Search Results (353)

Background: Malnutrition and systemic inflammation are increasingly recognized as important determinants of prognosis in patients with heart failure. Several immunonutritional indices, including the Prognostic Nutritional Index (PNI), the Controlling Nutritional Status (CONUT) score, and the C-reactive protein–albumin–lymphocyte (CALLy) index, have been proposed as markers of nutritional and inflammatory status. However, their prognostic value in elderly patients with heart failure with preserved ejection fraction (HFpEF) remains incompletely defined. This study aimed to evaluate the prognostic significance of these immunonutritional indices in elderly patients with HFpEF over a long-term follow-up period. Methods: This retrospective observational study included 200 elderly patients hospitalized with HFpEF (mean age 86.6 ± 6.5 years). Clinical, laboratory, and echocardiographic parameters were collected at admission. Nutritional status was assessed using PNI, CONUT score, and CALLy index. Patients were followed for mortality during long-term follow-up. Survival analyses were performed using Cox regression models, receiver operating characteristic (ROC) curves, and Kaplan–Meier analysis. Median follow-up was 3.8 years (IQR 2.1–5.9). Results: During follow-up, 123 patients (61.5%) died, while 77 patients (38.5%) were alive at the end of observation. In univariate analysis, PNI, CONUT score, left ventricular ejection fraction (LVEF), and the tricuspid annular plane systolic excursion to systolic pulmonary artery pressure (TAPSE/sPAP) ratio were significantly associated with mortality. In multivariate analysis, the CONUT score, LVEF, and the TAPSE/sPAP ratio remained independent predictors of mortality. ROC analysis showed strong prognostic performance for the TAPSE/sPAP ratio (AUC 0.932), CONUT score (AUC 0.925), and LVEF (AUC 0.897). Optimal cut-off values for mortality prediction were CONUT ≥ 6, LVEF ≥ 65%, and TAPSE/sPAP ≤ 0.55 mm/mmHg. Kaplan–Meier analysis confirmed significantly reduced survival among patients with higher CONUT scores, higher LVEF, and an impaired TAPSE/sPAP ratio. Conclusions: In elderly patients with HFpEF, nutritional status and cardiopulmonary functional parameters are important determinants of long-term prognosis. The CONUT score emerged as the most informative immunonutritional index, while echocardiographic parameters reflecting ventricular function and right ventricular–pulmonary arterial coupling provided additional prognostic information. Integrating nutritional assessment with echocardiographic evaluation may improve risk stratification in elderly patients with HFpEF. Full article

A key limitation in contemporary HF management is the marked heterogeneity of the syndrome, driven by diverse pathophysiological mechanisms that are not fully captured by traditional classifications based on left ventricular ejection fraction. Precision medicine has emerged as a promising approach to address this heterogeneity by integrating clinical characteristics, circulating biomarkers, advanced imaging, and computational phenotyping strategies. However, current frameworks predominantly emphasize myocardial dysfunction, while the contribution of vascular abnormalities remains underrepresented. The interaction between the left ventricle and the arterial system plays a fundamental role in cardiovascular performance. Arterial stiffness, commonly assessed by pulse wave velocity (PWV), represents a key determinant of vascular aging and a robust predictor of cardiovascular risk. Increasing evidence suggests that vascular dysfunction contributes significantly to the pathophysiology and clinical expression of HF, particularly in phenotypes characterized by preserved ejection fraction. This review synthesizes current evidence on precision medicine in HF and highlights the emerging role of arterial stiffness and PWV in multidimensional patient phenotyping. We propose that integrating vascular parameters into existing phenotyping frameworks may enhance risk stratification, improve mechanistic understanding, and support the development of more personalized therapeutic strategies in heart failure. Unlike previous reviews that have addressed arterial stiffness or heart failure phenotyping separately, this work uniquely integrates ventricular–vascular interaction and pulse wave velocity into a comprehensive precision medicine framework for heart failure. By bridging vascular physiology with data-driven phenotyping strategies, this review provides a novel conceptual model for incorporating arterial stiffness into multidimensional patient characterization across the full spectrum of heart failure phenotypes. Full article

