Search Results (264)

Tricuspid regurgitation (TR) is being increasingly recognized in the patient population. It is a common cardiac cause of chronic disability. This pathology is characterized by a heterogeneous and broad spectrum of clinical manifestations with signs and symptoms. The results from various and different analyses and studies suggest that TR-related deaths may have increased over the last 20 years. This trend may justify a greater focus on timely diagnosis and management of TR. For a long time, this problem has been underestimated or treated with only pharmacological therapy (diuretics). The use of the isolated surgical option remains infrequent, especially in patients at high surgical risk, for whom a significant number of patients with TR are still not treated, and a disability remains that is difficult to manage and rehabilitate. To date, there are emerging as an alternative to surgery in high-risk patients with severe TR multiple transcatheter devices that aim to reduce TR through different functional mechanisms. There are numerous minimally invasive treatments for TR, and many devices used for the treatment of this disabling pathology. In fact, there are various treatments with a transcatheter approach using ever-new devices. The use of heterotopic implantation of bioprosthetic valves in the superior and inferior vena cava represents an additional therapeutic armamentarium that, through caval reflux, can constitute an additional resource, too. Starting from a single clinical experience and describing a clinical case report, a narrative review has been undertaken by reviewing the various studies that have investigated this type of approach and their impact on the general, cardiac, and functional sides, to then discuss the cost–benefit ratio in light of knowledge on this specific topic. Full article

Background/Objectives: Atrial fibrillation (AF) may cause functional mitral regurgitation (MR) and tricuspid regurgitation (TR) through atrial remodeling and annular dilation. However, the prevalence and structural characteristics of combined MR/TR in AF are not well defined. We aimed to determine the prevalence, clinical profile, and factors associated with combined clinically significant MR and TR in AF patients. Methods: In this prospective observational study (REMO-FIB), 175 consecutive AF patients underwent comprehensive transesophageal echocardiography with three-dimensional mitral valve analysis. After excluding organic MR and significant aortic valve disease, 125 patients were analyzed. Patients were classified into four groups according to the presence of moderate/severe MR and/or TR. Multivariable logistic regression evaluated factors associated with the combined phenotype. Results: Among 125 patients, 53 (42.4%) had no significant MR/TR, 33 (26.4%) had isolated MR, 11 (8.8%) had isolated TR, and 28 (22.4%) had combined MR/TR. Compared with patients without regurgitation, those with combined MR/TR had higher symptom burden (EHRA class, p = 0.036), more heart failure (92.9% vs. 67.9%, p = 0.048), larger left (47.0 vs. 42.0 mm, p = 0.002) and right atria (42.0 vs. 38.0 mm, p < 0.001), higher pulmonary artery pressure (40.0 vs. 28.0 mmHg, p = 0.004), and lower left ventricular ejection fraction (47.5% vs. 55.0%, p = 0.006). Three-dimensional analysis showed larger mitral annular perimeter (129.0 vs. 121.0 mm, p = 0.009), greater annular area (12.7 vs. 11.1 cm², p = 0.014), longer anterior leaflet length (26.5 vs. 24.0 mm, p < 0.001), and greater tenting area (2.1 vs. 1.4 cm², p = 0.002). Factors independently associated with the combined phenotype were female sex (OR 4.60, p = 0.015), lower ejection fraction (OR 0.47 per SD, p = 0.005), and larger right atrial diameter (OR 1.85 per SD, p = 0.037). Model discrimination was good (AUC 0.81). Conclusions: Combined moderate/severe MR and TR affects over one-fifth of AF patients without organic valve disease and is associated with advanced biatrial remodeling, adverse symptoms, and heart failure. Comprehensive assessment of both atrioventricular valves should be considered in AF. Full article

