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Arch Cardiovasc Dis. 2025 Jun 12:S1875-2136(25)00325-0. doi: 10.1016/j.acvd.2025.04.056. Online ahead of print.

ABSTRACT

BACKGROUND: Despite the widespread adoption of percutaneous pulmonary valve implantation, there remains a lack of consensus on the optimal management of peri-interventional and long-term antithrombotic therapies because of a lack of evidence.

AIM: To clarify current practices in peri/postprocedural antithrombotic strategies for percutaneous pulmonary valve implantation.

METHODS: An online survey was submitted to the Interventional Working Group of the Association for European Paediatric and Congenital Cardiology, and was completed by 76 congenital interventional cardiologists in 2023-2024.

RESULTS: Overall, 86% had standardized protocols for anticoagulation/antiaggregation. Intraprocedural heparin administration of 100IU/kg was common (83%), and postprocedural strategies mostly included acetylsalicylic acid (aspirin) (45%) or a combination of antiaggregation and anticoagulation (29%). Long-term strategies comprised antiaggregation (88%), no therapy (11%) and anticoagulation only (1%). Acetylsalicylic acid monotherapy was prescribed by 91%, whereas 9% used dual antiaggregation therapy. Dual antiaggregation therapy was continued for suspicious medical history of thrombotic complication or microthrombi for 3-6 months. Testing for acetylsalicylic acid resistance was infrequent (36%), and only if clinically indicated. When patients had pre-established anticoagulation therapy, 59% changed their strategy. Treatment changes based on valve type were rare (8%). The primary reasons for anticoagulation/antiaggregation were to increase valve longevity (26%) and for both longevity and endocarditis prophylaxis (68%). Acute valve thrombosis was reported in 11 cases.

CONCLUSIONS: The survey reveals variability in practices after percutaneous pulmonary valve implantation. Most interventional cardiologists prefer acetylsalicylic acid for postprocedural and long-term management, whereas dual antiaggregation therapy is sometimes used in specific cases. Anticoagulation is limited to pre-existing therapy cases or isolated experiences for 3 months.

PMID:40544108 | DOI:10.1016/j.acvd.2025.04.056

J Am Soc Echocardiogr. 2025 Jun 19:S0894-7317(25)00332-3. doi: 10.1016/j.echo.2025.06.006. Online ahead of print.

ABSTRACT

BACKGROUND: Current guidelines recommend annual or biennial transthoracic echocardiograms for patients with d-transposition of the great arteries (d-TGA) who have undergone an arterial switch operation (ASO), but optimal imaging frequency is unknown. We sought to determine the utility of annual surveillance echocardiograms for asymptomatic patients.

METHODS: Clinical documentation from 2011-2023 for asymptomatic patients > 18 years old with history of d-TGA and ASO at a single large tertiary care center was reviewed to determine if routine surveillance echocardiograms resulted in changes in clinical management (ΔMGMT), categorized as procedures (surgery or catheterization) or noninvasive changes (medication changes, additional imaging, etc.). Echocardiograms obtained for symptoms or completed before age 18 were excluded from analysis. Data was evaluated with chi-square and Kruskal-Wallis tests, Kaplan-Meier analysis, and Cox proportional hazard analysis.

RESULTS: Of 416 echocardiograms from 127 patients, the median time from ASO to final echocardiogram was 22.2 years (IQR 19.1-25.7 years; range 15.2-34.1 years). Eighteen echocardiograms (4.32%) resulted in ΔMGMT for 12 patients including 8 (1.92%) medication changes, 7 (1.68%) cardiac CT or MRI studies, and 1 (0.24%) each for cardiac catheterization and surgery. A significantly larger proportion of patients with ΔMGMT underwent ASO at age >1 year compared to patients without ΔMGMT (36.36% vs 6.14%, P<0.01). Patients with a history of hypertension, arrhythmia, >2 sternotomies, or neo-aortic valve replacement had a significantly greater risk of ΔMGMT, as did those with neo-aortic root dilation >4.5cm and/or moderate or greater neo-aortic insufficiency.

CONCLUSIONS: Routine surveillance echocardiograms are low yield in asymptomatic adults up to 30 years after ASO for d-TGA, suggesting it may be reasonable to increase the time interval between routine echocardiograms without adversely impacting care. Higher risk sub-populations including those with ASO at older ages, >2 sternotomies, neo-aortic valve replacement, and/or neo-aortic valve/root pathology may benefit from continued frequent surveillance.

PMID:40543855 | DOI:10.1016/j.echo.2025.06.006

Ann Thorac Surg. 2025 Jun 19:S0003-4975(25)00530-2. doi: 10.1016/j.athoracsur.2025.05.038. Online ahead of print.

ABSTRACT

BACKGROUND: Gender-based pay disparity in compensation is widespread. In cardiothoracic surgery, women earn between 71-84% of men's salaries at comparable ranks. Limited data exist on how factors like subspecialty, practice type, and work efforts contribute to these disparities.

