Search Results (5,132)

Background: Poor sleep quality is an increasingly recognized, modifiable cardiovascular risk factor, yet data among patients with established coronary heart disease (CHD) in Central Asia are scarce. We estimated the prevalence of poor sleep quality and identified its correlates in a Kazakhstani CHD population. Methods: In this multi-center cross-sectional study, 398 patients 6–24 months after an index coronary event were assessed for sleep quality. Sleep quality was measured with the Pittsburgh Sleep Quality Index (PSQI; >5 = poor). Anxiety and depression, physical activity, cognition, and clinical and socio-demographic variables were recorded. Associations were examined using logistic regression with subgroup and interaction analyses. Results: Poor sleep quality was reported by 147 patients (36.9%). In the adjusted model, anxiety was the only independent factor associated with poor sleep (OR 1.88, 95% CI: 1.10 to 3.23). The subgroup analysis suggested anxiety (OR 3.94) and lower education (OR 2.58) as correlates in women, whereas retirement (OR 2.27) and low physical activity (OR 2.31) were linked to poor sleep in men. A significant sex–anxiety interaction demonstrated a weaker anxiety effect in men. Conclusions: More than one-third of CHD patients reported poor sleep quality, driven primarily by anxiety, with distinct sex- and age-specific determinants. Sleep and psychological screening should be integrated into secondary prevention, with personalized approaches. Full article

Background/Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as a systemic metabolic disorder associated with an elevated risk of cardiovascular disease. Mac-2 binding protein glycosylation isomer (M2BPGi), a noninvasive serum biomarker of hepatic fibrosis, has also been linked to adverse metabolic and cardiovascular outcomes. However, the association between serum M2BPGi levels and subclinical coronary atherosclerosis in individuals with MASLD remains unclear. We investigated the association between serum M2BPGi levels and coronary artery calcium score (CACS), an established imaging marker of subclinical atherosclerosis, in individuals with MASLD. Methods: This retrospective cross-sectional study included 6514 adults with MASLD who underwent health screening examinations between 2020 and 2025. Participants were categorized into quartiles according to serum M2BPGi levels: Q1 (<0.48), Q2 (0.48–0.61), Q3 (0.62–0.80), and Q4 (≥0.81). Coronary artery calcification (CAC) was defined as CACS > 0. Multivariable logistic regression analysis was performed after adjustment for age, sex, smoking status, liver enzymes, adiposity, dysglycemia, blood pressure, and lipid profile. Multivariable ordinal logistic regression analysis was additionally performed to evaluate the association between M2BPGi levels and CAC severity. Results: The prevalence of CAC increased progressively across M2BPGi quartiles (39.4%, 45.3%, 48.5%, and 57.4% for Q1–Q4, respectively; p < 0.001). In multivariable logistic regression analysis, participants in the highest M2BPGi quartile had significantly higher odds of CAC presence than those in the lowest quartile (OR, 1.32; 95% CI, 1.10–1.58; p = 0.0035). Higher M2BPGi quartiles were also independently associated with greater CAC severity in multivariable ordinal logistic regression analysis (OR, 1.33; 95% CI, 1.13–1.57; p = 0.0007 for Q4 vs. Q1). Conclusions: Higher serum M2BPGi levels were independently associated with both the presence and severity of CAC in individuals with MASLD. These findings suggest that M2BPGi may serve as a potential biomarker for identifying individuals with MASLD at increased risk of subclinical atherosclerosis and may complement conventional cardiovascular risk assessment. Full article

