Search Results (2,180)

Background: High-risk percutaneous coronary intervention (HR-PCI) in patients with severe left ventricular (LV) systolic dysfunction and complex coronary artery disease may be complicated by abrupt intraprocedural hemodynamic deterioration. Temporary mechanical circulatory support may be considered after individualized Heart Team assessment; however, clinical experience with the pulsatile iVAC2L device remains limited. Case Presentation: An 84-year-old man presented with inferior ST-segment-elevation myocardial infarction, acute decompensated heart failure, pulmonary edema, and an LV ejection fraction of 10–15%. Coronary angiography (CAG) showed a presumed chronic total occlusion of the right coronary artery (RCA) and critical disease of the left main (LMCA), left anterior descending (LAD), and left circumflex (LCx) arteries. Preparation for coronary artery bypass grafting was initiated, but clinical deterioration prompted PCI. The first attempt was aborted after cardiac arrest during coronary wiring. Following stabilization and repeat Heart Team assessment, iVAC2L-supported HR-PCI was performed. During 60 min of active pump support, five stents were implanted in the LMCA, LAD, and LCx. The patient remained conscious and hemodynamically stable without vasopressors. LV ejection fraction was approximately 20% at discharge after six hospital days, and the patient was transferred to inpatient rehabilitation. Conclusions: In this selected patient, iVAC2L-supported HR-PCI was technically feasible and was associated with maintained intraprocedural hemodynamic stability. A single case cannot establish comparative safety or efficacy; prospective studies are required to define patient selection, procedural protocols, and clinically meaningful outcomes. Full article

Acute coronary syndromes (ACS) remain a major cause of cardiovascular mortality and long-term morbidity worldwide despite substantial advances in revascularization techniques, antithrombotic therapies, and lipid-lowering strategies. Although contemporary management has significantly improved survival, a considerable residual risk of recurrent ischemic events, adverse ventricular remodelling, heart failure, and cardiovascular death persists following ACS. Consequently, accurate risk stratification has become increasingly important to guide individualized secondary prevention and optimize long-term outcomes. Traditional risk assessment after ACS relies largely on clinical characteristics, conventional cardiovascular risk factors, and established risk scores such as GRACE and TIMI. However, growing evidence indicates that several emerging biomarkers and pathophysiological pathways provide additional prognostic information beyond conventional models. These markers reflect distinct biological processes including residual inflammatory activity, myocardial injury and remodelling, renal dysfunction, metabolic impairment, and visceral adiposity. This review summarizes current evidence regarding both established and emerging prognostic markers after ACS across six major pathophysiological domains: lipid abnormalities and traditional cardiovascular risk factors; systemic inflammation and residual inflammatory risk; myocardial injury and adverse ventricular remodelling; cardiorenal dysfunction; visceral adiposity; and anti-inflammatory therapeutic strategies. For each domain, we discuss underlying biological mechanisms, key findings from major clinical trials and registries, and the potential incremental value of biomarkers in contemporary risk stratification. Collectively, these markers support a multidimensional approach to post-ACS risk assessment and may contribute to more personalized therapeutic strategies aimed at reducing residual cardiovascular risk. Full article

Background/Objectives: In heart failure with preserved ejection fraction (HFpEF), the gut–heart axis has emerged as a potential contributor to inflammation and cardiometabolic stress. We characterised gut microbiota composition, diversity, and predicted metabolic potential in HFpEF to assess their associations with disease status and clinical heterogeneity. Methods and Results: Faecal samples from 30 HFpEF patients and 28 healthy controls were profiled by means of bacterial ribosomal RNA gene sequencing. The groups were comparable in age (74 years in both groups) and sex (female: 60% vs. 60.7%). HFpEF patients exhibited lower community evenness (p = 0.04) and a trend toward lower diversity (p = 0.08), but no detectable shift in global community structure. The tested clinical and demographic variables explained only a modest proportion of the observed variation in community structure, with substantial residual variation across the beta-diversity analyses. No taxa were differentially abundant between groups at the predefined thresholds. Among clinical stratifications, New York Heart Association (NYHA) class showed the most consistent family-level associations, including stepwise depletion of Lachnospiraceae, Butyricicoccaceae, and Ruminococcaceae and enrichment of Akkermansiaceae; Enterobacteriaceae peaked in milder disease. These severity-associated taxonomic trajectories were accompanied by predicted functional shifts consistent with microbial adaptation to increasing metabolic constraints, including enrichment of stress-adaptation traits and, with increasing functional limitation, depletion of core metabolic and fermentative pathways and relative enrichment of oxidative stress-response pathways. Conclusions: HFpEF is associated with subtle gut microbiota alterations that appear to reflect severity- and context-dependent ecological reorganisation rather than uniform dysbiosis. These findings support severity-informed approaches targeting microbial metabolic function and ecological context rather than broad compositional changes. Full article