METHODS: The Society of Thoracic Surgeons (STS) conducted the Compensation Survey in 2023 among practicing members with at least a 0.5 full-time equivalent role. Collected data included compensation sources, predominant subspeciality of cardiothoracic surgery, work relative value units (wRVUs) generated, and demographics. Comparisons on gender-based salary across subspecialties, years of experience, and wRVUs were included.

RESULTS: Among 838 respondents, gender disparities were present in both base salary and total compensation across all subspecialties, with women earning 64-93% of men's salaries. Income disparity was greatest in cardiac surgery with 11-20 years of experience, where women earned 63-70% of men's compensation. Similarly, in thoracic surgery, women earned 59-72% of the compensation of men with 21-30 years of experience. Women with 11-20 years of experience earned less than both men and women colleagues with 6-10 years of experience. Women reported more compensation from teaching, while men reported more from call coverage.

CONCLUSIONS: Gender pay disparities exist among cardiothoracic surgeons, even when accounting for experience and productivity. Reasons for these disparities, including parenthood penalty, need to be further studied and corrections proposed.

PMID:40543696 | DOI:10.1016/j.athoracsur.2025.05.038

J Endovasc Ther. 2025 Jun 21:15266028251344541. doi: 10.1177/15266028251344541. Online ahead of print.

ABSTRACT

INTRODUCTION: The use of intravascular catheters has become increasingly widespread in children, due to their use in diagnostic procedures (such as coronary, intracardiac, cerebral, and renal angiography, as well as pressure monitoring) and for therapeutic purposes (including angioplasties, valvuloplasties, congenital defect closure, chemotherapy, among other uses). However, they are not free from complications, which may include catheter fracture and migration within the cardiovascular system, potentially leading to vascular or cavity perforation, arrhythmias, and even death.

OBJECTIVE: To define the clinical and hemodynamic characteristics of pediatric patients undergoing catheterization for the retrieval of intravascular foreign bodies.

MATERIALS AND METHODS: A retrospective cohort study of all patients under 18 years of age who underwent endovascular extraction of foreign bodies at a cardiovascular reference center.

RESULTS: A high percentage of successful retrieval of intravascular foreign bodies was noted, with the most frequently retrieved catheter being the chemotherapy catheter, primarily located in the right atrium, between the pulmonary trunk and the right ventricle, and in the brachiocephalic vein. Few secondary complications were observed, occurring in only 2 patients.

CONCLUSION: Endovascular retrieval of foreign bodies is a highly effective procedure, and complications are relatively low in pediatrics, even during the neonatal period and in low-birth-weight cases, making it a preferable alternative to surgical extraction.Clinical ImpactBy documenting favorable outcomes across a diverse group, it encourages clinicians to adopt catheter-based approaches more confidently. The use of tools like snare loops and balloon-tipped guidewires in this population reflects procedural innovation and adaptability. Early, minimally invasive intervention may reduce morbidity and hospital stay. These findings can influence clinical decision-making and protocol development in pediatric cardiovascular care, particularly in centers equipped for interventional procedures.

PMID:40542822 | DOI:10.1177/15266028251344541

Mol Med Rep. 2025 Sep;32(3):232. doi: 10.3892/mmr.2025.13597. Epub 2025 Jun 20.

ABSTRACT

The present study aimed to identify differentially expressed circRNAs in hypertrophic cardiac tissues and explored the potential regulatory role and mechanism of one differentially expressed circRNA in myocardial hypertrophy. RNA sequencing was used to identify differentially expressed circRNAs in hypertrophic and control cardiac tissues. CircRNA expression levels were verified by reverse transcription‑quantitative PCR. Isoproterenol (ISO) was used to induce hypertrophy of AC16 cells. The extent of cell hypertrophy was indicated by the cell size, protein/DNA ratio and levels of B‑type natriuretic peptide (BNP) and β‑myosin heavy chain (β‑MHC). The interactions between hsa_circ_0072107 and miR‑516b‑5p, as well as between miR‑516b‑5p and zinc ring finger protein 36 (ZFP36), were confirmed through dual luciferase assays, biotinylated probe pull‑down and anti‑AGO2 RNA immunoprecipitation assays. hsa_circ_0072107 was one of the most upregulated circRNAs in hypertrophic cardiac tissues. hsa_circ_0072107 overexpression and ISO treatment increased cell size, elevated the protein/DNA ratio and increased the levels of BNP and β‑MHC in AC16 cells, indicating that hsa_circ_0072107 aggravates AC16 hypertrophy. These changes induced by ISO treatment could be blocked by the knockdown of hsa_circ_0072107. The dual‑luciferase activity assay indicated that miR‑516b‑5p can bind to hsa_circ_0072107. miR‑516b‑5p binding site mutation blocked the effect of hsa_circ_0072107. ZFP36 is a target gene of miR‑516b‑5p, which suppresses AC16 hypertrophy. hsa_circ_0072107 overexpression alleviated the effect of miR‑516b‑5p overexpression on cell hypertrophy and ZFP36 expression. hsa_circ_0072107 is up‑regulated in hypertrophic cardiac tissues and potentially promotes AC16 hypertrophy and may play its role by acting as a competitive endogenous RNA of miR‑516b‑5p. Thus, hsa_circ_0072107 may be a novel target for the treatment of myocardial hypertrophy.