Purpose: Hypertension in women is a dynamic, hormone sensitive condition shaped by cumulative physiological changes across the life course. This review summarises current evidence relating vascular ageing, hormonal regulation, metabolic dysfunction, and reproductive history to blood pressure regulation in women. Materials and Methods: A narrative review of the literature was conducted using PubMed, Scopus and Google Scholar. Clinical, epidemiological, and mechanistic studies were synthesised to evaluate factors influencing hypertension in women. Reports in which menopausal status was not defined, or previous reproductive milestones were not documented, were excluded or interpreted with caution. Results: Evidence suggests that menopause, vascular ageing, metabolic dysfunction, androgen to oestrogen balance, and reproductive history interact to influence endothelial function, neurohormonal regulation, renal sodium handling, and vascular resistance. Ageing-related mechanisms, including cellular senescence, chronic low-grade inflammation, and genetic susceptibility, may contribute to increased cardiovascular risk. Hypertensive disorders of pregnancy identify women who are at higher risk of developing cardiovascular disease later in life and provide an opportunity for earlier risk assessment and prevention. Emerging therapies, including GLP-1 receptor agonists and SGLT2 inhibitors, may offer additional options for improving cardiovascular risk management, although their role in sex-specific prevention remains an evolving area of research. Conclusions: Hypertension in women is best understood within a life-course framework. Incorporating reproductive history, menopausal status, metabolic health, and emerging risk markers may improve cardiovascular risk assessment and support earlier intervention. Full article

Dephosphorylated uncarboxylated matrix Gla protein (dp-ucMGP) is considered a marker of vitamin K status and vascular calcification risk in chronic kidney disease. This study assessed the association of serum dp-ucMGP, alone and combined with albumin, with all-cause and cardiovascular mortality in maintenance hemodialysis patients. This single-center observational cohort study included 133 maintenance hemodialysis patients with a two-year survival follow-up. Analyses involving dp-ucMGP and albumin were performed in 113 patients with complete biomarker data. Baseline serum dp-ucMGP, albumin, inflammatory markers, and routine laboratory parameters were measured. Associations with all-cause and cardiovascular mortality were evaluated using group comparisons, ROC curve analysis, Kaplan–Meier analysis, and Cox regression. Patients who died had significantly lower dp-ucMGP and albumin levels and higher inflammatory and hematological indices than survivors, with similar findings for cardiovascular mortality. The combined dp-ucMGP–albumin model showed higher apparent discriminatory performance than either marker alone for all-cause mortality (AUC 0.793, 95% CI 0.708–0.878, p < 0.001) and cardiovascular mortality (AUC 0.778, 95% CI 0.687–0.868, p < 0.001). Lower dp-ucMGP levels were associated with worse survival. In multivariable Cox regression, higher dp-ucMGP and albumin were independently associated with lower mortality. Combined dp-ucMGP and albumin assessment may provide complementary prognostic information in hemodialysis patients but requires validation in larger cohorts. Full article

Background: Autoimmune diseases (AIDs) are associated with increased cardiovascular risk. However, specific protein mediators linking AIDs to major adverse cardiovascular events (MACE) and cardiovascular death (CV death) remain unexplored. This study identifies proteomic mediators linking AIDs to MACE via high-dimensional mediation analysis in the UK Biobank. Methods: We used UK Biobank data with proteomic profiling by Olink platform. Participants with prevalent myocardial infarction (MI), stroke, and heart failure at baseline were excluded. AIDs were categorized into musculoskeletal (MSK), vasculitis, gastrointestinal (GI), neurologic, and rheumatic fever subsets. Fine–Gray models assessed associations between AIDs and MACE and CV death. Proteome-wide association studies identified proteins associated with both AIDs and cardiovascular outcomes. High-dimensional mediation analysis (HIMA) explored protein-mediated pathways. All models adjusted for age, sex, lipids, BMI, smoking, hypertension, diabetes, chronic kidney disease, atrial fibrillation, and coronary artery disease. Results: Among 400,633 participants (median follow-up 14.5 years, 44.8% male), AIDs were present in 28,754 (7.2%). All AID categories were associated with increased MACE (sHR: MSK 1.34, vasculitis 1.67, GI 1.20, neurologic 1.33, rheumatic fever 1.38; all p < 0.001). For CV death, MSK, vasculitis, and rheumatic fever showed increased risk (sHR 1.34, 1.78, 1.51; all p ≤ 0.004), but not GI or neurologic AIDs. In 43,599 participants with proteomic data, HIMA identified 66 and 32 unique potential mediators linking AIDs to MACE and CV death, respectively. Four proteins (Growth Differentiation Factor 15, Interleukin-15, urokinase plasminogen activator receptor, and Tenascin C) mediated the AID-MACE relationship across multiple AID categories. Growth Differentiation Factor 15 and Interleukin-15 were shared mediators for CV death. Conclusions: This proteomic analysis identifies specific proteins that may mediate the association between AIDs and adverse cardiovascular outcomes, offering mechanistic insights into immune-related cardiovascular risk. These findings are hypothesis-generating and require replication and validation before the identified proteins can be considered causal mediators or adopted for clinical risk stratification. Full article

