Active and passive fixation leads are both commonly used in transvenous cardiac implantable electronic device procedures. Although active fixation leads (AFLs) are often selected over passive fixation leads (PFLs) for more precise positioning and the possibility of a potentially simpler future lead extraction, current evidence remains inconclusive regarding the delayed, post-discharge complications of lead dislodgement and cardiac perforation. This systematic review and meta-analysis aimed to compare these complications between AFLs and PFLs. Observational studies enrolling consecutive adult patients undergoing transvenous cardiac device implantation with either AFLs or PFLs were systematically identified. Studies reporting post-discharge lead dislodgement and/or cardiac perforation for both AFLs and PFLs were included. Pooled event rates were calculated using random-effects models, with sensitivity, cumulative and bootstrap analyses performed to assess robustness. Meta-regression and subgroup analyses for key variables were conducted to assess heterogeneity and possible effect modifications. Eighteen studies were included, encompassing 69,198 patients (77,248 leads: 38,250 AFL and 38,998 PFL) who were followed up for at least 1-month post-implantation. Post-discharge lead dislodgement was significantly less frequent with AFLs than with PFLs [Odds Ratio (OR) 0.71; 95% Confidence Interval (CI), 0.54-0.94, p = 0.015], driven by a marginally significant lower risk involving atrial leads (OR: 0.70; 95% CI, 0.49-1.00, p = 0.052). Additionally, AFLs were associated with a significantly higher risk of post-discharge cardiac perforation compared to PFLs (OR 1.78; 95% CI, 1.09-2.90, p = 0.02), driven by a marginally significant higher risk of ventricular leads (OR 1.94; 95% CI, 0.97-3.86, p = 0.06). Subgroup analyses revealed that, in implantable cardioverter-defibrillator implantation, AFLs were associated with a lower risk of dislodgement, but a higher risk of perforation compared with PFLs. Compared with PFLs, AFLs are associated with a higher risk of post-discharge cardiac perforation, mainly ventricular, but with a lower risk of post-discharge dislodgement, mainly atrial. A pragmatic approach might favour the use of AFLs in atrial positions and PFLs in apical or trabeculated ventricular positions. Fixation strategy should be individualized rather than routine preference, and integrated into a broader lead lifecycle perspective, encompassing complications, revisions, and potential future extraction.
Although the "I NEED HELP" criteria facilitate timely consideration of advanced heart failure (HF) therapies, patient classification based on the variables included in the criteria are scarcely investigated. This study aimed to identify phenotypically distinct subgroups of patients with advanced HF using unsupervised cluster analysis based on the variables included in these criteria. A multicenter registry was used to identify patients hospitalized with HF who met at least 1 I NEED HELP criterion. Latent class analysis was performed on 9 variables from the criteria. A total of 2520 patients (mean age, 74±13 years; 40% women) were included in this study. Latent class analysis identified 3 phenotypes: more de novo HF with the lowest number of applicable criteria (phenotype 1, 31%); younger age with the lowest left ventricular ejection fraction and highest number of applicable criteria (phenotype 2, 19%); and older age with more comorbidities and poorer renal function (phenotype 3, 49%). After multivariable adjustment, phenotypes 2 and 3 were associated with a higher incidence of composite all-cause death or rehospitalization for HF (phenotype 2: hazard ratio [HR], 1.96 [95% CI, 1.58-2.42]; phenotype 3: HR, 1.54 [95% CI, 1.28-1.84]; phenotype 1: reference) during the follow-up period (median, 461 [interquartile range, 130-730] days). This study describes a novel phenotypical classification based on the I NEED HELP criteria, with significantly different prognoses identified for patients with advanced HF. These classifications may facilitate risk stratification in this population with a complicated clinical profile.