PMID:40539438 | DOI:10.3892/mmr.2025.13597

Physiol Rep. 2025 Jun;13(12):e70425. doi: 10.14814/phy2.70425.

ABSTRACT

This study aims at defining a standardized workflow based on a customized ImageJ macro combined with a machine-learning algorithm to analyze morphometric features of isolated cardiomyocytes using high-resolution/high-content photomicrographs and to identify key and specific morphological features of cardiomyocytes isolated from various murine cardiac hypertrophy models. For that purpose, we set up and optimized a Langendorff based protocol for isolating cardiomyocytes from mouse hearts. This optimized protocol yielded in a significantly high number of formaldehyde-fixed cardiomyocytes, with more than 97% of rod shaped cells. Moreover, our method allowed for reliable gene expression analysis and conservation of cell integrity through multiple freeze-thaw cycles. Next, we successfully applied our analytical workflow on formaldehyde-fixed cardiomyocytes isolated from various murine cardiac hypertrophy models and defined distinct morphological features in Angiotensin II, Isoproterenol, and age-induced hypertrophy. Taken together, our study provides an effective and standardized workflow for high-throughput morphological and molecular characterization of isolated cardiomyocytes, and could constitute a robust and reliable analytical tool to distinguish healthy versus diseased states and assess the ability of a potential therapeutic agent or strategy to reverse the situation.

PMID:40538075 | PMC:PMC12179408 | DOI:10.14814/phy2.70425

Crit Care. 2025 Jun 20;29(1):255. doi: 10.1186/s13054-025-05495-4.

ABSTRACT

BACKGROUND: A systemic inflammatory response can contribute to poor outcomes in an advanced stage of cardiogenic shock (CS). We investigated the efficacy of extracorporeal endotoxin and cytokine adsorption using oXiris in patients with CS undergoing venoarterial extracorporeal membrane oxygenation (VA-ECMO).

METHODS: In this prospective, single-center, randomized, open-label pilot trial, 40 patients with CS who were undergoing VA-ECMO were randomly assigned to receive either oXiris for 24 h (n = 20) or usual care (n = 20). The primary endpoint was endotoxin levels at 48 h. Secondary endpoints included changes in inflammatory cytokines, vasoactive-inotropic score (VIS), ECMO weaning success, and in-hospital and 30-day mortality.

RESULTS: The median endotoxin levels at 48 h were 0.5 (IQR 0.4-1.0) in the oXiris group and 0.4 (IQR 0.2-0.5) in the control group, with no significant difference between them (P = 0.097). The oXiris group showed significant temporal reductions in GDF-15 and IL-6 levels, with IL-6 revealing significant reductions from baseline to 24 h (P = 0.020) and from baseline to 7 days (P = 0.003). VIS decreased significantly from baseline to 48 h (-13.63, 95% CI: -20.90 - -6.34, P < 0.001) and 7 days (-12.19, 95% CI: -21.0 - -3.31, P = 0.007) in the oXiris group, but intergroup differences were insignificant. ECMO weaning success, duration of ECMO support, and mortality rates were similar between the groups.

CONCLUSION: In this pilot study conducted on CS patients requiring VA-ECMO, oXiris treatment did not significantly reduce endotoxin levels or improve patient centered clinical outcomes.

TRIAL REGISTRATION: NCT05642273, registered 8 December 2022.

PMID:40542431 | PMC:PMC12181899 | DOI:10.1186/s13054-025-05495-4

Cardiovasc Revasc Med. 2025 Jun 4:S1553-8389(25)00288-X. doi: 10.1016/j.carrev.2025.06.003. Online ahead of print.

ABSTRACT

BACKGROUND: Impella is a catheter-based, continuous blood flow left ventricle assist device used in selected patients undergoing high-risk percutaneous coronary interventions (HR PCI). We aimed to evaluate outcomes in patients undergoing Impella-assisted HR-PCI and identify independent predictors of 12-month mortality.

METHODS: Consecutive HR-PCI patients enrolled in the national, multicentre, retrospective IMPELLA-PL registry (n = 253) in 20 Polish interventional cardiological centres from October 2014 until December 2021 were included in the analysis. The main endpoints were (i) procedural success defined as revascularization of all preplanned lesions, (ii) device-related complications, (iii) 12-month mortality and major adverse cardiovascular events (MACE).