Background/Objectives: Cardiovascular risk (CVR) prediction using SCORE2 may incompletely capture the burden of subclinical atherosclerosis in patients with chronic inflammatory conditions. Identifying simple, accessible markers to refine risk stratification remains an unmet need. This study aimed to evaluate whether serum urate improves detection of subclinical atherosclerosis beyond SCORE2 in a psoriatic arthritis cohort. Methods: We conducted a cross-sectional study including 250 patients with psoriatic arthritis fulfilling CASPAR criteria. Vascular assessment comprised carotid and femoral ultrasound and abdominal radiography. Atherosclerotic plaque was defined according to Mannheim criteria. The main outcomes were global plaque (≥1 vascular territory) and extended plaque (≥2 territories). Multivariable logistic regression adjusted for SCORE2 categories assessed independent associations. Incremental value was evaluated using decision curve analysis (DCA), category-free net reclassification improvement (cfNRI), and integrated discrimination improvement (IDI). Results: Hyperuricemia prevalence was 21.6%. Patients with hyperuricemia showed a higher prevalence of global plaque (88.9% vs. 62.8%, p < 0.001). After adjustment for SCORE2, serum urate was independently associated with global plaque (OR 4.23, 95% CI 1.26–14.2). Notably, 64.3% of patients classified as low–moderate risk already exhibited plaque. In the 50–69-year subgroup, adding serum urate improved reclassification (cfNRI +0.60; IDI +0.031) and was associated with higher net clinical benefit across decision thresholds. The combined model (SCORE2+HU+cIMT) achieved the highest curves, although with limited incremental gain over HU alone. Conclusions: SCORE2 categories showed substantial discordance with imaging-defined subclinical atherosclerotic burden in this population. Serum urate, an inexpensive and widely available marker, may help refine cardiovascular risk stratification and identify patients who could benefit from further vascular assessment. Full article

Background/Objectives: Finerenone improves cardiovascular and renal outcomes in diabetic kidney disease (DKD), but hyperkalemia remains a key safety concern. Patients with elevated baseline potassium levels (≥4.9 mEq/L) are largely excluded from clinical trials, and real-world data in this population are scarce. Methods: In this retrospective multicenter cohort study derived from the FINE-TURK cohort, adults with DKD who initiated finerenone with baseline potassium ≥ 4.9 mEq/L were included. The primary outcome was clinically significant hyperkalemia (K ≥ 5.5 mEq/L) within three months. Multivariable logistic regression analyses were used to identify associated factors, with multiple sensitivity analyses performed. Results: A total of 166 patients were included, of whom 47 (28.3%) had baseline potassium levels between 5.1 and 5.5 mEq/L. Of the 166 patients, 35 (21.1%) reached the primary outcome, and 10 (6%) patients had follow-up potassium ≥ 6.0 mEq/L. 126 (76.8%) patients required no intervention, 24 (14.6%) were initiated on potassium binders, and finerenone was discontinued in only 12 (7.3%) patients. Lower baseline estimated glomerular filtration rate, baseline urinary albumin, loop diuretic use and 20 mg finerenone dose were associated with the primary outcome. In contrast, baseline potassium was not associated with the primary outcome. Conclusions: In patients with DKD and elevated baseline potassium levels, finerenone initiation was associated with manageable rates of hyperkalemia. Our findings support the cautious use of finerenone in selected patients under close monitoring, as well as highlight the need for a multidimensional approach to hyperkalemia risk assessment. Full article