Cardiac arrest is a way of demise of patients who are affected by heart failure (HF), being more frequent in those with HF with a reduced left ventricular ejection fraction (HFrEF), and is, as such, responsible for 30–50% of cardiac death. Specific data on the risk of sudden cardiac death (SCD) related to HF with a preserved ejection fraction (HFpEF) and HF with a mildly reduced ejection fraction (HFmrEF) are lacking, as well as data regarding ventricular arrhythmias in this population. Considering the 0.3% person/year incidence rate of investigator-reported ventricular tachycardia (VT) and ventricular fibrillation (VF), the rate of SCD in the analyzed population seems to be 1.3% per year. Age, gender, history of diabetes and myocardial infarction, left bundle branch block (LBBB) on electrocardiogram (ECG), and a natural logarithm of N-terminal pro B-type natriuretic peptide (NT-proBNP), identified a subgroup of HFpEF patients with a higher risk (5-year cumulative incidence of 11%) of sudden death (SD). In HFpEF patients, both glifozins and finerenone did not demonstrate a beneficial effect on SCD incidence in comparison to placebo. A significantly lower rate of SCD emerged in patients who were treated with dapaglifozin (10 vs. 26 pts) among patients with HF with an improved ejection fraction (HFimpEF), who were defined as patients with a previous left ventricular ejection fraction (LVEF) < 40%. Promising methods discussed include cardiac magnetic resonance, myocardial scintigraphy, genetic assessment, and electrophysiologic studies for predicting SCD in those patients. In conclusion, arrhythmic SCD in HFpEF patients should not be considered merely as an effect of VT/VF; bradyarrhythmia is probably more frequent and dangerous. The effects of drugs in preventing SCD in HFpEF have not been demonstrated yet. Full article

Acute myocardial infarction (AMI) with reduced or preserved left ventricular ejection fraction (LVEF) is associated with distinct prognoses and differing risk factor profiles. However, the use of new-onset atrial fibrillation (NOAF) burden in risk stratification of AMI patients, particularly across LVEF subgroups, remains unclear. We analyzed consecutive AMI patients without prior AF who developed their first in-hospital AF episode between 2014 and 2022. The patients were stratified by LVEF (AMIrEF: <40%; AMIpEF: ≥40%) and AF burden (>10.87% vs. ≤10.87%). The primary endpoint was a major adverse cardiovascular event (MACE), including cardiovascular death and heart failure hospitalization. Among 644 patients with LVEF data, 178 (27.6%) were AMIrEF and 466 (72.4%) were AMIpEF; 248 (38.5%) had a high AF burden. Over a median follow-up time of 4.2 years, the MACE incidence was 18.9 and 23.0 per 100 person-years in low- and high-burden AMIrEF patients, and 7.2 and 17.5 in AMIpEF patients, respectively. After multivariable adjustment, a high NOAF burden was significantly associated with increased MACE in AMIpEF patients [hazard ratio (HR): 2.63, 95% confidence interval (CI): 1.82–3.79], but not in AMIrEF patients [HR: 1.29, 95% CI: 0.79–2.10]. Propensity-matched analysis yielded concordant results [AMIrEF: 1.15 (0.69–1.90); AMIpEF: 2.45 (1.75–3.45)]. In conclusion, a high NOAF burden is strongly associated with adverse long-term cardiovascular outcomes in AMIpEF patients, highlighting its potential utility for risk stratification in this population. Full article