暂无摘要（点击查看详情）
Acute respiratory distress syndrome (ARDS), characterized by inflammation-induced pulmonary reactive oxygen species (ROS) elevation, causes severe alveolar epithelial cells damage and promotes M1 polarization of alveolar macrophages (AMs). M1-polarized AMs generate substantial ROS and potent pro-inflammatory cytokines, triggering a widespread secondary inflammatory cascade. Therefore, ARDS is trapped in a vicious "ROS-M1 macrophages polarization-inflammation-ROS" cycle, which markedly exacerbates disease progression. Constrained by this, previous monotargeted therapeutic approaches exhibited suboptimal efficacy and failed to meet clinical needs. Herein, a vicious cycle-normalizing strategy was introduced to target the dual pathogenic mediators in the ARDS microenvironment. Specifically, phosphatidylserine-modified and metformin-loaded biomimetic honeycomb manganese dioxide nanoparticles (PS-HM/M NPs) were developed, with superoxide dismutase (SOD) and catalase (CAT)-mimetic properties to eliminate excessive intracellular ROS while metformin efficiently promotes phenotypic transition of AMs toward the pro-resolution M2 state. In an acute lung injury (ALI) model, PS-HM/M NPs successfully interrupted the malignant cycle and significantly resolved inflammation. In conclusion, this work highlighted the critical role of regulating the ROS-macrophage crosstalk and provided a promising avenue for ARDS therapy.
Early rhythm control reduces cardiovascular events in patients with atrial fibrillation (AF) and cardiovascular comorbidities. Whether this effect is consistent across severities of different AF-associated conditions is not known. In the EAST-AFNET 4 biomolecule study (n=1,586; median age 70 years; 45% women), 14 circulating biomarkers reflecting inflammation, fibrosis, ageing, cardiac strain, and myocardial damage were quantified. Log-transformed, winsorized biomarkers were analysed in quintiles to detect non-linear associations and as continuous parameters. Cox proportional hazards models evaluated associations with the primary outcome (cardiovascular death, stroke, or unplanned hospitalization for heart failure or acute coronary syndrome) and the safety outcome (death, stroke, or major bleeding) of the trial, including interaction terms for biomarkers and randomized treatment (early rhythm control [ERC] vs usual care). [UC]). Two independent cohorts, BBC-AF resembling UC and a TRUST snapshot resembling ERC were combined for external replication. All tests were exploratory. ERC reduced the primary outcome consistently across biomarker concentrations. No signal for treatment interaction was observed for 13 of 14 biomarkers for the primary outcome. For BMP10, a nominal interaction was observed in categorical analyses, suggesting an attenuated treatment effect of ERC in patients in the lowest BMP10 quintile. No interaction was detected for continuous parameters. Similar patterns were observed in exploratory analyses of the replication cohort. Early rhythm control therapy is effective across patients with different severities of conditions associated with atrial fibrillation as quantified by biomolecule concentrations. A potentially attenuated effect of ERC with low BMP10 concentrations warrants further research.
Little is known about the differences in left atrial (LA) volume and strain assessed with two-dimensional (2DE) and three-dimensional echocardiography(3DE). Therefore, this study aimed to compare 2DE and 3DE parameters in healthy subjects. We obtained LA volumes and strains by 3DE and 2DE in 328 healthy subjects (52 ± 13 years; 51.83% men). Means of 3DE LA volume indexes (LAVIs) were higher than those derived from 2DE (maximal LAVI: 26.75 vs. 22.66 mL/m2; minimal LAVI: 11.76 vs. 9.30 mL/m2; preA LAVI: 19.52 vs. 16.23 mL/m2, respectively, all p < 0.001). Conversely, means of 3DE LA phasic strains were lower than those derived from 2DE (LA reservoir strain: 25.16 vs. 32.01%; LA conduit strain: 13.09 vs. 16.52%; LA contractile strain: 12.12 vs. 15.52%, respectively, all p < 0.001). Similarly, total, passive, and active LA emptying fractions (EF) were lower with 3DE than those with 2DE (all p < 0.05). Correlation between 3DE and 2DE was moderate for LAVIs (all r > 0.65, all p < 0.001), with 2DE showing a systematic underestimation (bias: -4.09 mL/m2 for maximal LAVI; -2.46 mL/m2 for minimal LAVI, -3.30 mL/m2 for preA LAVI). For LA strain parameters, only conduit strain showed moderate correlation (r = 0.65, p < 0.001) with an overestimation bias of +3.42%, while reservoir and contractile strains correlated poorly between modalities with wide limits of agreement. LAEFs also demonstrated poor inter-modality agreement. 2DE yielded lower LAVIs but higher LA strain and EF values compared to 3DE. Although there was a significant correlation between the 2D and 3D parameters, agreement analysis indicated that their normal reference values were not interchangeable.