RESULTS: The majority of patients presented with multivessel disease including left main (63.6 %). The median Syntax Score II was 43.0 (32.4-55.0). The procedural success was achieved in 83.0 % of patients. Device-related complications included access site bleeding (14.6 %), limb ischemia (2.4 %) and hemolysis (1.6 %). The in-hospital MACE included 1 cardiosurgical intervention (0.4 %), 12 exacerbations of heart failure (4.7 %), 11 myocardial infarctions (4.3 %), 32 cases of acute kidney injury (12.6 %), 35 inflammatory complications (13.8 %) and 32 major bleeding complications (13.4 %). In-hospital mortality rate was 8.3 %, 12-month mortality rate was 18.2 % and MACE rate post-discharge was 22.5 %. The 12-month-mortality was increased by pre-existing, atrial fibrillation (OR 3.50, 95 % CI 1.38-8.95) and chronic kidney disease (OR 2.77, 95 % CI 1.06-7.26) and decreased by Impella removal in the cath-lab (OR 0.11, 95 % CI 0.02-0.76) and RAAS inhibitor use (OR 0.26, 95 % CI 0.08-0.89).

CONCLUSIONS: Despite high anatomical complexity of coronary artery disease of patients included in the IMPELLA-PL registry, the procedural success rate was relatively high and the mortality relatively low.

PMID:40541478 | DOI:10.1016/j.carrev.2025.06.003

Cardiovasc Drugs Ther. 2025 Jun 20. doi: 10.1007/s10557-025-07735-9. Online ahead of print.

ABSTRACT

PURPOSE: The association between the intra-procedure quantitative flow ratio (QFR) and clinical outcomes after drug-coated balloon (DCB) angioplasty has not been investigated. This study aimed to investigate the clinical predictive value of pre-DCB QFR, a functional assessment of lesion preparation, for clinical outcomes in de novo coronary lesions after DCB angioplasty.

METHODS: This retrospective study included 170 consecutive patients undergoing DCB angioplasty for 177 de novo coronary lesions between January 2021 and December 2022. The QFR was computed at baseline, pre-DCB, and post-DCB. The primary endpoint was major adverse cardiac events (MACE), defined as a composite of all-cause death, cardiac death, target vessel myocardial infarction, and target lesion revascularization.

RESULTS: During 2-year follow-up, 37 patients with 38 lesions have experienced MACE. The pre-DCB QFR, measured after pre-dilation, was significantly lower in the MACE group. Receiver operator characteristic curve analysis showed the optimal pre-DCB QFR cut-off value for predicting MACE was 0.925 (area under curve = 0.782, 95% confidence interval [CI] 0.702-0.861, sensitivity = 78.9%, specificity = 74.8%, p < 0.001). A pre-DCB QFR < 0.925 was associated with a significantly higher risk of MACE compared with a value > 0.925 (46.1% vs. 7.1%, p < 0.001). In multivariable Cox regression analyses, pre-DCB QFR < 0.925 was associated with an over sixfold increased risk of MACE (hazard ratio = 7.483, 95% CI 3.363-16.653, p < 0.001).

CONCLUSION: The pre-DCB QFR was a promising predictor of unfavorable clinical outcomes in de novo coronary lesions after DCB angioplasty.

PMID:40540079 | DOI:10.1007/s10557-025-07735-9

Cardiol Rev. 2025 Jun 20. doi: 10.1097/CRD.0000000000000971. Online ahead of print.

ABSTRACT

Dual antiplatelet therapy is a standard treatment after percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS), but the optimal monotherapy agent post-dual antiplatelet therapy remains unclear. Clopidogrel and aspirin are widely used, yet their comparative effectiveness and safety in this patient population have not been fully established. This systematic review and meta-analysis compared the efficacy and safety of clopidogrel and aspirin monotherapy following PCI in patients with ACS. A comprehensive search of PubMed, Embase, and Web of Science was conducted from inception to March 31, 2025. Randomized controlled trials (RCTs) comparing clopidogrel and aspirin monotherapy in adult ACS patients post-PCI were included. Primary outcomes were all-cause death, myocardial infarction (MI), and ischemic stroke. Secondary outcomes included target-vessel and target-lesion revascularization, cardiovascular and noncardiovascular death, and stent thrombosis. The risk of bias was assessed using the Cochrane RoB 2 tool, and the GRADE methodology was applied to evaluate the certainty of evidence. Three RCTs involving 16,056 patients (clopidogrel: 8103; aspirin: 7953) were included. Clopidogrel significantly reduced MI (risk ratio = 0.71; 95% confidence interval: 0.55-0.92; P = 0.01) and target-vessel revascularization (risk ratio = 0.77; 95% confidence interval: 0.60-0.97; P = 0.03). No significant differences were found in all-cause death, ischemic stroke, or other secondary outcomes. Sensitivity analysis suggested a potential reduction in noncardiovascular death favoring clopidogrel. Clopidogrel monotherapy after PCI may offer superior protection against MI and target-vessel revascularization compared with aspirin, with no increased risk of death or stroke.

PMID:40539811 | DOI:10.1097/CRD.0000000000000971

Cureus. 2025 May 20;17(5):e84471. doi: 10.7759/cureus.84471. eCollection 2025 May.