Background: Heart failure (HF) is a complex disease and one of the major causes of morbidity and mortality in the world. Increased B-type natriuretic peptide (BNP) levels have been associated with HF. The NPPB:rs198389 (c.-381T > C) promoter polymorphism has been found to modulate BNP levels. Aim: To investigate possible associations among the NPPB:rs198389 polymorphism, N-terminal pro-BNP (NT-proBNP) concentrations, and phenotypic features in Polish patients with HF. Methods: The study group comprised 250 patients with HF. Genomic DNA was extracted from blood, and genotyping was performed using PCR-RFLP. Results: There were no significant differences in the distributions of NPPB genotypes or alleles between HF females and HF males. Except for body height, there were no significant differences in phenotypic features among HF patients regarding NPPB:rs198389 genotypes. There were also no significant differences in the distributions of either NPPB:rs198389 genotypes or alleles across NT-proBNP concentration terciles. However, age, left-ventricular-mass index, C-reactive-protein levels, serum-creatinine concentrations, and the incidence of myocardial infarction, left ventricular hypertrophy, or reduced ejection fraction (EF) were significantly lower in patients from the lower tercile (LT) than in patients from the middle and/or upper terciles. EF and the frequency of preserved EF in LT patients were significantly higher than those from other terciles. Conclusions: Our results did not confirm associations between NPPB:rs198389 and NT-proBNP serum concentrations or clinical phenotypes in Polish patients with HF. Full article

Background: Left ventricular global longitudinal strain (GLS) measured by speckle-tracking echocardiography (STE) has become a key marker of myocardial systolic function, yet normal reference values remain heterogeneous, and the magnitude of physiological sex differences is not fully defined. We performed a systematic review and meta-analysis to establish pooled GLS reference estimates in healthy individuals, quantify sex-related differences, and contextualize deformation findings relative to conventional systolic function. Methods: A systematic search of PubMed, Scopus, and EMBASE identified observational studies reporting GLS in healthy adults assessed by two-dimensional or three-dimensional STE. Random-effects meta-analysis using standardized mean differences (SMD) compared GLS between women and men. Descriptive pooled reference values were derived using weighted median and interquartile range (IQR) reconstruction from study-level distributions. Meta-regression analyses explored demographic, clinical, and methodological sources of heterogeneity. A complementary analysis evaluated sex-related differences in left ventricular ejection fraction (LVEF) within the same populations. Results: Thirty-two studies, including 19,157 healthy individuals, were analyzed. The pooled population had a weighted median age of 47.5 years and 53% female participants. Overall, GLS demonstrated a weighted median of 20.3% (IQR 17.8–22.5). Women showed higher GLS values than men (20.8% [18.4–23.1] vs. 19.4% [17.0–21.6]). Meta-analysis of 28 studies confirmed significantly greater GLS in females (SMD 0.487, 95% CI 0.409–0.565; p < 0.001), with consistent findings across imaging modalities and no subgroup interaction. Between-study heterogeneity was substantial (I² = 82.7%), although effect direction was uniform. Meta-regression analyses identified no significant moderators, and sensitivity analyses confirmed stable estimates without publication bias. Segmental analysis demonstrated a physiological base-to-apex strain gradient. In contrast, LVEF was largely comparable between sexes, with no clinically meaningful difference (SMD 0.257, 95% CI 0.186–0.327; p < 0.001), indicating preserved global systolic performance despite differences in myocardial deformation. Conclusions: GLS demonstrates a consistent physiological range in healthy populations, with women exhibiting higher longitudinal deformation than men, independent of the imaging modality. These findings support the adoption of sex-specific GLS reference values and highlight the complementary roles of deformation and volumetric indices in improving the interpretation of myocardial function and reducing misclassification in clinical practice. Full article