Atrial fibrillation (AF) is the most common arrhythmia, affecting up to 6 million in the United States, and is associated with significant morbidity and mortality. Despite higher rates of AF clinical and social risk factors, underrepresented racial and ethnic group individuals have lower AF incidence. Structural factors, such as neighborhood-level racial and ethnic residential segregation, have been associated with incident cardiometabolic disease, particularly among underrepresented individuals. However, as data on segregation and incident AF are sparse our objective was to examine the association of segregation on AF. Data from MESA (Multi-Ethnic Study of Atherosclerosis; baseline 2000-2002) were used to identify those with a diagnosis of AF during follow-up. Own-group racial and ethnic segregation was defined by local Gi* statistic, which compares the percentage of each racial and ethnic group in a current census tract to the surrounding area. Racial- and ethnic-stratified Cox proportional hazard models were used to estimate hazard ratios comparing across segregation levels. Models were adjusted for demographic, participant, and neighborhood level socioeconomic, and clinical factors. Our cohort comprised 5375 participants (31% Black, 25% Hispanic/Latino, 44% White). During a median follow-up of 16.6 years, 1035 participants (19.3%) were diagnosed with AF. Black and Hispanic/Latino participants had the highest prevalence of AF risk factors at baseline and were more likely to reside in segregated neighborhoods than White participants. After adjusting for demographic, socioeconomic, and clinical factors, neighborhood segregation was not found to be associated with AF across racial and ethnic groups. In this longitudinal analysis we did not observe an association between residential segregation and AF incidence for Black, Hispanic/Latino, or White participants in fully adjusted models. Further research is needed to understand how individual factors may intersect with clinical, health care, and structural factors to drive previously described differential risk of AF.
暂无摘要（点击查看详情）
To describe the proportion and severity of fatigue among out-of-hospital cardiac arrest (OHCA) survivors and to investigate the association between age group (working-age 18-64 years vs ≥65 years) and fatigue. This cross-sectional study used data from the Danish Cardiac Survivorship (DANCAS) survey, including adult (≥18 years) OHCA survivors. Fatigue (the Modified Fatigue Impact Scale, MFIS), anxiety and depression (Hospital Anxiety and Depression Scale, HADS), and disability (WHO Disability Assessment Schedule, WHODAS 2.0) were assessed. Descriptive statistics characterised fatigue across age groups. Linear regression models (unadjusted and adjusted) investigated the association between age group and fatigue, reported as regression coefficients (β) and 95% confidence intervals (CI).In total, n = 1236 survivors (median age 67 years, IQR 57-74) were included, of whom 551 were of working age and 685 were ≥65 years. Working-age survivors reported significantly higher (worse) levels of fatigue (median 19, IQR 6-38) compared to those aged ≥65 years (median 13, IQR 5-28). Working age was significantly associated with higher fatigue scores after adjustment for sex and age (β 4.80, 95% CI 2.63-6.98). The association was reduced but remained statistically significant after further adjusting for anxiety, depression, and disability (β 1.57, 95% CI 0.22-2.92). Working-age OHCA survivors reported higher levels of fatigue compared with survivors aged ≥65 years, particularly in the non-physical domains. The association was reduced after adjustment, suggesting overlap between fatigue, psychological distress and disability. These findings highlight the need for multidimensional and age-specific assessment of post-OHCA fatigue.
Although cardiovascular events increase sudden cardiac arrest (SCA) risk, the impact of recurrent events on subsequent SCA risk in a contemporary population is unknown. This study assessed whether patients with a first-time acute coronary syndrome (ACS) or heart failure (HF) hospitalization who experience a recurrent cardiovascular event have increased SCA risk. The OSCAR (Observational Study of Cardiac Arrest Risk) is a prospective cohort with adjudicated SCA outcomes. The current study followed up patients who survived a first ACS or HF hospitalization (the index ACS or HF cohorts) for recurrent cardiovascular events and SCA. Recurrent event was a time-dependent variable in Cox models predicting SCA. Findings were validated in the FHS (Framingham Heart Study). Among 2946 patients in the index ACS cohort, incidence of SCA was higher following a recurrent ACS event than without (3.70 versus 1.28 per 100 patient-years). A recurrent ACS event was associated with higher risk of SCA (adjusted hazard ratio [HR], 3.15 [95% CI, 2.06-4.83]; P<0.0001). Among 6711 patients in the index HF cohort, incidence of SCA was higher following a recurrent HF event than without (1.35 versus 0.97 per 100 patient-years), and SCA risk was higher with recurrent HF (HR, 1.79 [95% CI, 1.44-2.23]; P<0.0001). In the FHS cohort, risk of SCA was higher with recurrent ACS (HR, 2.85 [95% CI, 1.66-4.90]; P=0.0002); the association was not significant for recurrent HF (HR, 1.49 [95% CI, 0.73-3.03]; P=0.27). Recurrent events were associated with higher risk of SCA; dynamic clinical trajectories of recurrent cardiovascular events may inform prevention of SCA.