Immune checkpoint inhibitors (ICIs) have transformed the therapeutic landscape of advanced melanoma, significantly improving long-term survival. Nevertheless, these therapies may induce immune-related cardiovascular adverse events, which are uncommon but potentially life-threatening. Myocarditis is the best-characterized and most severe manifestation, although a broad spectrum of cardiovascular complications—including pericardial disease, arrhythmias, conduction abnormalities, heart failure, Takotsubo syndrome, and vascular events—has increasingly been recognized. Emerging evidence suggests that melanoma itself and dual immune checkpoint blockade may confer a higher risk of cardiotoxicity than other malignancies or single-agent immunotherapy. This narrative review summarizes current evidence regarding the epidemiology, pathophysiological mechanisms, clinical presentation, diagnostic evaluation, cardiovascular surveillance, and management of ICI-associated cardiotoxicity in patients with melanoma. Diagnosis relies on integrating clinical findings with electrocardiography, cardiac biomarkers, echocardiography, cardiac magnetic resonance imaging, and, in selected cases, endomyocardial biopsy. Prompt interruption of ICI therapy, early administration of high-dose corticosteroids, and escalation to additional immunosuppressive therapies in refractory cases remain the cornerstone of treatment. As the use of ICIs continues to expand, improving cardiovascular risk stratification and implementing evidence-based surveillance strategies will become increasingly important. A multidisciplinary cardio-oncology approach is essential to ensure early diagnosis, optimize cardiovascular outcomes, and preserve the anticancer efficacy of immunotherapy. Full article

Background. White adipose tissue (WAT) is increasingly recognized as an endocrine organ involved in cardiovascular physiology. However, the specific contributions of distinct adipose depots to cardiac homeostasis and adaptation to pathological stress remain poorly understood. We investigated the consequences of visceral (VAT) or subcutaneous (SAT) lipectomy (Lpx) on cardiac phenotype in male and female C57BL/6J mice and evaluated its impact on the response to a stress-inducing heart failure with preserved ejection fraction-like phenotype. Methods. VAT or SAT depot removal was performed in young adult mice. Ten weeks later, we assessed cardiac morphology, function, circulating adipokines, and left ventricular (LV) gene expression. We then exposed separate cohorts to angiotensin II infusion combined with a high-fat diet. We also conducted experiments in ovariectomized (Ovx) females to evaluate the contribution of ovarian hormones. Results. Lpx induced marked depot- and sex-specific effects on body composition, cardiac morphology, and echocardiographic parameters. Changes in LV mass, atrial size, and diastolic indices were observed despite the absence of overt pathology. These alterations were accompanied by substantial modulation of genes involved in cardiac hypertrophy, calcium handling, extracellular matrix remodelling, and energy metabolism. VAT and SAT removal also differentially affected circulating adiponectin, leptin, and MCP-1 levels. Lpx modified the cardiac hypertrophic response to cardiometabolic stress in a sex- and depot-dependent manner. Ovx altered several of these responses and was associated with evidence of increased pulmonary congestion in VAT-lipectomized females. Conclusions. These findings show that WAT contributes to maintaining cardiac homeostasis and influences adaptation to pathological stress through mechanisms highly dependent on adipose depot location, biological sex, and ovarian hormone status. Full article