Hypertensive heart disease (HHD) is a major global cause of cardiovascular mortality and disability-adjusted life years (DALYs). We used an age–period–cohort model to assess mortality and DALY trends (1992–2021) across sociodemographic regions and their association with healthcare quality. Using Global Burden of Disease (GBD) data (1992–2021), we applied an age–period–cohort model to HHD mortality and DALYs in adults aged 20–54 across SDI regions and examined associations with healthcare quality. HHD mortality and DALYs declined across most SDI regions over 29 years, with high-middle SDI females showing the greatest reductions (ASMR: −3.2% annually; ASDR: −2.9%). Conversely, high-SDI regions exhibited rises of ~1.7% and ~1.2% in males and females, respectively. Low-SDI regions maintained the highest absolute burden, with 2021 mortality rates 10-fold higher in males and 13.7-fold higher in females versus high-SDI regions, despite the steepest declines. The male-to-female mortality ratio ranged from 1.74× (high-middle SDI) to 1.14× (low SDI). Age-related patterns diverged markedly: high-SDI females showed a 46.7% risk decline for ages 20–54, while males experienced a 92–111% lifespan risk increase. Period effects showed pre-2002 peak risk in lower-SDI versus post-2002 increases in high-SDI regions (males: +36%; females: +24%). The 1997–2001 birth cohort in high-SDI regions showed the highest risk (males: RR 1.75–1.85; females: RR 1.45–1.50). No significant correlation was found between HHD burden and HAQI (ASMR: r = 0.40; ASDR: r = 0.42; p > 0.05). HHD remains a major global health concern, with rising burden in high-SDI regions and persistent male predominance. Healthcare quality alone is insufficient, highlighting the need for targeted prevention focused on modifiable risk factors in working-age adults. Full article

Background/Objectives: Endothelial dysfunction represents an early stage of vascular injury in type 2 diabetes mellitus (T2DM) and contributes to increased cardiovascular risk. Leptin, a hormone involved in metabolic and inflammatory regulation, has been implicated in vascular dysfunction. However, its association with digital thermal monitoring (DTM)-derived peripheral vascular reactivity in T2DM remains unclear. Methods: This cross-sectional study enrolled 88 patients with T2DM to investigate the association between serum leptin levels and peripheral vascular reactivity, assessed using the digital thermal monitoring-derived vascular reactivity index (VRI). Based on the VRI values, patients were categorized as having good (VRI ≥ 2.0), intermediate (VRI of 1.0–1.9), or poor (VRI < 1.0) vascular reactivity. Serum leptin levels were quantified using an enzyme immunoassay. Results: Patients with poor vascular reactivity were older and had higher total cholesterol, triglyceride, fasting glucose, glycated hemoglobin, urine albumin-to-creatinine ratio, and leptin levels. In the primary parsimonious multivariable logistic regression model adjusted for age, sex, body mass index (BMI) and eGFR, higher serum leptin levels were associated with vascular reactivity dysfunction. Linear regression analysis also showed that log-transformed leptin levels were negatively associated with VRI. Exploratory analyses, including poor vascular reactivity models and penalized regression models, showed generally consistent findings but were interpreted cautiously because of the limited number of outcome events. Conclusions: Higher serum leptin levels were associated with impaired DTM-derived peripheral vascular reactivity in clinically stable patients with T2DM after adjustment for age, sex, BMI, and eGFR. These findings should be interpreted cautiously and require validation in larger prospective studies. Full article