IntroductionLymphoma survivors are at increased cardiovascular risk due to cardiotoxic therapies and commonly experience reduced cardiorespiratory fitness and quality of life. Telehealth-supported home-based exercise (HBE) may extend access to cardio-oncology rehabilitation (CORE); however, evidence from randomized trials in lymphoma survivors remains limited. This trial compared the short-term effects of telehealth-supported HBE versus center-based exercise (CBE) in lymphoma survivors entering CORE.Materials and MethodsIn this single-center, single-blind, parallel-group randomized controlled trial, lymphoma survivors in remission were randomized 1:1 to a 12-week telehealth-supported HBE program or supervised CBE. The primary endpoint was cardiorespiratory fitness, operationalized as peak oxygen uptake (pVO2, mL·kg-1·min-1) assessed by cardiopulmonary exercise testing (CPET) at 12 weeks. Key secondary outcomes were maximal workload (W) and SF-36 Physical Functioning. Between-group effects were estimated using ANCOVA with baseline adjustment (intention-to-treat; missing outcomes handled by multiple imputation).ResultsEighty participants were randomized (HBE n=40; CBE n=40); post-intervention CPET outcomes were available for 69 participants (HBE n=34; CBE n=35). pVO2 improved in both groups, with no significant baseline-adjusted between-group difference at 12 weeks (adjusted mean difference HBE-CBE -0.60 mL·kg-1·min-1, 95% CI -2.38 to 1.17; p=0.504). No between-group differences were observed for maximal workload (2.05 W, 95% CI -9.20 to 13.30; p=0.721) or SF-36 Physical Functioning (1.69 points, 95% CI -3.37 to 6.74; p=0.512). Adherence was high in both groups (HBE 80.1% vs CBE 77.9%). No adverse events were reported. Costs per participant were CZK 13,032 for HBE versus CZK 24,900 for CBE (48% lower for HBE).ConclusionTelehealth-supported HBE achieved comparable short-term improvements in exercise capacity and physical functioning to supervised CBE among lymphoma survivors entering CORE, with high adherence, no reported adverse events, and substantially lower provider costs. Telehealth-guided HBE represents a pragmatic, lower-cost delivery option to expand access to CORE.
Epicardial adipose tissue volume (EATV) is increasingly recognized as a cardiometabolic risk marker associated with adverse outcomes. The most established approach for EATV quantification is cardiac computed tomography (CT). MRI offers a radiation-free alternative allowing simultaneous assessment of myocardial function and tissue characteristics; however, standardization and validation are limited. To evaluate a standardized MRI-based method for EATV quantification and determine its agreement with CT. Retrospective. 127 patients with aortic stenosis (AS) (78 ± 6 years; 38% female) who underwent paired CT and MRI and 11 volunteers (74 ± 7 years, 45% female) who underwent repeat MRI after ≥ 6 weeks. Short-axis balanced steady-state free precession cine sequence at 3T (AS patients) and 1.5T (volunteers). On CT, EATV was quantified by manual delineation of the visceral pericardium and voxel-thresholding (-190 to -30 HU). MRI-based EATV quantification used manual volumetry with delineation of the visceral pericardium and epicardium on end-diastolic short-axis cine stacks. Inter-modality agreement was assessed by Spearman correlation and Bland-Altman analysis. Reproducibility was evaluated in 20 patients using intraclass correlation coefficient (ICC) and coefficient of variation (CoV). Scan-rescan reproducibility for MRI-derived EATV quantification was assessed using ICC and linear regression. p < 0.05 was considered significant. Median EATV was significantly higher on MRI than CT (47 vs. 38 mL/m2), with a significant moderate correlation (ρ = 0.627) between measures. Inter- and intra-observer analyses showed excellent reproducibility for both modalities (CT: intra-observer ICC: 0.983, inter-observer ICC: 0.994; MRI: intra-observer ICC: 0.955, inter-observer ICC: 0.970). MRI-derived EATV quantification also showed excellent scan-rescan reproducibility (ICC: 0.985). The standardized MRI-based approach enabled highly reproducible EATV measurements with excellent repeatability. Agreement with CT was moderate, with systematically higher values on MRI, limiting direct comparability. 3. 2. Epicardial adipose tissue (EAT) is recognized as a marker of cardiometabolic risk. While it is usually measured using CT, MRI offers a radiation‐free alternative and can simultaneously assess tissue function and characteristics. This study evaluated an MRI‐based method for measuring EAT and compared it with CT. 127 patients undergoing CT and MRI and 11 volunteers undergoing repeat MRI were included. MRI measurements showed a moderate correlation with CT but consistently higher values. Importantly, the MRI method demonstrated excellent reproducibility between readers and across repeated scans. Because MRI and CT yield systematically different values, their measurements should not be used interchangeably.