Background: Diabetes mellitus is frequently complicated by cardiovascular, neurological, and limb-threatening conditions, yet these complications are often evaluated separately. Heart failure, peripheral neuropathy, and lower-limb amputation may coexist in patients with advanced diabetes and may define a clinically severe cardio-neurovascular multimorbidity phenotype. This study evaluated the real-world overlap between these complications. Methods: This retrospective hospital-based study used four routinely generated patient-level exports from the electronic diabetes registry/clinical information system of the Clinical County Emergency Hospital Bihor, Oradea, Romania. The primary cohort comprised 2246 unique patients with diabetes and a recorded heart failure diagnosis; linked exports identified peripheral neuropathy and below- or above-ankle amputation. Results: Peripheral neuropathy was documented in 1028 patients (45.8%). Patients with neuropathy were older (median 70 [IQR 63–76] vs. 67 [IQR 59–73] years, p < 0.001) and had longer diabetes duration (15 [IQR 9–21] vs. 6 [IQR 1–11] years, p < 0.001) than patients without neuropathy. Any lower-limb amputation occurred in 35 patients (1.6%) and was more frequent among patients with neuropathy than among those without neuropathy (2.6% vs. 0.7%, p < 0.001). In the adjusted analysis, male sex, diabetes duration, and insulin therapy were independently associated with lower-limb amputation, whereas the association with neuropathy was attenuated. Conclusions: In this hospital-based retrospective cohort, peripheral neuropathy was common and identified a subgroup with longer-standing diabetes, more intensive therapy, and greater amputation burden. The findings indicate associations within a selected clinical population and should not be interpreted as causal or population-based estimates. Full article

Background/Objectives: Patients with ST-segment elevation myocardial infarction (STEMI) may develop gastrointestinal (GI) bleeding. We aimed to assess the impact of GI bleeding on in-hospital outcomes in patients with STEMI. Methods: This retrospective study was performed using the National Inpatient Sample from the United States of America from the years 2016–2021 to identify STEMI hospitalizations. Index admissions were stratified according to concomitant GI bleeding. The primary outcome was in-hospital mortality; secondary outcomes were inflation-adjusted total charges, total costs, length of stay ≥7 days, acute kidney injury, and cardiogenic shock. Multivariable analysis with a logistic regression model was used to identify associations with in-hospital mortality and several secondary outcomes. Results: Of 1,013,800 index admissions with STEMI, 22,260 (2.2%) had concomitant GI bleeding. Patients with GI bleeding were older and more frequently had comorbidities such as chronic heart failure, liver disease, and chronic kidney disease. In-hospital mortality was higher in patients with GI bleeding (27.8% versus 7.6%, p < 0.001). GI bleeding was associated with 2.30 times (2.11–2.51, p < 0.001), 3.78 times (3.50–4.07, p < 0.001), 2.99 times (2.76–3.24, p < 0.001), and 2.62 times (2.42–2.83, p < 0.001) increased odds of in-hospital mortality, length of stay ≥7 days, acute kidney injury, and cardiogenic shock, respectively. However, liver disease was most strongly positively associated with in-hospital mortality (odds ratio [OR]: 5.50 [5.21–5.80], p < 0.001), acute kidney injury (OR: 6.50 [6.18–6.84], p < 0.001), and cardiogenic shock (OR: 5.47 [5.22–5.74], p < 0.001). Conclusions: GI bleeding was associated with in-hospital mortality, adverse outcomes, and increased resource utilization in patients with STEMI, highlighting the need for risk stratification, implementation of preventative strategies, and timely treatment of GI bleeding. Full article

Trimethylamine N-oxide (TMAO), a gut microbiota-derived metabolite of dietary choline and L-carnitine, has emerged as a leading molecular mediator of the gut–heart–kidney axis in heart failure (HF). This state-of-the-art narrative review synthesizes evidence from 14 observational studies (13 prospective cohorts and one cross-sectional analysis), encompassing a heterogeneous range of HF settings, including established chronic HF, acute decompensated HF, incident HF in community cohorts, and subclinical myocardial injury. Across these populations, elevated circulating TMAO has been associated with adverse outcomes, including mortality, rehospitalization, and major adverse cardiovascular events, although the strength and consistency of associations vary by HF phenotype, renal function status, and population ancestry. The prognostic independence of TMAO is attenuated after adjusting for renal function in several cohorts, reflecting both obligatory renal clearance and a potentially bidirectional relationship with kidney injury. TMAO was not reduced during neurohormonal GDMT uptitration in the BIOSTAT-CHF study, suggesting that gut microbiota dysbiosis may represent a pathophysiological axis not reached by current HF treatment. The field has evolved through three thematic stages: TMAO as a single prognostic biomarker, TMAO within cardiorenal pathophysiology, and multimetabolite and multipathway risk profiling. Beyond the TMAO pathway, emerging evidence for phenylacetylglutamine (PAGln), short-chain fatty acids (SCFAs), and protein-bound uremic toxins as parallel gut-derived cardiovascular mediators supports a multidimensional metabolite profiling approach. Several cohorts suggest that selected multimetabolite panels may provide additional prognostic information beyond TMAO alone, although their composition, calibration, and external validity remain uncertain. Population-specific variation in TMAO levels and prognostic thresholds complicates universal clinical application. Without human interventional data demonstrating that lowering TMAO improves cardiovascular outcomes, TMAO remains a prognostic risk marker rather than a validated clinical target. Clinical translation requires resolving the renal confounding problem, validating multimetabolite panels across diverse populations, and conducting intervention trials targeting the gut–heart–kidney axis. Full article