Background: Trisomy 21 (T21) is strongly associated with congenital heart disease, particularly atrioventricular septal defect (AVSD), ventricular septal defect (VSD), atrial septal defect (ASD) and selected conotruncal and arch anomalies. First- and second-trimester ultrasound, Doppler and fetal cardiac MRI enable increasingly early and detailed characterization of these lesions, while advances in molecular cardiogenesis have linked specific phenotypes to dosage-sensitive genes on chromosome 21. Methods: This narrative review synthesizes contemporary evidence on structural and functional cardiovascular anomalies in T21 fetuses in the first and second trimester, integrating fetal echocardiography, Doppler assessment and fetal cardiac MRI with embryologic and molecular insights, and summarizing trimester-specific detectability and pathophysiologic links to candidate genes in the Down syndrome-critical region. Approximately one quarter to one third of T21 fetuses have major congenital heart disease on high-quality prenatal echocardiography, with AVSD representing about half of all lesions and VSD, tetralogy of Fallot (TOF), arch anomalies, venous return abnormalities and functional markers (increased nuchal translucency, tricuspid regurgitation, ductus venosus abnormalities) comprising the remainder. Results: First-trimester detection relies on functional markers and early four-chamber and outflow-tract views, whereas second-trimester studies refine anatomic definition and hemodynamics, with MRI reserved for complex cases. Overexpression of genes such as DSCAM, COL6A1/COL6A2, DYRK1A and RCAN1 perturbs endocardial cushion, conotruncal and vascular development. Conclusions: Early, protocol-driven cardiac imaging in T21 supports timely diagnosis, risk stratification and multidisciplinary counselling, and links fetal imaging phenotypes with chromosome 21 gene dosage to advance personalized management and future genotype–phenotype research. Full article

Background/Objectives: Cardiovascular involvement is among the most consequential sequelae of SARS-CoV-2 infection. Myocardial injury, arrhythmia, and thromboembolic disease have been characterized in depth, yet the relationship between COVID-19 and valvular heart disease (VHD), and its interplay with heart failure (HF), has received comparatively limited synthesis. This narrative review consolidates current evidence on the mechanisms, diagnosis, differential assessment, and clinical outcomes linking acute and post-acute COVID-19 to valvular dysfunction and to incident or worsening heart failure, with emphasis on practical implications for cardiologists and internists. Methods: We searched PubMed, Scopus, and Web of Science (January 2020–January 2026) for studies on valvular dysfunction, heart failure, myocardial injury, and endothelial pathology in SARS-CoV-2 infection, and synthesized findings narratively. Results: Convergent pathways—endothelial injury, systemic hyperinflammation, micro- and macrovascular thrombosis, and pressure–volume overload—contribute to functional and, less frequently, structural valvular changes. Available evidence suggests that clinically relevant post-COVID valvular abnormalities are more often secondary/functional (mitral and tricuspid regurgitation) than primary structural lesions, although dedicated prospective valvular studies remain scarce. Pre-existing severe VHD markedly worsens acute COVID-19 prognosis. Elevated NT-proBNP, troponin, and interleukin-6 consistently predict decompensation and mortality, and a substantial minority of survivors show persistent fibrotic pulmonary changes and restrictive ventilatory defects on follow-up (pulmonary rather than cardiac findings). Conclusions: Post-COVID valvular dysfunction appears, on currently available but largely indirect evidence, predominantly functional and inflammation-related, and may overlap with HFpEF phenotypes in selected patients when objective diagnostic criteria are fulfilled. Biomarker-guided, multimodality follow-up is reasonable in high-risk survivors, and prospective longitudinal studies with standardized valvular endpoints remain a priority. Dedicated longitudinal evidence on valvular outcomes specifically remains very limited. Full article