Carbon dioxide (CO2) can regulate blood flow and is applied therapeutically in intensive care units to treat brain injury, as well as in balneotherapy for peripheral arterial disease (PAD) and diabetic angiopathy; however, its mode of action remains unclear. The vasoactive CO2 effects were tested in arteries of healthy C57BL/6J mice, hypertensive apolipoprotein E-deficient mice, and soluble guanylyl cyclase (sGC) knockout mice in a small vessel myograph with and without pharmacologically intervening in endothelium- and/or vascular smooth muscle-mediated vasodilation. CO2-based Near Infrared Spectroscopy (NIRS-CO2) was developed to assess vasoreactivity of the skin microcirculation to CO2 in healthy individuals, PAD and coronary artery disease (CAD) patients, and was compared with flow-mediated dilation (FMD). We identified CO2 as a triple vasodilator mimicking the actions of endothelium-derived relaxing factor (nitric oxide, NO), endothelium-derived hyperpolarization factor (EDHF), and direct myogenic vasodilators. CO2 engaged endothelial NO/sGC, endothelial small-/intermediate-conductance calcium-activated potassium channels (SKCa/IKCa), and myogenic voltage-gated (KV) and IKCa potassium channels, respectively, acting as a triple vasodilator. CO2-evoked vasodilator responses were blunted and delayed in diseased human and murine arteries. In the human cohort, the NIRS-CO2-derived time-to-intersection (TTI) of the HbO2 and HHb curves, capturing the delay phenotype, showed a strong association with PAD/CAD status and, in exploratory analyses, also distinguished young individuals with cardiovascular risk factors, supporting NIRS-CO2 as a physiological readout that integrates endothelial and myogenic components of microvascular reactivity. Duration and extent of CO2 vasodilation were coupled to tissue metabolism through vascular carbonic anhydrases (CAs), providing a mechanism for vasculometabolic coupling and one for clinically approved CA inhibitors. NIRS-CO2 provides a feasible readout of CO2-evoked microvascular responsiveness and shows disease-associated alterations in our PAD/CAD cohort. Larger studies will validate generalizability across vasculopathies and clarify the relative contributions of NO-sGC versus K+ channel-linked mechanisms for future therapeutic translation.
Oxidative stress and antioxidant balance play critical roles in carcinogenesis, particularly among older adults who experience increased oxidative burden. This study explored the association between the composite dietary antioxidant index (CDAI) and cancer prevalence in the elderly. Data from 4,907 elderly participants were analyzed and categorized into quartiles (Q1-Q4) according to CDAI. Logistic regression models estimated odds ratios (ORs) and 95% confidence intervals (CIs) for cancer across quartiles, adjusting for demographic and clinical covariates. Subgroup analyses were performed to evaluate the consistency across subgroups. Participants with higher CDAI levels were more likely to be male, educated, and have lower diabetes prevalence. The prevalence of cancer increased across CDAI quartiles (19.6% in Q1 to 27.5% in Q4, P < 0.001). In fully adjusted models, Q4 had higher odds of cancer (OR = 1.26, 95% CI 1.02-1.54, P = 0.029). Subgroup analyses indicated stronger associations among women and those with diabetes. Unexpectedly, higher CDAI was associated with a greater prevalence of cancer among elderly individuals, suggesting complex, context-dependent effects of dietary antioxidants on cancer prevalence.