Background/Objectives: General cardio-oncology guidance describes cardiovascular toxicity from BRAF/MEK inhibitors and immune checkpoint inhibitors (ICIs), but it does not resolve how treatment decisions should change when heart failure (HF) is already present. This critical narrative review separates direct HF-specific evidence from indirect evidence and proposes an HF-centered framework for systemic melanoma. Methods: MEDLINE/PubMed, Embase, and the Cochrane Library were searched for English-language sources published from January 2015 to April 2026, with targeted guideline, prescribing-information, interaction, and geriatric-oncology updates through July 2026. Sources were classified as direct, indirect, or extrapolated. This review follows SANRA principles but does not claim systematic-review conduct, pooled estimates, formal risk-of-bias assessment, or GRADE certainty. Results: Only case-level evidence directly describes systemic melanoma treatment in established HF; most cardiotoxicity rates are derived from selected longitudinal and real-world cohorts. We therefore organize decisions across four domains: HF phenotype and current stability; oncological urgency and alternatives; treatment-specific toxicity phenotype; and detectability, reversibility, and patient priorities. Each domain is graded ordinally and generates its own decision output, and explicit precedence rules resolve situations in which several domains are simultaneously abnormal; the pathway from assessment to documented output is presented as a decision flowchart and applied to illustrative clinical cases. This approach modifies interpretation of symptoms, biomarkers, ventricular function, surveillance, drug interactions, treatment interruption, and rechallenge. Every actionable statement is labeled as guideline-supported or author-proposed, therapy-specific baseline and follow-up monitoring are tabulated separately for each treatment class, and heart failure with preserved ejection fraction is addressed as a phenotype in which clinical deterioration may occur without any change in ejection fraction. Patient-level priorities in older adults—survival, quality of life, avoidance of hospitalization, tolerance of frequent monitoring, oral versus infusion treatment, and functional expectation—are specified as items to be recorded rather than inferred. Conclusions: Stable HF is not an automatic contraindication to effective melanoma therapy, whereas recent or active decompensation requires stabilization or monitored treatment when oncological delay is unsafe. The proposed framework operationalizes guideline principles for an understudied population while making the limits of the evidence explicit. It makes a procedural rather than an empirical claim: it is a transparent structure for documenting a decision that must be made anyway, not an algorithm derived from or validated against outcome data. Full article

Depression and cardiovascular disease (CVD) are two of the heaviest burdens carried by modern medicine, and a growing body of evidence now suggests that they are linked by a bidirectional, mutually reinforcing relationship rather than by a simple cause-and-effect chain. Patients with major depressive disorder appear to carry an elevated risk of incident coronary artery disease, heart failure, and stroke, while patients with established CVD, particularly those recovering from an acute coronary syndrome, frequently go on to develop clinically significant depressive symptoms that worsen prognosis independently of traditional risk factors. Several shared pathophysiological pathways help explain this dangerous liaison, among them autonomic dysfunction, dysregulation of the hypothalamic–pituitary–adrenal axis, chronic low-grade inflammation, platelet hyperreactivity, endothelial dysfunction, and unhealthy behavioral patterns that tend to accumulate once mood suffers. Despite this growing mechanistic understanding, translating this knowledge into effective treatment has proven far from straightforward: several randomized trials of antidepressants and psychotherapy have improved mood, yet they have not consistently reduced hard cardiovascular endpoints, with a handful of notable exceptions. This review brings together the current evidence on epidemiology, biological mechanisms, prognostic implications, and management strategies at the depression–CVD interface, and closes by outlining priorities for future research and for integrated cardiac–behavioral care. Full article