Background/Objectives: SGLT2 inhibitors (SGLT2i) became a cornerstone of heart failure with preserved ejection fraction (HFpEF) pharmacotherapy in the recent years However, their actual influence on pulmonary veins isolation (PVI) efficacy in this population remains unclear. The aim of the study was to evaluate an impact of SGLT2i on one-year first-time PVI efficacy and clinical course of patients with HFpEF and atrial fibrillation (AF). Methods: This is a single-center retrospective study including 105 HFpEF and AF individuals, who underwent the first-time PVI (51 (48.6%) males; mean age at PVI: 65.2 ± 9.5 years). 53 patients treated with SGLT2i (hospitalized for PVI since 2023) and 52 patients without such a treatment (2020-mid-2023) were assessed according to the clinical presentation and hard endpoints. The primary endpoint was arrhythmia recurrence rate. The secondary endpoint was a composite of major adverse cardiovascular and cerebrovascular events (MACCE). Results: SGLT2i therapy was associated with greater symptom reduction after PVI (90.6% vs. 62.7%; p < 0.001). There was a statistical trend toward reduced all-cause mortality in SGLT2i (0% vs. 5.8%; p = 0.076). Although overall AF recurrence rates were similar between subgroups, Kaplan–Meier analysis showed a non-significant trend toward lower recurrence in the SGLT2i group (p = 0.096). The analysis did not reveal significant differences in terms of cardiovascular hospitalizations, stroke/transient ischemic attack (TIA) and MACCE incidence between the subgroups. Non-vitamin K antagonist oral anticoagulants (NOACs) administration was associated with a lower risk of AF recurrence (OR 0.27; 95% CI 0.096 to 0.77; p = 0.014). MACCE occurrence was predicted by higher CHA₂DS₂-VA (Congestive heart failure, Hypertension, Age ≥ 75, Diabetes, Stroke, Vascular disease, Age 65–74) (OR 5.63; 95% CI 1.57–20.12; p = 0.008), lower left ventricular ejection fraction (LVEF) (OR 0.74; 95% CI 0.57–0.99; p = 0.028) and (vitamin K antagonists) VKA use (OR 97.44; 95% CI 3.2–2962.57; p = 0.009). Conclusions: SGLT2i pharmacotherapy in the study population was linked to higher efficacy in symptom reduction, with a probability of AF recurrence and all-cause mortality reduction, which may suggest a potential beneficial role of SGLT2i in this cohort. Full article

Background: Atrial fibrillation (AF) frequently coexists with heart failure (HF) and worsens clinical outcomes. However, factors associated with AF in HF with preserved (HFpEF) and mildly reduced ejection fraction (HFmrEF) remain poorly defined. This study aimed to identify clinical, laboratory, and echocardiographic determinants of AF in these HF phenotypes. Methods: This retrospective single-center observational study included 700 consecutive patients with HF hospitalized between January 2018 and December 2023. The median age was 74 years (IQR 66–80). Women predominated in the cohort (55.3% vs. 44.7%, p < 0.001). Based on echocardiographically assessed left ventricular ejection fraction, patients were stratified into groups with preserved (≥50%), mildly reduced (41–49%), and reduced (≤40%) ejection fraction. Determinants of AF were evaluated using univariate and multivariate logistic regression analyses, and model discrimination was assessed using ROC analysis. Results: Strongest determinants of AF in our patients with HFpEF and HFmrEF were left atrial size (OR 1.114 per mm increase; 95% CI 1.054–1.177; p < 0.001), moderate and severe tricuspid regurgitation (OR 4.092; 95% CI 1.977–8.466; p < 0.001 and OR 6.957; 95% CI 2.482–19.499; p < 0.001), male gender (OR 1.680; 95% CI 1.076–2.621; p = 0.022) and advanced age (OR 1.070 per year; 95% CI 1.032–1.109; p < 0.001). Conclusions: In patients with HFpEF and HFmrEF, AF is strongly associated with atrial remodeling, with left atrial enlargement as the key structural determinant. The identified associations may contribute to an improved understanding of AF in HFpEF and HFmrEF; however, their potential role in risk stratification requires validation in prospective studies. Full article