暂无摘要（点击查看详情）
暂无摘要（点击查看详情）
暂无摘要（点击查看详情）
Pan-vascular diseases pose a significant and growing global public health burden. However, the burden of pan-vascular diseases remains unknown, especially regarding its trends through 2050. The global burden of ischemic heart disease (IHD), ischemic stroke (IS), and lower extremity peripheral arterial disease (LEPAD) was analyzed in this study. We investigated the prevalence trends of these pan-vascular diseases from 1990 to 2021 across 204 countries and territories, assesses the impact of population aging, lifestyle changes, and epidemiological shifts on the prevalence of pan-vascular diseases, examines health inequalities between countries, and forecasts trends through 2050.In 2021, the estimated global cases of IHD, IS, and LEPAD reached 254.3 million, 69.9 million, and 113.7 million, respectively. The age-standardized prevalence rates (ASPR) were 3031, 1018, and 1337 per 100,000 population, with estimated annual percentage changes (EAPC) of 0.61%, 0.95%, and 0.1%, respectively. Over recent years, population growth contributed most to the increasing burden of IHD, IS, and LEPAD, with a slightly higher impact in females for IS and LEPAD. Notably, epidemiological factors (-18.9%) partially mitigated the burden of LEPAD despite demographic pressures. Trend projections indicate a slow increase in IHD ASPR, particularly among females, while males exhibit a relatively stable trend through 2050. A similar pattern was observed for IS, whereas ASPR for LEPAD is expected to remain stable. Significant absolute and relative inequalities in disease burden were observed across countries with varying sociodemographic index (SDI) levels. The burden of pan-vascular diseases continues to rise globally, driven primarily by demographic changes (population growth and aging). Despite improvements in healthcare, significant cross-country health inequalities persist, particularly in high-SDI countries, where the disease burden has intensified. As prevalence trends are projected to increase further, targeted public health interventions and policies are urgently needed to mitigate the growing impact of pan-vascular diseases and reduce global health disparities.
Percutaneous LAAO is an established stroke-prevention strategy in atrial fibrillation patients unsuitable for long-term anticoagulation. Device embolization is uncommon but can cause severe complications requiring urgent intervention. We report 2 related cases of device embolization associated with left atrial appendage occlusion and subsequent peri-device leak closure. The first involved early Amulet occluder embolization with mitral inflow obstruction and hemodynamic instability. The second occurred during peri-device leak closure after prior WATCHMAN implantation, when a 6 × 4-mm vascular occluder embolized upon release. In both cases, intraprocedural transesophageal echocardiography and fluoroscopy guided successful snare-based percutaneous retrieval with coaxial sheath-assisted extraction, avoiding surgery. Both devices were retrieved intact without major complications. Percutaneous retrieval of embolized LAAO devices is achievable with systematic planning and multidisciplinary preparedness. Growing LAAO volumes and leak reinterventions underscore the need for structured embolization rescue protocols.
Sodium-glucose co-transporter 2 (SGLT2) inhibitors have emerged as cornerstone therapies for heart failure with reduced ejection fraction (HFrEF), owing to their cardioprotective and hematologic effects. While their impact on hemoglobin and hematocrit levels is increasingly recognized, the influence of SGLT2 inhibitors on mean platelet volume (MPV), a surrogate marker of platelet activation and cardiovascular risk, remains underexplored in HFrEF patients. While SGLT2 inhibitors' effects on MPV have been studied in DM, this is the first study examining MPV changes specifically in HFrEF patients with adjustment for diuretic therapy. This retrospective study included 80 HFrEF patients receiving guideline-directed medical therapy to which SGLT2 inhibitors were subsequently added. Baseline and 6-month follow-up data on hematological and biochemical parameters were collected. Exclusion criteria included active infection, malignancy, advanced renal failure, hematologic disorders, and recent transfusions. MPV and platelet counts were analyzed using standardized protocols and equipment. Following 6 months of SGLT2 inhibitor therapy, MPV values decreased significantly (p < 0.05), while platelet counts increased significantly (p < 0.05). Although hemoglobin and hematocrit levels showed upward trends, these changes were not statistically significant. No significant correlation was observed between ΔMPV and ΔPLT. Other biochemical markers remained stable throughout the study period. SGLT2 inhibitor therapy was associated with a significant reduction in MPV and an increase in platelet count among patients with HFrEF. These hematological changes may represent an additional mechanism by which SGLT2 inhibitors exert cardiovascular benefit. However, prospective, randomized trials are needed to validate these findings and explore the clinical significance of MPV modulation in heart failure management.