Background/Objectives: Heart failure (HF) phenotype based on left ventricular ejection fraction (LVEF) may be associated with outcomes after coronary revascularization, but data comparing patients with HF with preserved EF (HFpEF) and HF with mildly reduced EF (HFmrEF) undergoing coronary artery bypass grafting (CABG) remain limited. We compared clinical outcomes and longitudinal echocardiographic changes between patients with HFpEF and HFmrEF undergoing isolated off-pump CABG (OPCAB). Methods: We retrospectively analyzed 362 patients with HF who underwent isolated OPCAB between 2012 and 2020, including 273 with HFpEF (LVEF ≥ 50%) and 89 with HFmrEF (LVEF 41–49%). Overall survival was analyzed using Cox regression, and composite cardiovascular adverse events (CCAEs) and their individual components were analyzed using Fine–Gray models. Inverse probability of treatment weighting (IPTW) was used to reduce measured baseline confounding. Longitudinal echocardiographic changes were evaluated using linear mixed-effects models. Results: Patients with HFmrEF had higher baseline NT-proBNP levels and more adverse echocardiographic features than those with HFpEF. In IPTW-weighted analyses, HFmrEF was associated with all-cause mortality (HR, 3.09; 95% CI, 1.39–6.89; p = 0.006), HF readmission (sHR, 5.72; 95% CI, 2.12–15.45; p < 0.001), and CCAEs (sHR, 2.67; 95% CI, 1.37–5.19; p = 0.004). A significant group-by-time interaction was observed for LVEF (p < 0.001), with an early postoperative increase in LVEF in the HFmrEF group. Conclusions: In patients with HF undergoing isolated OPCAB at a single center, HFmrEF was associated with poorer long-term outcomes than HFpEF, although an early postoperative increase in LVEF was observed. These associations may partly reflect differences in baseline HF severity rather than EF category alone. Full article

Background: Depression is a major health issue among older adults and is frequently accompanied by chronic physical conditions. Conventional care of depression in older adults is delivered through primary care settings and often fails to address the complex interactions between mental health, physical illness, and social determinants of health in this population. Integrated care models, characterized by coordinated, multidisciplinary, and patient-centered approaches, have emerged as a promising strategy for improving depression outcomes in late life. Objective: This scoping review aimed to characterize integrated care models for managing depression in older adults. The review examined the structure and implementation of these models and evaluated depression-related outcomes. Methods: A systematic literature search was conducted in PubMed and Google Scholar. Studies published in English between 2006 and February 2026 were considered. Eligible studies included randomized controlled trials (RCTs), cluster RCTs, and quasi-RCTs that evaluated integrated care interventions targeting depression in adults aged 65 years or older or mixed adult populations that included older adults. One reviewer conducted the search and initial screening, and four additional reviewers evaluated the eligibility of full-text reports and extracted data using a structured template. Results were synthesized descriptively. Results: Seventeen studies met the inclusion criteria. Integrated care interventions were implemented across primary care clinics, community health centers, and home healthcare programs in several countries. Participants commonly had depression alongside chronic medical conditions, including diabetes, hypertension, heart failure, or chronic obstructive pulmonary disease. Integrated care models varied in staffing, therapeutic components, specialist involvement, delivery intensity, and comparator conditions. Most interventions incorporated multidisciplinary care teams; structured symptom monitoring; care coordination; behavioral or psychological interventions; and, in some studies, chronic disease management, social support, or technology-supported follow-up. Thirteen studies reported a favorable depression-related finding at one or more assessment points; however, benefits were not always sustained, and some studies reported null- or comparator-favoring findings. Conclusions: Integrated care for depression in older adults encompasses heterogeneous models implemented across diverse healthcare contexts. Common themes included multidisciplinary collaboration, coordinated follow-up, structured psychological or behavioral treatment, symptom monitoring, and integration of mental and physical health management. Favorable outcomes were reported in most studies, but findings varied by population, setting, comparator, intervention intensity, and follow-up duration. These findings may inform future program design, although the effectiveness of the integrated care models and the independent contribution of individual components remain uncertain. Full article