The advent of transcatheter aortic valve implantation (TAVI) has redefined the treatment of aortic stenosis over the last two decades, evolving from a therapy reserved for patients that were deemed to be of prohibitive surgical risk to the standard of care for a large group of patients presenting with symptomatic disease. With improvements in technology, operator and institutional experience and longer-term outcome data, recent guidelines have supported the broadening of indications to low-risk and asymptomatic patients in addition to other pathologies including the management of failed surgical bioprosthetic valves and aortic regurgitation. The rapid developments in the field have resulted in a rapid expansion of TAVI. The focus has moved from the technical aspects of the procedure itself that are now well established to the lifetime management of patients with aortic stenosis, particularly younger patients with regard to valve durability, planning for a further intervention after TAVI and associated considerations including future coronary access. Beyond aortic stenosis, TAVI technology is also increasingly being utilized for the management of failed surgical bioprostheses, bicuspid valve disease, aortic incompetence and mitral/tricuspid disease and these represent future areas of focus in the field. Full article

Background and Clinical Significance: Carcinoid heart disease (CHD) is an uncommon valvular manifestation of neuroendocrine tumours, usually affecting right-sided cardiac valves. Left-sided involvement is rare and is generally associated with bronchopulmonary carcinoid, right-to-left shunting, or markedly elevated circulating vasoactive substances. Therapeutic decision-making is particularly challenging in advanced disease when severe tricuspid regurgitation occurs in patients at prohibitive surgical risk. Case Presentation: We report the case of a 61-year-old male patient with progressive dyspnoea, abdominal distension, lower-limb oedema, facial flushing, and 15 kg of unintentional weight loss. Transthoracic and transoesophageal echocardiography demonstrated torrential tricuspid regurgitation caused by thickened, retracted, and immobile leaflets, with additional mitral and aortic valve involvement, raising strong suspicion of CHD. An agitated-saline contrast study demonstrated delayed right-to-left shunting without patent foramen ovale, suggesting an extracardiac, likely intrapulmonary, shunt. Somatostatin receptor PET/CT identified a pancreatic lesion with metastatic disease, and bone marrow biopsy confirmed neuroendocrine tumour infiltration. Owing to prohibitive surgical risk, as reflected by a Tricuspid Regurgitation Impact Score (TRI-SCORE) with an estimated in-hospital mortality of 65%, unfavourable tricuspid anatomy for repair, and refractory venous congestion, heterotopic bicaval valve implantation was performed (TricValve system -P&F). Discussion: This case highlights the role of echocardiography in recognising the characteristic phenotype of CHD, detecting occult right-to-left shunting, and supporting selection of a palliative transcatheter intervention. It also illustrates the value of a multimodality diagnostic strategy integrating echocardiography, functional oncological imaging, and histopathology in tumour-related cardiac disease. Conclusions: In selected inoperable patients with advanced carcinoid-related tricuspid regurgitation, heterotopic bicaval valve implantation may represent a feasible strategy for reducing venous congestion and improving functional status. Full article

Troponin T is a molecular marker of cardiomyocyte injury, whereas left ventricular ejection fraction (LVEF) and tricuspid regurgitation velocity (TRV) reflect downstream ventricular and cardiopulmonary measures. This study evaluated whether synchronized troponin T and echocardiographic data can identify mortality risk in critically ill patients with heart failure, while separating statistical association from clinically meaningful incremental discrimination. Adult intensive care unit admissions with heart failure diagnoses were identified from MIMIC-IV and MIMIC-IV-ECHO. The primary endpoint was 28-day all-cause mortality; one-year mortality was secondary. Multivariable Cox models were adjusted for demographics, comorbidity, illness severity, organ support, and laboratory covariates. Restricted cubic splines, proportional hazards diagnostics, variance inflation factors, prespecified subgroup interaction tests, complete-case analyses, and multiple imputation sensitivity analyses were performed. The final cohort included 4362 patients, and 1072 patients (24.6%) died within 28 days. In the primary complete-case Cox model (n = 2087; 659 deaths), higher log-transformed troponin T was associated with higher 28-day mortality (hazard ratio [HR], 1.09; 95% confidence interval [CI], 1.03–1.15; p = 0.003), and higher LVEF was associated with lower mortality (HR per percentage point, 0.99; 95% CI, 0.99–1.00; p = 0.004). After severity and organ-support covariates were entered, troponin T and LVEF produced statistically detectable but very small C-statistic gains. Measurable TRV was available in 1546 patients and was associated with mortality in that subset (HR, 1.28; 95% CI, 1.08–1.52; p = 0.005). Troponin T, LVEF, and TRV were associated with mortality in ICU heart failure. Their contribution was best interpreted as risk enrichment within a clinical severity framework rather than a stand-alone decision rule. Full article