Background: The prognostic value of discharge renin–angiotensin–aldosterone system inhibitor (RASi) therapy in contemporary PCI-treated acute myocardial infarction (AMI) survivors with preserved or mildly reduced left ventricular ejection fraction (LVEF) remains uncertain. Methods: A retrospective cohort study of 2530 AMI patients (2019–2022) stratified by RASi use. Exclusion criteria were in-hospital mortality, LVEF < 40%, contraindications to the use of RASis or no percutaneous coronary intervention (PCI). Primary endpoints included heart failure (HF) events, recurrent acute coronary syndrome (ACS), and all-cause mortality. Kaplan–Meier analyses and inverse probability of treatment weighting (IPTW)-weighted Cox models were applied. Results: Over a mean follow-up of 49 months, discharge RASi therapy was not associated with all-cause mortality overall, but was associated with fewer HF rehospitalizations (HR 0.62, 95% CI 0.40–0.95; p = 0.03). Mortality associations differed by AMI type and hypertension status, particularly for NSTEMI (HR 0.36, 95% CI 0.14–0.91; p = 0.03; p for interaction = 0.02) and hypertension (HR 0.36, 95% CI 0.15–0.84; p = 0.02; p for interaction = 0.04). Conclusions: In this single-center observational cohort of PCI-treated AMI survivors with LVEF ≥ 40%, discharge RASi therapy was associated with fewer HF rehospitalizations but not with lower overall mortality. Exploratory subgroup analyses suggested potential heterogeneity according to NSTEMI status and hypertension, but these findings should be considered hypothesis-generating and require confirmation. Full article

Obesity is a chronic, highly prevalent disease affecting nearly one-third of the global population and represents a major independent risk factor for heart failure (HF), particularly heart failure with preserved ejection fraction (HFpEF). Excess adiposity—especially visceral and epicardial adipose tissue (EAT)—acts as an active endocrine and immune organ, promoting chronic low-grade inflammation, oxidative stress, endothelial dysfunction, and adverse myocardial remodeling. Expanded EAT exerts both paracrine inflammatory effects and mechanical constraint on the myocardium, contributing to diastolic dysfunction, microvascular impairment, atrial arrhythmogenesis, and elevated filling pressures despite preserved systolic function. Evidence demonstrates a dose–response relationship between increasing body mass index and incident HF. Clinically, obesity-related HFpEF is characterized by concentric left ventricular hypertrophy, impaired relaxation, increased plasma volume, reduced exercise tolerance, and relatively low natriuretic peptide levels, complicating diagnosis. HF management includes traditional treatment with diuretics, renin-angiotensin system inhibitors, β-blockers, mineralocorticoid receptor antagonists, and angiotensin receptor-neprilysin inhibitors. These agents widely remain foundational as they primarily target hemodynamic and neurohormonal pathways in HF. In contrast, sodium–glucose cotransporter 2 inhibitors consistently reduce HF hospitalizations across the ejection fraction spectrum, while glucagon-like peptide-1 receptor agonists and dual incretin therapies (e.g., tirzepatide) promote substantial weight loss, improve symptoms, and demonstrate promising anti-remodeling effects in obesity-related HFpEF. Recognizing obesity-driven HF as a distinct cardiometabolic entity supports an integrated therapeutic strategy combining structured weight reduction with guideline-directed HF polypharmacotherapy to address both hemodynamic burden and upstream adiposity-related mechanisms. Full article

Ischemic cardiomyopathy is defined as coronary artery disease accompanied by left ventricular dysfunction with an ejection fraction equal to or less than 40%. The substrate of ischemic cardiomyopathy is heterogeneous, characterized by the coexistence of normal, stunned, hibernating, and scarred myocardium within the same myocardial region. Altogether, these components may represent different phases of a single pathological process. It is well-established that the assessment of isolated myocardial viability and ischemia alone has failed to reliably guide the indication for coronary artery bypass grafting (CABG). CABG in patients with low ejection fraction carries a significant risk of perioperative mortality and morbidity, largely related to the development of postcardiotomy shock. Preoperative optimization with pharmacologic or mechanical circulatory support (MCS) is often essential; the decision requires integrating multiple complex factors, including clinical presentation, response to optimization therapy, myocardial viability, the presence of hibernating or scarred myocardium, left ventricular end-systolic volume index, coronary angiography findings, hemodynamic assessment, and the Pulmonary Arterial Pressure Index score. A preoperative evaluation that incorporates anatomical, morphological, functional, and hemodynamic domains enables more precise selection and timing of MCS. Preemptive left ventricular unloading mitigates the physiological impact of cardiopulmonary bypass, preserves end-organ perfusion, and reduces the need for high-dose vasopressors. However, the risk–benefit ratio remains uncertain and may be associated with serious complications. Careful judgment regarding the indications for MCS has the potential to enhance the safety of CABG in high-risk patients, but robust, long-term, prospective studies are needed to determine its true impact on clinical outcomes. In this review, we will examine the indications and criteria for the use of MCS in patients with advanced ischemic cardiomyopathy, as well as the various devices available for preoperative or intraoperative support, including technical considerations, advantages and disadvantages, and associated complications. Full article