Molecular mechanisms underlying the progression from compensated eccentric hypertrophy to heart failure in chronic aortic regurgitation (AR) remain poorly understood. We investigated associated transcriptional changes induced by chronic volume overload in an experimental model of severe AR. AR was induced in male Wistar rats (n = 10) by retrograde aortic valve perforation and compared with age-matched control rats (n = 8). Sixty days after surgery, cardiac remodeling was evaluated by echocardiography, invasive hemodynamics and myocardial gene-expression profiling using RT-qPCR. Chronic AR induced marked left ventricular dilatation and systolic dysfunction, consistent with decompensated eccentric hypertrophy. These functional alterations were accompanied by coordinated transcriptional changes involving pathways related to apoptosis, oxidative balance, metabolic regulation and calcium handling. AR hearts exhibited an increased BAX/BCL2 ratio, together with reduced SOD2 and increased GPX1 expression, suggesting a transcriptional profile consistent with activation of pro-apoptotic and antioxidant responses. Metabolic remodeling was characterized by decreased AMPKα1, PPARγ and GLUT4 expression, together with increased OLR1 and 15-LOX. KLK10 expression was increased. Reduced SERCA2A expression was observed, consistent with transcriptional alterations involving calcium-handling pathways. Chronic AR is associated with marked structural and functional cardiac remodeling accompanied by coordinated transcriptional alterations across multiple pathways implicated in myocardial dysfunction. This provides potential molecular pathways for further investigation. Full article

Objectives: Severe mitral regurgitation (MR) has been associated with significant morbidity and mortality, necessitating effective risk stratification. The H2FPEF score has demonstrated prognostic value in other cardiac disorders. This study evaluates the prognostic utility of a modified version of the H2FPEF score for severe MR with preserved ejection fraction. Methods and Results: Patients from a tertiary cardiovascular referral center with consecutive index echocardiographic diagnoses of severe MR were included. We excluded patients with secondary MR, reduced LVEF (<50%) and/or missing information for modified H2FPEF score calculation. A modified H2FPEF score was utilized in view of differing obesity cutoffs in our Asian population (BMI > 25 kg/m²) as opposed to the original cutoff (BMI > 30 kg/m²). Patients were stratified based on the modified score into low (0–1), intermediate (2–5), and high (6–9) groups. The primary endpoint, a composite of all-cause mortality and first heart failure hospitalization (HFH), was analyzed using multivariate Cox regression. A total of 388 patients (low 57 [14.7%]; intermediate 218 [56.2%]; high 113 [29.1%] modified H2FPEF score) were included with a median follow-up duration of 4.53 years (interquartile range 2.61 to 6.60). Patients with a high modified H2FPEF score were older, more likely to have hyperlipidemia, diabetes, end-stage renal disease, higher NYHA class, and lower LVEF. Malay ethnicity, hyperlipidemia, diabetes, end-stage renal disease and a higher indexed left atrial diameter were independently associated with greater modified H2FPEF score. High and intermediate modified H2FPEF scores were associated with the primary endpoint (HR 9.17, 95% CI 2.15–39.1 and 6.71, 95% CI 1.62–27.9 respectively) versus low scores. However, a Fine–Gray regression showed no difference in subdistribution hazards of first HFH between high and intermediate scores. Conclusions: The modified H2FPEF score may facilitate risk stratification for all-cause mortality and first HFH in patients with severe primary MR and preserved ejection fraction. Full article

Background/Objectives: Despite advances in diagnostics, prevention, and therapy, heart failure (HF) remains the leading cause of death among cardiovascular diseases. The prognosis for patients remains unfavorable, and their quality of life is severely reduced. In end-stage HF, the only remaining treatment options are heart transplantation (OHT) or the use of long-term mechanical circulatory support (MCS). Methods: This study had a cross-sectional, observational design. Three research tools were utilized: (1) an original metric–clinical questionnaire covering sociodemographic variables (age, sex, education, weight, height, place of residence) and self-reported clinical data (Left ventricular assist device (LVAD) pump model, date of implantation, controlled parameters, comorbidities, estimated ejection fraction, physical activity); (2) the Minnesota Living with Heart Failure Questionnaire (MLHFQ)—a validated, standardized, and translated into Polish anonymous questionnaire; and (3) the Short-Form Survey (SF-36)—a validated, standardized, and translated into Polish anonymous questionnaire. Results: The conducted analysis revealed that patients treated with MCS demonstrated higher quality of life (QoL) across all analyzed aspects. The effect size for the differences was moderate (for bodily pain assessment) or strong (for all other dimensions). The presence of LVAD support explained the largest percentage of variance in QoL, determining the QoL score at 21.9%. Conclusions: The use of MCS is associated with a significantly higher patient QoL in all analyzed dimensions compared to individuals without support. The obtained results emphasize the importance and role of LVAD therapy as an effective therapeutic option associated with higher QoL in patients diagnosed with end-stage HF, which serves as a compelling argument in clinical decision-making regarding qualification for treatment. Full article