Background/Objectives: Atrial fibrillation (AF) is common in heart failure with preserved ejection fraction (HFpEF) and is associated with worse symptoms and prognosis. Emerging evidence suggests that sex modifies the AF–HFpEF relationship through differences in atrial remodeling, comorbidity burden, and hemodynamic vulnerability. This study aimed to evaluate how sex and AF jointly relate to differences in cardiac structure, clinical characteristics, and outcomes in HFpEF. Methods: We retrospectively analyzed 622 patients with HFpEF admitted between January 2019 and May 2023. Patients were categorized into four predefined clinical subgroups: women without AF, women with AF, men without AF, and men with AF. The primary endpoint was first rehospitalization for HF decompensation. Results: Over a mean follow-up of 48.6 ± 16.4 months, 181 patients (29.1%) were rehospitalized for worsening HF, with the highest event burden observed in men with AF. Sex and AF were each associated with distinct clinical and remodeling profiles, without significant sex-by-AF interaction effects. AF was independently associated with a higher risk of HF rehospitalization (HR 1.45, 95% CI 1.06–1.99, p = 0.021), whereas female sex was protective (HR 0.71, 95% CI 0.53–0.97, p = 0.032). Men with AF exhibited the most adverse remodeling profile, characterized by the largest unindexed left atrial and left ventricular dimensions, the highest prevalence of significant tricuspid regurgitation, and the lowest event-free survival (HR 1.92, 95% CI 1.23–2.99, p = 0.004). In contrast, women with AF more frequently displayed concentric remodeling and significant mitral regurgitation. Independent predictors of rehospitalization included higher NYHA functional class and lower left ventricular EF within the preserved EF range. Conclusions: Sex and AF were independently associated with substantial differences in cardiac structure, clinical characteristics and prognosis in HFpEF. Men with AF represent the highest-risk subgroup, driven by more advanced structural remodeling and valvular dysfunction. These findings suggest that simple sex- and rhythm-based classification may provide complementary information for risk stratification and management in HFpEF. Further validation in independent cohorts is warranted. Full article