Background/Objectives: There are significant gaps in knowledge regarding the heterogeneity of heart failure (HF) phenotypes, particularly among patients with preserved left ventricular ejection fraction (HFpEF). Our aim was to identify phenotypes within the hospitalized North-Eastern Romanian HFpEF cohort and their impact on short-term outcomes. Methods and Results: We derived a cluster model from 924 patients with HFpEF hospitalized over an 18-month interval in the Internal Medicine II Department of the “Sf. Spiridon” Emergency Clinical County Hospital in Iași, Romania. The median age of the patients was 74 years [range 30–101], 59.8% were women, and the most frequent comorbidities were arterial hypertension (93.2%), valvular heart disease (68.7%), atherosclerotic cardiovascular disease (ASCVD, 64.6%) and atrial fibrillation (43%). Statistical analysis identified five distinct phenotypes: cluster 1 (21.6% of patients) consisted of normal-weight patients with valvular disease predominance; cluster 2 (18.2%) described a severe cardiometabolic phenotype; cluster 3 (19.6%) defined a young, hypertensive, and atherosclerotic phenotype; cluster 4 (21.26%) described a hypertensive–atrial fibrillation phenotype; and cluster 5 (18.9%) included elderly, hypertensive non-diabetic patients with severe vascular burden (ASCVD 100%). Conclusions: This study defines five distinct phenotypes within the HFpEF population in our region which differ in terms of clinical characteristics and heart failure pharmacological therapy. These results confirm the significant heterogeneity of HFpEF. The identified phenotypes were not associated with significant differences in composite short-term outcomes, including in-hospital mortality and 30-day rehospitalization for heart failure. Full article

Background: Prognostic heterogeneity in heart failure (HF) is substantial and not fully captured by conventional left-sided echocardiographic parameters. Growing evidence highlights the importance of right ventricular–pulmonary arterial (RV–PA) interaction in HF pathophysiology and outcomes. The echocardiographic tricuspid annular plane systolic excursion-to-systolic pulmonary artery pressure (TAPSE/sPAP) ratio has been proposed as a simple noninvasive surrogate of RV–PA coupling, yet its prognostic value across the HF spectrum remains incompletely defined. Methods: This systematic review followed PRISMA guidelines and was registered in INPLASY. PubMed, Scopus, and EMBASE were searched from inception through January 2026 for observational studies evaluating the prognostic value of TAPSE/sPAP in adult patients with HF. Study selection, data extraction, and risk-of-bias assessment were performed independently by two reviewers. Owing to substantial heterogeneity, a qualitative synthesis with weighted pooled descriptive statistics was performed. Results: Fifteen observational studies including 5389 patients were analyzed, with a median follow-up of approximately 1.9 years, ranging from in-hospital outcomes to long-term follow-up of up to 15 years. Study populations encompassed a wide range of HF phenotypes and clinical settings, including acute and chronic HF, preserved and reduced ejection fraction, valvular heart disease, infiltrative cardiomyopathies, and advanced HF. Across studies, reduced TAPSE/sPAP was generally associated with adverse outcomes, including all-cause mortality and HF-related events, with reported hazard ratios ranging from approximately two- to five-fold. Prognostically relevant TAPSE/sPAP cut-off values tended to cluster within a relatively narrow range, with most thresholds between 0.36 and 0.40 and a weighted median of approximately 0.36. When reported, TAPSE/sPAP showed favorable discriminative performance for adverse outcomes. Overall methodological quality was predominantly fair. Conclusions: Across heterogeneous HF populations, impaired TAPSE/sPAP appears to be a consistent marker of adverse prognosis. These findings support TAPSE/sPAP as a practical, noninvasive indicator of RV–PA uncoupling that may contribute to risk stratification and phenotyping in heart failure. Prospective studies focusing on specific HF phenotypes are needed to clarify its role in longitudinal monitoring and therapeutic decision-making. Full article