Background/Objectives: Systemic inflammation is common in patients with cancer and may reflect tumor activity, disease extent, and the patient’s overall clinical condition. The systemic immune-inflammation index (SII), calculated from neutrophil, platelet, and lymphocyte counts, is a simple marker, but its relationship with tumor type, cardiovascular burden, and mortality is not fully clarified. To compare patients with respiratory system malignancies (RSM) and gastrointestinal tract malignancies (GITM) in terms of cardiovascular comorbidity, inflammatory profile, tumor-related characteristics, and recorded all-cause mortality, and to assess the association between SII and mortality. Methods: We analyzed 879 patients with solid malignancies, including 350 with RSM and 529 with GITM. SII was calculated as platelet count × neutrophil count/lymphocyte count. Cardiometabolic and cardiovascular burden was assessed according to the number of recorded cardiometabolic risk factors and cardiovascular diseases. The main outcome was recorded all-cause mortality. Results: Patients with RSM were younger and more often male, and more frequently had stage IV disease, whereas patients with GITM had a more pronounced cardiometabolic risk profile. Mortality was higher in RSM than in GITM (42.3% vs. 29.9%), and SII was also higher in RSM (median 1117.8 vs. 716.8). In the overall cohort, higher SII was associated with mortality after adjustment for age, sex, cancer type, stage, and metastatic disease (OR 1.11 per 1000-unit increase, 95% CI 1.02–1.21; p = 0.013). Mortality increased across SII tertiles from 22.5% to 34.5% and 47.4%. Adding SII to the clinical model led to only a small increase in AUC, from 0.719 to 0.729. Conclusions: SII was higher in patients with RSM and was associated with recorded all-cause mortality. However, its added prognostic value was modest. SII should therefore be interpreted as a supportive inflammatory marker, together with tumor stage, metastatic disease, and the broader clinical condition of the patient. Full article

Background/Objectives: Psoriatic disease (PsD) is a chronic cutaneous and systemic inflammatory condition associated with an increased risk of metabolic-dysfunction-associated steatotic liver disease (MASLD) and its complications. Our objective was to determine the prevalence of MASLD in our overall cohort and to analyze it across PsO, PsA, and healthy control groups. The secondary objective was to describe hepatic steatosis and fibrosis using transient elastography (FibroScan^®) and to characterize hepatic scores within each study group. The third objective was to assess whether specific cardiovascular risk factors were associated with the development of hepatic steatosis or fibrosis in individuals with PsD and healthy controls. Methods: A cross-sectional study was conducted at a single tertiary care center, enrolling consecutive patients from the Dermatology and Rheumatology Departments. Individuals with pre-existing liver disorders were excluded. The control cohort comprised 102 healthy volunteers without chronic inflammatory or hepatic conditions. All participants underwent comprehensive clinical assessments, serum biomarker analysis, and FibroScan^®. Results: A total of 330 participants were included, 228 with PsD (101 with psoriasis (PsO) and 127 with psoriatic arthritis (PsA)) and 102 healthy controls. MASLD was present in 39% of the overall cohort, with a prevalence of 47.5% in PsO, 32.2% in PsA, and 8.8% in healthy controls (p < 0.001). FibroScan^® measurements indicated a tendency toward increased liver stiffness and higher controlled attenuation parameter (CAP) values in patients with PsD. Both PsO and PsA groups showed a higher prevalence of cardiometabolic risk factors compared with controls (p < 0.05). Non-invasive fibrosis indices were also significantly altered in both patient groups. Conclusions: Patients with PsD demonstrated a higher prevalence of MASLD, hepatic fibrosis, and cardiometabolic abnormalities compared with healthy controls in our cohort. Full article