Background: Pulmonary arterial hypertension is a rare but life-threatening condition in children, with hereditary forms often being linked to mutations in genes such as bone morphogenetic protein receptor type 2 (BMPR2), caveolin 1 (CAV1), and potassium channel subfamily K member 3 (KCNK3). Among these, CAV1 mutations are associated with severe disease phenotypes, though cases resulting from de novo heterozygous CAV1 mutations with multi-system involvement remain rarely reported. The CAV1 mutation (c.424C > T, p.Q142X) disrupts caveolin-1 function, leading to dysregulated pulmonary vascular remodeling and multi-system abnormalities. Methods: This was a retrospective case study of a pediatric patient with hereditary PAH. The patient was followed at our hospital from initial presentation until death. Clinical data were collected from medical records, including physical examinations, laboratory tests, echocardiography, chest X-ray, computed tomography pulmonary angiography (CTPA), and genetic analysis. The patient was treated sequentially with various PAH-targeted medications. This report also includes a review of the relevant literature on CAV1-associated PAH. Results: A female aged 3 years and 11 months was diagnosed with hereditary PAH associated with a de novo heterozygous CAV1 mutation (c.424C > T, p.Q142X). Both parents underwent genetic testing and were negative for the mutation, confirming its de novo origin. Clinical manifestations included special facial features, congenital telangiectasia, cutis marmorata (marbled skin), congenital cataract, hereditary lipodystrophy, and severe PAH. The patient presented with progressive exercise intolerance, syncope, and worsening dyspnea over nine years. Echocardiography revealed pulmonary hypertension with an estimated pulmonary artery systolic pressure of 69–105 mmHg, right heart enlargement, right ventricular hypertrophy, and moderate tricuspid regurgitation. Blood and urine metabolic screenings were normal. A chest X-ray showed progressive enlargement of the cardiac silhouette and bulging of the pulmonary artery segment. CTPA demonstrated pulmonary hypertension, secondary right heart dysfunction, decompensated right ventricular function, and mosaic perfusion in both lungs, suggestive of small arterial branch occlusion. Right heart catheterization was declined by the parents. Thus, the diagnosis of PAH was established based on clinical, echocardiographic, CTPA, and genetic findings. The patient was hospitalized four times and lost to follow-up from 2017 to 2023. She received sequential treatment with digoxin, hydrochlorothiazide, tadalafil, ambrisentan, selexipag, and treprostinil. Despite these therapies, pulmonary artery pressure continued to rise with progressive clinical deterioration. The patient ultimately died at 13 years of age due to a pulmonary hypertensive crisis and multiple organ failure following a severe episode of gastroenteritis. Conclusions: Despite aggressive treatment with multiple targeted reduced pulmonary artery pressure drug therapies, managing hereditary PAH caused by CAV1 mutations in children remains a significant challenge, with a high mortality rate. Early genetic diagnosis, regular follow-up, and individualized treatment are crucial. It requires the joint efforts of patients, parents, and healthcare providers. Full article

Background: Tricuspid regurgitation (TR) is a common valvular heart condition associated with significantly increased mortality. It is often underdiagnosed and undertreated due to limited insight into patient-specific risk prediction and optimal timing of intervention. Machine learning (ML) methods offer the potential to address these gaps by identifying high-risk patients, estimating survival probabilities, and uncovering key risk markers that influence outcomes. Methods: We developed and evaluated models to predict survival curves for a cohort of 949 patients with moderate or severe TR. Three modeling approaches were compared: Cox proportional hazards (Cox PH), Random Survival Forests (RSF), and DeepSurv (a deep learning-based survival model). Models were trained on clinical and imaging features extracted from cardiac magnetic resonance (CMR) studies and patient records. Performance was assessed using the concordance index (C-index) and time-dependent area under the receiver operating characteristic curve (AUC). Kaplan–Meier analysis and multivariable Cox regression were used to identify significant predictors of mortality. Results: RSF achieved the best predictive performance with a C-index of 78% and AUC of 82%, followed by DeepSurv (C-index 72%, AUC 78%) and Cox PH (C-index 66%, AUC 76%). Predicted survival curves for low- and high-risk groups demonstrated clear separation, underscoring the models’ ability to distinguish patient risk. Key predictors of poor survival included older age, tobacco exposure, right ventricular dilation and hypertrophy, right atrial enlargement, and the presence of non-ischemic myocardial fibrosis. These features were independently associated with elevated mortality risk and showed distinct survival differences in Kaplan–Meier analysis. Conclusions: Machine learning-based survival models, particularly RSF and DeepSurv, offer beneficial tools for individualized risk stratification in patients with advanced TR. Structural abnormalities of the right heart and myocardial fibrosis were among the most significant predictors of mortality, highlighting the importance of early detection and timely intervention. Integrating AI-driven survival prediction into clinical workflows could potentially benefit decision-making and enable more personalized management of TR. Full article