ABSTRACT

Background The healthcare landscape is notably divided between investor-owned and nonprofit hospitals, raising questions about the impact of hospital ownership on patient outcomes, especially for high-stakes conditions such as cardiogenic shock resulting from ST-elevation myocardial infarction (STEMI) treated with percutaneous coronary intervention (PCI). This study analyzed whether differences in hospital ownership are associated with variations in mortality, length of stay (LOS), and healthcare costs. Methodology We conducted a retrospective cohort study using the National Inpatient Sample (NIS) from 2016 to 2021, identifying 95,260 adult patients with STEMI-induced cardiogenic shock treated with PCI. Identification was based on validated International Classification of Diseases, Tenth Revision, Clinical Modification coding algorithms. The primary outcome was in-hospital mortality, with LOS and total hospital charges (inflation-adjusted via the Consumer Price Index) as secondary outcomes. All outcomes were assessed using multivariable regression models adjusting for patient demographics (age, sex, race/ethnicity), comorbidities, insurance type, and hospital-level factors (region, teaching status, and bed size). Regional cost variation and case mix were also accounted for. Propensity score matching was additionally performed to validate results. Results The analysis revealed no significant difference in mortality rates between investor-owned (27.22%) and nonprofit hospitals (26.93%, adjusted odds ratio (aOR) = 1.03, p = 0.60; 95% confidence interval (CI) = 0.91-1.16). Propensity score-matched analysis confirmed similar findings (aOR = 0.98, p = 0.696). Investor-owned hospitals, however, incurred significantly higher healthcare costs (average charges = $325,543 vs. $222,528; p < 0.001). The average cost difference of $103,015.50 remained statistically and systemically significant after adjustment and may reflect differences in resource utilization and/or billing practices. LOS was slightly shorter in investor-owned hospitals (6.51 vs. 7.27 days); while statistically significant (p < 0.001), this difference was not clinically meaningful after adjustment (coefficient = 0.19, p = 0.334). Key demographic and clinical predictors included age, insurance status, comorbidity index, hospital bed size, and teaching status. Racial and insurance-based disparities, particularly among Hispanic patients and Medicaid enrollees, were associated with higher costs, though not fully explained by hospital ownership. Conclusions In this national analysis, hospital ownership was not associated with differences in mortality for STEMI-induced cardiogenic shock treated with PCI, but was independently associated with substantially higher hospital charges in investor-owned hospitals. These findings demonstrate association, not causation, and highlight the need for future research into cost drivers and initiatives to promote high-value, standardized care across all hospital types.

PMID:40539141 | PMC:PMC12178224 | DOI:10.7759/cureus.84471

Front Cardiovasc Med. 2025 Jun 5;12:1611019. doi: 10.3389/fcvm.2025.1611019. eCollection 2025.

ABSTRACT

This study delineates the diagnostic and therapeutic strategies for acute myocardial infarction occurring years after stent implantation for Stanford type A aortic dissection. Emergency coronary angiography presented substantial technical challenges attributable to the lack of recent aortic imaging data and marked tortuosity of the brachiocephalic trunk resulting from postoperative anatomical changes. Consequently, while selective left coronary angiography was successfully completed, visualization of the right coronary artery necessitated non-selective contrast administration via a pigtail catheter. This case underscores the pivotal role of preoperative aortic computed tomography angiography (CTA) in hemodynamically stable patients, as it provides essential vascular anatomical information that may circumvent procedural complexities during coronary angiography. Building upon these observations, we advocate an "aorto-coronary combined assessment" strategy for post-aortic surgery patients, integrating systematic imaging surveillance to facilitate early identification of coronary lesions. Such an approach permits the timely implementation of intensive medical therapy or elective revascularization, thereby mitigating the risk of acute cardiovascular events.

PMID:40538917 | PMC:PMC12176840 | DOI:10.3389/fcvm.2025.1611019

Sci Rep. 2025 Jun 20;15(1):20195. doi: 10.1038/s41598-025-06206-3.

ABSTRACT

Acute myocardial infarction (MI), a serious manifestation of ischemic heart disease, remains the culprit for mortality among coronary heart disease patients. Astaxanthin has demonstrated the ability to alleviate inflammation-induced myocardial damage while maintaining a balance between oxidants and antioxidants. This study investigates the cardioprotective potential of astaxanthin (ASX), particularly when encapsulated in nanostructured lipid carriers (NLCs), in isoprenaline (ISO)-induced myocardial infarction in rats. The study involved 48 rats separated into 6 groups. ASX and Nano-ASX (5 mg/kg) were administrated orally for 21 days before MI induction (isoprenaline, 85 mg/kg, subcutaneously). Blood and cardiac tissue samples were taken 24 h following the last isoprenaline injection for biochemical and histopathological investigation. The findings reveal that nano-formulated ASX significantly reduces oxidative stress and cardiac injury markers, including CK-MB, Troponin-I, and LDH. Additionally, it enhances antioxidant enzyme activities (GSH, GPx, and GSH-RD) and decreases inflammatory markers (COX-2 and VEGF). The study further demonstrates that nano-ASX stimulates autophagy by upregulating critical genes such as Beclin-1, ULK1, and LC3B, which are vital for cardiac protection and repair. Histological analysis confirms these biochemical outcomes, showing reduced myocardial damage and inflammation in the nano-ASX-treated groups. This study concludes the potential of ASX nano-formulations as an advanced therapeutic approach for myocardial infarction, leveraging improved bioavailability and targeting oxidative stress, inflammation, and autophagic mechanisms.