Background: Breast cancer patients are exposed to cardiovascular complications related to both pre-existing cardiovascular risk factors and cardiotoxic cancer therapies. Heart failure with preserved ejection fraction (HFpEF) is an emerging and often under-recognized condition in this population, potentially present before treatment initiation and further influenced by oncologic therapies. This study aimed to characterize baseline HFpEF probability and its longitudinal evolution using validated scoring systems in a real-world cardio-oncology cohort. Methods: We retrospectively evaluated 145 women with breast cancer undergoing baseline cardio-oncology assessment before initiation of potentially cardiotoxic therapies. HFpEF probability was estimated using three validated algorithms (H₂FPEF, ABA, and HFA-PEFF). A subgroup of 89 patients underwent exploratory reassessment after 12 ± 3 months to investigate longitudinal changes in HFpEF probability according to treatment. Results: At baseline, HFpEF probability varied substantially according to the scoring system applied, with 14.8–41.5% of patients classified as having intermediate-to-high probability. Agreement among the three algorithms was limited, particularly between HFA-PEFF and H₂FPEF/ABA scores. Exploratory longitudinal analyses showed no significant changes in HFpEF probability categories during follow-up. Conclusions: HFpEF probability assessment in breast cancer patients showed substantial baseline heterogeneity across validated scoring systems, with clinically relevant differences in risk classification and limited inter-score agreement. These findings provide novel insights into an underexplored cardio-oncology phenotype and suggest that currently available HFpEF scoring systems may not be directly interchangeable in this clinical setting. Prospective studies including provocative testing are needed to determine the clinical relevance of HFpEF probability scores in breast cancer patients. Full article

Background/Objectives: Metabolic-obesity phenotypes are dynamic, yet little is known about how their longitudinal transitions affect cardiovascular disease (CVD) risk. We aimed to characterize these transitions and examine their associations with incident CVD in middle-aged and older Chinese adults. Methods: We included 4516 participants from the China Health and Retirement Longitudinal Study (CHARLS) who were free of CVD at the follow-up baseline (wave 3). Metabolic-obesity phenotypes (metabolically healthy non-obese [MHNO], metabolically unhealthy non-obese [MUNO], metabolically healthy obese [MHO], and metabolically unhealthy obese [MUO]) were assessed in 2011 and 2015, and six trajectory patterns were defined. Incident CVD (heart disease or stroke) was ascertained from 2015 to 2020. Cox proportional hazards models estimated associations between trajectory groups and incident CVD, and Kaplan–Meier curves compared cumulative incidence across groups. Results: Stable MHNO accounted for 35.96% of the cohort, whereas the stable non-MHNO group accounted for 28.06%. After multivariable adjustment, the small obesity recovery group (n = 89) showed an elevated CVD risk estimate compared with the stable MHNO (HR 2.32, 95% CI 1.33–4.05), while stable non-MHNO group were associated with higher CVD risk (HR 1.72, 95% CI 1.36–2.18). Incident obesity showed elevated but non-significant risk (HR 1.71, 95% CI 0.94–3.10), and metabolic decline showed borderline significance (HR 1.36, 95% CI 1.00–1.85). Sex-stratified analyses showed heterogeneous risk patterns. Conclusions: Metabolic-obesity phenotypes are dynamic, but unfavorable phenotypes often persist. The obesity recovery group, defined using BMI, may represent a heterogeneous group and does not necessarily indicate true cardiometabolic recovery; the observed association should not be interpreted as evidence that weight loss itself increases CVD risk. These findings highlight the importance of jointly considering longitudinal changes in metabolic health and obesity when examining their associations with incident CVD. Full article

