factors initiating individual HLHS patterns, as well as how they might contribute to HLHS in general, were critically analyzed. Results: The flow theory is strongly supported by animal models and in utero interventions that demonstrate the impact of altered hemodynamics on cardiac morphogenesis. However, the flow theory fails to identify initial causes of disturbed flow or related histological features of HLHS like endocardial fibroelastosis. The myocardial and valve-first models suggest an important role in developmental defects, but do not necessarily have a strong experimental basis that provides explanations for how they mediate HLHS. Genetic studies in patients with HLHS have identified several candidate causal mutations. However, such genetic causes of HLHS exhibit incomplete phenotypic penetrance and clinical impact. A multifactorial framework attempts to integrate these diverse mechanisms and may provide the most coherent explanation that can accommodate the heterogeneity and variable presentation of HLHS. Such a framework may identify multiple forces that drive disease but does not provide useful pathways for future research about HLHS. Conclusions: No single hypothesis has fully explained how HLHS is initiated, progresses, and presents with the clinical conditions that are encountered by cardiac surgeons and cardiologists. The most current models suggest that the spectrum of HLHS reflects acomplex interaction between genetic susceptibility, flow-dependent cardiac remodeling, and environmental factors in utero. A multifactorial model integrates these diverse mechanisms and may provide the most coherent explanation for the various phenotypic variations in HLHS. Based on our analysis of the most current data and the strengths and weaknesses of the current theoretical frameworks, we propose a novel research strategy aimed at identifying specific cardiac progenitor cell populations whose dysregulation may represent a unifying explanation for the etiology of the various phenotypes of HLHS. Based on the arguments made throughout this manuscript that evaluate the various genetic, structural, and hemodynamic models of initiation of disease, we believe that the significant phenotypic variability across the spectrum of HLHS (i.e., the different anatomic subtypes for "classic" HLHS) most likely reflects different underlying etiologies and mechanisms. At the very least, it is very likely that the timing of the insult is critical in determining anatomic subtype. Based on the published data and the arguments within this manuscript, it seems naive to think that there is a single unifying mechanism explain all forms of HLHLS.

Background/Objectives: Although comprehensive transthoracic echocardiography (TTE) is part of the diagnostic workup in acute ischemic stroke, it is not cost-effective to use it for all patients. Guidelines recommend using it only for selected patients to guide secondary prevention. Neurologist-led, stroke-focused cardiac ultrasound (S-FoCUS) is an emerging bedside screening tool that optimizes cardiac evaluation in acute stroke care. We hypothesize that the implementation of S-FoCUS screening may reduce resource utilization in terms of hospital stay and TTE procedures. Methods: We conducted a retrospective before-and-after cohort study of patients with suspected acute ischemic stroke or TIA admitted to our comprehensive stroke center. We compared two 6-month periods: the pre-S-FoCUS period, during which patients underwent TTE as the initial cardiac imaging modality; and the post-S-FoCUS period, during which patients initially underwent S-FoCUS, with subsequent TTE performed only in the presence of abnormal findings or at the clinician's discretion. We compared the time from admission to first cardiac ultrasound assessment, length of stay, relative reduction in TTE procedures and estimated in-hospital costs. Results: The pre-S-FoCUS period included 224 patients, and the post-S-FoCUS period included 229 patients. The S-FoCUS protocol reduced the median time to first cardiac ultrasound assessment by two days (median [IQR] 3 [2-5] vs. 1 [1-2], p < 0.001) and the median length of stay by one day (6 [4-9] vs. 5 [3-10], p = 0.014). Implementing the S-FoCUS protocol was associated with an exploratory estimate of lower in-hospital costs (approximately €716 per screened patient) driven mainly by a shorter length of stay. The distribution of the frequency of predefined cardioembolic sources was similar between both periods. There was a high agreement rate between the S-FoCUS and TTE findings in patients who underwent both tests: mitral stenosis (κ = 0.78), left atrial severe enlargement (κ = 0.74), left ventricular hypokinesia/akinesia (κ = 0.84), and depressed LVEF (κ = 0.88). Conclusions: Neurologist-led S-FoCUS is a feasible triage strategy to improve efficiency in the acute stroke pathway.

Aortic stenosis (AS) and mitral stenosis (MS) are progressive valvular heart diseases associated with substantial morbidity and mortality once symptoms develop. Over the past decade, the management of isolated AS has undergone profound evolution, driven by refinements in surgical aortic valve replacement, the adoption of minimally invasive techniques, and the rapid expansion of transcatheter aortic valve replacement across all surgical risk categories. In contrast, patients with concomitant AS and MS represent a complex and understudied population, frequently excluded from randomized trials and only marginally addressed in contemporary clinical practice guidelines. The management requires individualized guideline-directed decision-making led by a multidisciplinary Heart Team. The paucity of high-quality data in combined AS-MS underscores the need for dedicated prospective studies and international registries. The aim of this narrative review is to describe current strategies to treat AS both when isolated and concomitant with MS. We also discuss the need for updated, specific guidelines.

Background: Reintervention after mitral valve repair represents a relevant clinical challenge, yet the mechanisms and timing of repair failure remain incompletely defined. Understanding how the interval between index repair and reoperation affects failure mechanisms and the feasibility of repeat repair may help refine surgical strategies. Methods: We retrospectively analyzed 194 patients undergoing repeat mitral valve surgery between 2010 and 2025 after prior repair. Median age was 70 years and 61.3% were male. Patients were stratified by time to reoperation: 0-5 years (n = 91), 6-10 years (n = 42), and >10 years (n = 61). Median left ventricular ejection fraction was 58%, atrial fibrillation prevalence 32.5%, minimally invasive approach 21.6%, and EuroSCORE II 4.8%. Results: Baseline characteristics and operative risk were comparable across groups. However, mechanisms of repair failure differed significantly. Early failures were more commonly due to recurrent leaflet prolapse (47.8%), whereas late failures showed a higher incidence of mitral stenosis (63.9%). The rate of repeat mitral repair decreased over time, being higher in early failures compared with intermediate and late failures (17.6% vs. 14.3% vs. 8.2%). Conclusions: Timing of mitral repair failure is associated with distinct mechanisms and influences surgical management. Early failures are more frequently related to prolapse recurrence and are more amenable to re-repair, whereas late failures are characterized by structural degeneration and more often require valve replacement.

A 26-year-old woman at 14 weeks gestation with her third pregnancy presented with severe bioprosthetic mitral valve stenosis, which represents very high maternal and fetal risk. Pregnancy termination was recommended but declined, and valve surgery was deemed to be of prohibitive risk. After multidisciplinary discussion, she underwent valve-in-valve transcatheter mitral valve replacement in the second trimester. She had an uncomplicated vaginal delivery at term. This represents a novel use of transcatheter valve replacement to stabilize a pregnant patient with a high-risk valvular lesion. This approach may be considered after multidisciplinary discussion in appropriately selected patients.