Background: Right heart failure (HF) and tricuspid regurgitation (TR) are closely interrelated conditions, linked by a bidirectional and self-perpetuating pathophysiological relationship. Alterations in right-ventricular (RV) loading conditions, pulmonary vascular impedance, and ventriculo-arterial (VA) coupling play a central role in the development and progression of TR, which in turn exacerbates RV volume overload and end-organ dysfunction. Methods: This review provides a comprehensive overview of the pathophysiology of right HF and TR, focusing on the mechanisms underlying RV dysfunction, pressure–volume (PV) relationships, and pulmonary vascular load. We further examine the clinical implications of this interaction and summarize current strategies for risk stratification, with particular emphasis on disease-specific risk models. Results: TR emerges both as a consequence and a driver of RHF. Conditions such as pulmonary hypertension (PH) and left-sided heart disease promote annular dilation and leaflet tethering, leading to functional TR. Conversely, TR increases RV volume overload, worsening chamber dilation, reducing effective forward stroke volume (SV), and accelerating disease progression. This vicious cycle results in progressive RV impairment, impaired left-ventricular filling through ventricular interdependence, and systemic venous congestion affecting renal and hepatic function. Traditional risk scores fail to capture this complex pathophysiology. In this context, TRISCORE integrates clinical, biological, and echocardiographic (TTE) parameters reflecting RV dysfunction and systemic involvement, providing a more comprehensive assessment of disease severity and prognosis. Conclusions: TR should be considered not only a marker but also a key determinant of right HF progression. A multiparametric approach integrating pathophysiology and disease-specific risk stratification is essential to identifying the optimal therapeutic window and guiding clinical decision making. Full article

Increasing recognition of the clinical impact of isolated tricuspid regurgitation has led to rapid expansion of surgical and transcatheter tricuspid valve interventions. Given the close anatomic relationship between the tricuspid valve and the atrioventricular conduction system, both surgical and transcatheter approaches carry a significant risk of new conduction disturbances and permanent pacemaker implantation. A three-dimensional understanding of the atrioventricular conduction axis is essential to anticipate and mitigate these complications. This review provides a comprehensive overview of conduction system anatomy and physiology in the context of tricuspid valve interventions, highlighting the mechanisms underlying procedure-related conduction abnormalities. We also discuss contemporary management strategies, including approaches to pre-existing transvalvular leads, valve-sparing pacing alternatives, and the evolving role of electrophysiologists within the multidisciplinary heart team. Full article

Background and Objectives: Pulmonary hypertension (PH) is a major contributor to morbidity and mortality in sickle cell disease (SCD), yet reliable and accessible biomarkers for cardiopulmonary risk stratification remain limited. This study aimed to evaluate whether the platelet-to-neutrophil ratio (PNR) is independently associated with echo-estimated PH (ePH) in adolescents and adults with SCD and to compare its predictive value with hemoglobin composition and genotype. Materials and Methods: A retrospective cohort study was conducted at King Fahd Hospital of the University, Al Khobar, Saudi Arabia (January 2019–January 2025). Clinical, laboratory, and echocardiographic data from 114 patients with confirmed SCD who underwent transthoracic echocardiography (TTE) were analyzed. ePH was defined as tricuspid regurgitant velocity (TRV) ≥ 2.5 m/s or pulmonary artery acceleration time (PAAT) ≤ 105 ms. Multivariable logistic and linear regression models were used to assess associations between PNR, hemoglobin fractions, genotype, and pulmonary pressure estimates. Results: Overall, 43% of patients met the criteria for ePH. PNR was not independently associated with ePH or TRV in adjusted analyses. In contrast, higher fetal hemoglobin (HbF) levels were independently associated with lower odds of ePH (adjusted OR 0.92 per 1% increase, 95% CI 0.86–0.98) and lower TRV values. The HbS/β⁰ genotype was significantly associated with increased odds of ePH (adjusted OR 5.44, 95% CI 1.37–24.0). Exploratory analyses demonstrated an inverse association between PNR and lactate dehydrogenase, suggesting that PNR reflects hemolytic activity rather than pulmonary vascular involvement. Conclusions: In this retrospective cohort of patients with SCD, PNR was not independently associated with ePH or TRV after multivariable adjustment. In contrast, hemoglobin composition and genotype, particularly higher HbF and the HbS/β⁰ genotype, were significantly associated with pulmonary pressure estimates. Full article