Background and Objectives: Atrial secondary mitral regurgitation (A-SMR), also referred to as atrial functional mitral regurgitation, has emerged as a distinct clinical phenotype characterized by left atrial enlargement, mitral annular dilatation, and preserved left ventricular geometry and systolic function. Frequently associated with long-standing atrial fibrillation (AF) and heart failure with preserved ejection fraction (HFpEF), A-SMR challenges the traditional ventricular-centered classification of functional mitral regurgitation (MR) and is increasingly recognized as a clinically relevant condition. Materials and Methods: This narrative review provides an updated and critical overview of current evidence on A-SMR. We summarize available data on pathophysiology, diagnostic imaging, natural history, and therapeutic strategies, with particular emphasis on implications for cardiac surgery and clinical decision-making. Evidence was derived from observational studies, registry analyses, interventional reports, and contemporary guideline documents. Results: A-SMR is primarily driven by atrial remodeling and annular dilatation, with minimal contribution from ventricular distortion or leaflet tethering. Echocardiography and Magnetic Resonance Imaging (MRI) play a central role in diagnosis and phenotypic characterization, allowing differentiation from ventricular functional MR and identification of distinct A-SMR subtypes with potential therapeutic implications. A-SMR is a progressive condition associated with worsening symptoms and adverse clinical outcomes. Rhythm control strategies may reduce MR severity in selected patients by promoting atrial reverse remodeling. Transcatheter edge-to-edge repair (TEER) represents a treatment option for selected high-risk patients, although concerns regarding long-term durability remain in this predominantly annular disease. From a pathophysiological standpoint, surgical mitral valve repair based on annuloplasty directly targets the dominant mechanism of A-SMR and has been associated with favorable outcomes in appropriately selected patients. Conclusions: A-SMR is a distinct and increasingly recognized form of functional MR requiring a mechanism-oriented diagnostic and therapeutic approach. The 2025 ESC/EACTS Guidelines for the management of valvular heart disease have acknowledged A-SMR as a specific clinical phenotype, although dedicated phenotype-specific management recommendations remain limited. Surgical mitral valve repair, particularly when combined with AF ablation, represents a rational treatment strategy in selected patients and may improve long-term outcomes. Full article

Background: The pathophysiology of HFpEF is complex and characterized by systemic inflammation, metabolic dysregulation, and endothelial dysfunction. Trace element involvement in redox balance, mitochondrial function, and calcium signaling is postulated. This cross-sectional analysis aimed to investigate possible differences in hair scalp trace element concentrations in patients with HFpEF and controls. Material and methods: Fifty-eight consecutive patients were enrolled (HFpEF n = 37; controls n = 21). HFpEF diagnosis was established using the HFA-PEFF diagnostic algorithm by two independent cardiologists blinded to hair analysis results. Scalp hair samples were analyzed using inductively coupled plasma mass spectrometry (ICP-MS). Results: HFpEF patients demonstrated higher hair concentrations of magnesium (17.8 (7.3–47.5) vs. 14.0 (6.7–29.0) µg/g, p = 0.037), copper (57.24 (33.87–84.76) vs. 12.96 (9.85–26.02) µg/g, p < 0.001), calcium (322 (106–1330) vs. 145 (74–672) µg/g, p = 0.006), and lead (0.257 (0.164–0.563) vs. 0.159 (0.079–0.283) µg/g, p = 0.03). Conclusions: In this exploratory analysis, HFpEF was associated with differences in selected scalp hair trace element concentrations. The interaction between magnesium, calcium, copper, and lead were noted, with higher concentrations in HFpEF phenotypes. These findings are hypothesis-generating and warrant confirmation in larger cohorts incorporating serum/urine measurements and exposure assessment. Full article