Thoracic morphology is increasingly recognized as an important determinant of cardiopulmonary phenotype, influencing cardiovascular mechanics, respiratory physiology, and the interpretation of diagnostic imaging findings. Although the radiological Haller Index (HI) remains the reference standard for quantifying pectus excavatum severity, its dependence on computed tomography and ionizing radiation limits widespread clinical implementation, particularly in settings requiring serial evaluations. To overcome these limitations, the Modified Haller Index (MHI) was developed as a simple, non-invasive, radiation-free alternative that combines external thoracic anthropometry with echocardiographic assessment. Since its introduction, the MHI has undergone clinical validation and has progressively expanded beyond the assessment of chest wall deformities, demonstrating that thoracic conformation is not merely an anatomical characteristic but a clinically relevant determinant of cardiovascular and respiratory physiology. Growing evidence indicates that thoracic morphology influences cardiac chamber geometry, ventricular filling, stroke volume, myocardial deformation, ventricular–arterial coupling, exercise stress echocardiography findings, pulmonary function, and symptom perception across a broad spectrum of cardiovascular and respiratory diseases. Elevated MHI values identify individuals with a reduced antero-posterior thoracic diameter and a distinctive cardiopulmonary phenotype characterized by external cardiac compression, smaller cardiac chambers, restrictive ventilatory physiology, and apparent alterations in myocardial mechanics despite the absence of intrinsic myocardial disease. Building upon the clinical validation of the MHI, a novel patented anatomical measurement device was engineered to standardize thoracic morphometric assessment by enabling direct acquisition of both latero-lateral and antero-posterior thoracic diameters within a single measurement procedure. The device integrates dedicated anatomical reference elements, an innovative adjustable sternal pointer, movable measurement components, and a standardized acquisition workflow into a portable, low-cost, and radiation-free platform, thereby improving measurement reproducibility while simplifying bedside MHI determination. This narrative review summarizes the historical evolution of thoracic morphometry, the development and clinical validation of the MHI, the engineering rationale, structural architecture, and measurement workflow of the patented device, and the growing evidence supporting the clinical significance of thoracic conformation across cardiovascular and respiratory medicine. Together, the MHI and the proposed anatomical measurement device establish a practical platform for standardized, radiation-free thoracic morphometry that may facilitate routine bedside phenotyping. Future integration with digital technologies, artificial intelligence, and advanced imaging systems may further enable next-generation digital thoracic phenotyping for personalized cardiovascular and respiratory characterization, risk stratification, and precision medicine. Full article

Background: Current ESC/EACTS guidelines recommend bioprosthetic valves for aortic valve replacement (AVR) in patients > 65 years, yet their use is increasing among younger individuals. The INSPIRIS Resilia (IR) valve, a next-generation bioprosthesis, was designed to improve durability and reduce structural valve degeneration (SVD). This study compares clinical and valve-related outcomes up to six years in patients undergoing AVR with either the IR or its predecessor, the Perimount Magna Ease (PME) valve. Methods: Between January 2017 and December 2023, 2053 patients underwent isolated or combined AVR at a single institution (1602 PME; 451 IR). Propensity-score matching identified 224 patient pairs with comparable baseline characteristics. Outcomes were assessed over follow-up extending up to six years, focusing on cardiovascular and valve-related adverse events. Transvalvular gradients were also assessed at follow-up. Results: After matching, mean age was 64.2 ± 7.7 years in both groups. Freedom from cardiovascular mortality at six years was similar between PME and IR (96.6% vs. 98.2%; p = 0.34), as were rates of stroke, rehospitalization, prosthetic valve endocarditis, and reintervention. A total of 12 PME (5.4%) and six IR valves (2.5%) were explanted during follow-up (p = 0.15), with prosthetic endocarditis representing the leading cause of reintervention. Only one case of severe SVD was observed in both groups. Conclusions: In patients undergoing AVR with comparable baseline risk profiles, IR and PME valves demonstrated similar clinical, valve-related, and hemodynamic outcomes up to six years of follow-up. Prosthetic valve endocarditis represented the leading cause of valve failure, whereas structural valve deterioration remained rare. Longer follow-up and a greater number of valve-related events will be necessary to determine whether differences in bioprosthetic valve degeneration emerge over time. Full article