Tricuspid regurgitation (TR) is a prevalent cardiovascular disorder with significant clinical impact. TR is frequently silent and underdiagnosed and is estimated to impact over 70 million people globally. Characterized by retrograde blood flow from the right ventricle into the right atrium due to incomplete valve closure, TR leads to right heart dilation, systemic congestion, and eventually right-sided heart failure. Importantly, TR may contribute to the onset of atrial fibrillation (AF), the most common sustained arrhythmia, affecting approximately 59 million individuals worldwide. Despite its growing clinical importance, the pathophysiology of TR remains incompletely understood, and current animal models of TR, based on direct valve manipulation, limit translational applicability. We present a novel, minimally invasive porcine model of TR established via femoral/jugular vein catheterization with deployment of an inferior vena cava (IVC) filter. The filter partially impedes tricuspid valve closure, inducing TR without valvular injury. Validation was achieved through multimodal imaging, including fluoroscopy, echocardiography, and electrocardiography, confirming hallmark features of TR, including right atrial and ventricular enlargement and arrhythmic activity. This model provides a reproducible, minimally invasive platform for studying selected features of TR progression. Its minimally invasive nature and preservation of native valvular structure make it a useful preclinical platform for mechanistic and translational research. Full article

Background/Objectives: Totally endoscopic mitral valve repair reduces surgical trauma and accelerates recovery but can be technically challenging, particularly for precise annuloplasty suturing. The VirtuoSEW^® (LSI Solutions, Victor, NY 14564m, USA) automated annular suturing system was developed to standardize and simplify suture placement. This study was an early evaluation of this technology’s safety, efficacy, and feasibility in totally endoscopic microInvasive mitral valve repair (µMVr). Methods: We conducted a retrospective observational study of 20 patients with severe mitral valve disease of various etiologies. All patients underwent mitral valve repair using the VirtuoSEW^® system for automated placement of annuloplasty sutures, combined with leaflet resection or chordal management as appropriate. Postoperative outcomes were assessed at one month using echocardiography and clinical evaluation. Perioperative and postoperative complications and early mortality were systematically recorded. Results: VirtuoSEW^®-assisted mitral valve repair was safe and effective, achieving complete elimination of severe mitral regurgitation in all patients (N = 20, 100%). Annuloplasty rings included Physio-ring (N = 12, 60%), Memo 3D (N = 4, 20%), and Memo 4D (N = 4, 20%), combined with leaflet repair techniques: leaflet plication (N = 5, 25%), neochordae implantation (N = 7, 35%), sliding plasty (N = 2, 10%), commissural repair (N = 1, 5%), and hemibutterfly repair (N = 1, 5%). Concomitant procedures included: tricuspid valve repair (N = 1, 5%) and atrial septal defect closure (N = 1, 5%). Mitral annulus diameter decreased from 42.0 ± 5.3 mm to 34.2 ± 2.2 mm (p = 0.001). Mean total surgery, cardiopulmonary bypass, and aortic cross-clamp times were 170.3 ± 21.3, 143.4 ± 21.5, and 80.4 ± 7.9 min, respectively. ICU stay was 1.0 ± 0.2 days, with a hospital stay of 8.0 ± 1.9 days. No perioperative complications—including bleeding (N = 0, 0%), stroke (N = 0, 0%), infections (N = 0, 0%), or 30-day mortality (N = 0, 0%)—occurred. Conclusions: µMVR invasive mitral valve repair using the VirtuoSEW^® system is safe, effective, and reproducible, as well as compatible with almost all repair techniques, providing complete restoration of valve competence with no early device-related complications. To our knowledge, this is the first clinical study reporting outcomes with this device, supporting its potential to streamline mitral repair and improve procedural efficiency. Full article