PMID:40542058 | PMC:PMC12181253 | DOI:10.1038/s41598-025-06206-3

Chem Biol Interact. 2025 Jun 18;418:111607. doi: 10.1016/j.cbi.2025.111607. Online ahead of print.

ABSTRACT

Myocardial ischemia can induce myocardial infarction, posing a severe threat to human health. Although restoration of blood and oxygen supply alleviates tissue damage and reduces infarct size, reperfusion may trigger additional injury that exacerbates myocardial structural and functional disturbances, a phenomenon termed myocardial ischemia-reperfusion injury (MIRI). Ginkgolide B (GB), a terpenoid compound extracted from Ginkgo biloba leaves, exhibits cardiovascular protective properties. This study investigates the potential anti-MIRI effects of GB, with specific emphasis on elucidating the role of the GAS6/Axl signaling pathway in its cardioprotective mechanisms. In vivo experiments demonstrated that GB improved cardiac function and serum biochemical parameters in mice, concurrently suppressing apoptosis and mitigating oxidative stress. In vitro studies further revealed that GB protected HL-1 cardiomyocytes from hypoxia-reoxygenation (HR) injury, as evidenced by enhanced cell viability, reduced apoptosis rates, decreased ROS and LDH levels, alongside upregulated expression of GAS6, Axl, Bcl2, antioxidant-related proteins, and mitochondrial function-associated proteins. Crucially, the protective effects of GB were reversed by GAS6 knockdown or genetic ablation in the HL-1 cell HR model. Collectively, this study confirms the definitive cardioprotective efficacy of GB against MIRI and delineates the critical involvement of the GAS6/Axl signaling pathway, thereby establishing a robust theoretical foundation and scientific rationale for the clinical application of GB in MIRI management.

PMID:40541647 | DOI:10.1016/j.cbi.2025.111607

Cardiovasc Revasc Med. 2025 May 30:S1553-8389(25)00284-2. doi: 10.1016/j.carrev.2025.05.031. Online ahead of print.

ABSTRACT

BACKGROUND: High-risk percutaneous coronary intervention (HRPCI) procedures supported by percutaneous left ventricular assist devices (pLVAD) are increasingly common, but existing PCI risk scores were developed in patients across the risk spectrum, including few pLVAD-assisted patients.

OBJECTIVES: Assess the performance of existing PCI risk scores in patients receiving pLVAD-assisted HRPCI and create a novel risk score specific to this group.

METHODS: Patients in the PROTECT III multicenter, observational (46 US centers) study undergoing pLVAD-assisted HRPCI were assessed. The National Cardiovascular Data Registry (NCDR) bedside risk score and the Complex High-Risk Indicated PCI (CHIP-PCI) risk score were calculated for each patient, and their accuracy in predicting in-hospital events was assessed. A novel risk score for in-hospital mortality was created using pre-procedural variables which were significant in univariable and multivariable regressions.

RESULTS: Among 1237 patients, the NCDR bedside risk score showed modest discrimination (C-index 0.71) but poor goodness of fit (R2 = 0.30). The CHIP-PCI score had poor discrimination (C-index 0.61) and reasonable goodness of fit (R2 = 0.62). Five independent predictors of in-hospital mortality were identified: age >80 years, eGFR <30, left main disease, acute myocardial infarction, and left ventricular ejection fraction <30 %. These formed the "HRPCI" risk score (C-index 0.75), which correlated with 30-day mortality (5.4 % vs. 17.0 %, p<0.0001).

CONCLUSIONS: Existing PCI risk scores perform poorly in patients undergoing pLVAD-assisted HRPCI. A novel easily, calculable HRPCI risk score can assist in clinical decision making once validated.

CLINICAL TRIAL INFORMATION: Trial Name: The Global cVAD Study (cVAD). URL: https://clinicaltrials.gov/ct2/show/NCT04136392?term=cvad&draw=2&rank=2 ClinicalTrial.gov Identifier: NCT04136392.

PMID:40541479 | DOI:10.1016/j.carrev.2025.05.031

FASEB J. 2025 Jun 30;39(12):e70734. doi: 10.1096/fj.202402897RR.

ABSTRACT

ELABELA (ELA) has been identified as a potential cardiovascular protective factor. However, the source of endogenous ELA and its molecular mechanism in myocardial fibrosis inhibition remain incompletely understood. Herein, we found that aerobic exercise significantly improved renal apoptosis caused by MI, inhibited inflammation, attenuated structural damage, enhanced renal function, and increased expression and secretion levels of renal ELA. Aerobic exercise stimulated the circulation of renal-derived ELA to reach the MI heart and played a protective role. Under aerobic exercise intervention, renal-specific Elabela overexpression improved myocardial pathological remodeling, decreased cardiomyocyte apoptosis, and enhanced cardiac function. Renal-specific Elabela knockdown significantly increased cardiac apoptosis, inflammation, and fibrosis levels in MI mice, leading to severe impairment of cardiac function. Following AMPK agonist intervention, ELA expression in HKC cells and culture medium increased in a concentration-dependent manner. ELA-14 significantly activated the APJ-AMPK-Sirt1 signaling pathway and inhibited Tgf-β1 transcription by regulating Sirt1 translocation, and AMPK inhibitor weakened ELA-14 function. In cultured cardiac fibroblasts (CFs), the intervention of ELA-14 significantly inhibited the activity of the TGFβ1-Smad2/3 signaling pathway, downregulated the expression of fibrosis-related proteins, increased apoptosis, and lowered the cell migration rate. After TGFβR1 inhibitor intervention, ELA-14 showed a loss of regulation of CFs. Aerobic exercise stimulates the expression of renal-derived ELA, which reaches the MI heart through blood circulation. Renal-derived ELA partly exerts its antifibrotic effects by activating the APJ-AMPK-Sirt1 pathway and inhibiting the TGFβ1-Smad2/3 signaling pathway, contributing to its cardiac protective effects.

PMID:40540261 | DOI:10.1096/fj.202402897RR

Cardiol Rev. 2025 Jun 20. doi: 10.1097/CRD.0000000000000971. Online ahead of print.

ABSTRACT

Dual antiplatelet therapy is a standard treatment after percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS), but the optimal monotherapy agent post-dual antiplatelet therapy remains unclear. Clopidogrel and aspirin are widely used, yet their comparative effectiveness and safety in this patient population have not been fully established. This systematic review and meta-analysis compared the efficacy and safety of clopidogrel and aspirin monotherapy following PCI in patients with ACS. A comprehensive search of PubMed, Embase, and Web of Science was conducted from inception to March 31, 2025. Randomized controlled trials (RCTs) comparing clopidogrel and aspirin monotherapy in adult ACS patients post-PCI were included. Primary outcomes were all-cause death, myocardial infarction (MI), and ischemic stroke. Secondary outcomes included target-vessel and target-lesion revascularization, cardiovascular and noncardiovascular death, and stent thrombosis. The risk of bias was assessed using the Cochrane RoB 2 tool, and the GRADE methodology was applied to evaluate the certainty of evidence. Three RCTs involving 16,056 patients (clopidogrel: 8103; aspirin: 7953) were included. Clopidogrel significantly reduced MI (risk ratio = 0.71; 95% confidence interval: 0.55-0.92; P = 0.01) and target-vessel revascularization (risk ratio = 0.77; 95% confidence interval: 0.60-0.97; P = 0.03). No significant differences were found in all-cause death, ischemic stroke, or other secondary outcomes. Sensitivity analysis suggested a potential reduction in noncardiovascular death favoring clopidogrel. Clopidogrel monotherapy after PCI may offer superior protection against MI and target-vessel revascularization compared with aspirin, with no increased risk of death or stroke.

PMID:40539811 | DOI:10.1097/CRD.0000000000000971

Cytojournal. 2025 May 6;22:49. doi: 10.25259/Cytojournal_12_2025. eCollection 2025.

ABSTRACT

OBJECTIVE: Ischemia-reperfusion (I-R) injury in the myocardium is a considerable challenge in cardiovascular medicine, posing a severe threat to life. Given that galectin-3 possibly regulates myocardial I-R damage, this study aims to investigate the detailed mechanisms underlying galectin-3's effects on myocardial I-R injury.

MATERIAL AND METHODS: The expression levels of galectin-3 in vivo and in vitro myocardial I-R models were determined by Western blot and quantitative real-time polymerase chain reaction. The effects of galectin-3 on inflammatory factors and oxidative stress factors in myocardial I-R were measured with an enzyme-linked immunosorbent assay, and the extent of myocardial tissue damage was assessed using hematoxylin-eosin staining. The influence of galectin-3 on peroxisome proliferator-activated receptor g (PPARg) signaling pathway-related proteins in myocardial I-R was determined by Western blot.

RESULTS: Myocardial I-R damage was associated with increased galectin-3 expression, and the blood levels of creatine kinase-myocardial band and creatine kinase were favorably correlated with the messenger RNA levels of galectin-3 in mice with cardiac I-R damage. The inhibition of galectin-3 alleviated oxidative stress and inflammatory response, and galectin-3 promoted reactive oxygen species production in myocardial I-R cells. Furthermore, the cardiac I-R damage mouse model exhibited decreased expression of proteins linked to the PPARg signaling pathway, but galectin-3 inhibition enhanced the expression of these proteins.

CONCLUSION: Galectin-3 plays a crucial role in exacerbating myocardial I-R injury, and its up-regulation is associated with increased oxidative stress, inflammatory responses, and inhibition of the protective PPARg signaling pathway. The alleviation of these harmful effects by galectin-3 inhibition suggests that targeting galectin-3 is a potential therapeutic method for reducing myocardial I-R injury.

PMID:40539121 | PMC:PMC12178088 | DOI:10.25259/Cytojournal_12_2025

Front Pharmacol. 2025 Jun 5;16:1516836. doi: 10.3389/fphar.2025.1516836. eCollection 2025.

ABSTRACT

INTRODUCTION: Traumatic brain injury (TBI) is a leading cause of death and disability globally. Several studies have shown that 5-lipoxygenase (5-LOX) inhibition reduces leukotriene (LT) release and the inflammatory response, attenuating the development of respiratory diseases, myocardial infarction, and ischemic cerebral injury. However, its role in the pathophysiology of TBI remains unclear.

METHODS: Controlled cortical impact injury was induced to construct a mouse model of TBI. Pericontusional brain tissue samples from sham and TBI mice at 7 days after injury were used for RNA-seq analysis. Altered gene enrichment following TBI, based on Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, was quantified through real-time polymerase chain reaction (RT-PCR). Immunocytochemistry, Western blotting, and single-cell sequencing experiments were also performed to analyze 5-Lox protein expression. Arachidonic acid (AA) was detected through liquid chromatography mass spectrometry/mass spectrometry. Enzyme-linked immunosorbent assay was used to detect LTB4 release after TBI with or without zileuton treatment. Brain damage, blood-brain barrier disruption, and neuronal apoptosis were detected through histological examination. Neurological outcomes were determined through rotarod and fear conditioning tests.

RESULTS: TBI induced significant upregulation of genes related to the AA metabolic pathway, particularly the AA/5-LOX/LT axis, as verified by RT-PCR. AA and LTB4 production increased significantly after TBI. The expression levels of Pla2g4a, which hydrolyses phospholipids to release AA, and 5-Lox, which in turn act downstream to convert AA to LT, were dramatically upregulated up to 7 days after TBI. 5-LOX accumulated in the cytoplasm of activated ameboid microglial cells. In vivo, 5-LOX inhibition with zileuton blocked LT release and reduced microglial activation and the production of inflammatory cytokines, including Il-1β, Ccl7, Spp1, Ccr1, Ccl2, and Il-10. Zileuton also reduced TBI-induced lipid ROS and neuronal cell apoptosis, ameliorating brain damage compared to the vehicle group and improving neurological outcomes after TBI. Mechanically, TBI-induced LT upregulation may stimulate BV2 microglial activation through the ERK, NF-κB, and Akt pathways.

CONCLUSION: Our findings demonstrated the role of 5-LOX in TBI and its potential as a therapeutic target in TBI treatment.

PMID:40538546 | PMC:PMC12176805 | DOI:10.3389/fphar.2025.1516836

Acta Pharmacol Sin. 2025 Jun 20. doi: 10.1038/s41401-025-01597-5. Online ahead of print.

ABSTRACT

Cardiac hypertrophy as one of the major predisposing factors for chronic heart failure lacks effective interventions. It has been shown that protein ubiquitination plays an important role in cardiac hypertrophy. SMURF2 (SMAD-specific E3 ubiquitin ligase 2) is an important member of NEDD4 (neuronal precursor cell expressed developmentally downregulated 4) family of HECT E3 ubiquitin ligases. In this study we investigated the regulatory role of SMURF2 in cardiac hypertrophy. Experiment models were established in mice by transverse aortic constriction (TAC) in vivo, as well as in neonatal rat cardiomyocytes (NRCMs) by treatment with angiotensin II (Ang II, 1 μM) in vitro. We showed that the expression levels of SMURF2 were significantly elevated in cardiac tissues from patients with cardiac hypertrophy and the two experiment models. In NRCMs, SMURF2 knockdown or treatment with a specific SMURF2 inhibitor heclin (8 μM) significantly inhibited Ang II-induced cardiomyocyte hypertrophy, evidenced by reduced mRNA levels of Anp, Bnp and β-Mhc as well as cell surface. Prophylactic or therapeutic administration of heclin (10 mg·kg-1·d-1, i.p., for 5 or 4 weeks) effectively suppressed TAC-induced cardiac hypertrophy, and rescued heart function. We demonstrated that SMURF2 interacted with AXIN1 and increased ubiquitination degradation of AXIN1 in myocardial tissues, activating the Wnt/β-catenin signaling pathway. Heclin inhibited the ubiquitination degradation of AXIN1 by SMURF2 to alleviate cardiac hypertrophy. In conclusion, upregulated SMURF2 leads to AXIN1 ubiquitination and degradation, thereby facilitating the progression of cardiac hypertrophy. SMURF2 inhibitor heclin may serve as a therapeutic strategy for the treatment of cardiac hypertrophy.

PMID:40542282 | DOI:10.1038/s41401-025-01597-5