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Ann Nucl Med. 2025 Jun 27. doi: 10.1007/s12149-025-02077-w. Online ahead of print.

ABSTRACT

PURPOSE: The study aimed to assess the prognostic value of non-perfusion parameters for gated myocardial perfusion imaging (MPI) performed using Cadmium-Zinc-Telluride (CZT) single-photon emission computed tomography (SPECT) for individuals with normal myocardial perfusion.

METHODS: We analyzed data from consecutive patients who underwent thallium-201 MPI SPECT with normal perfusion. Major adverse cardiovascular events (MACEs) were recorded during a 2-year follow-up. Non-perfusion parameters were evaluated as predictors of MACEs.

RESULTS: Among 1570 patients with normal SPECT perfusion, 80 (5.1%) experienced MACEs over a mean follow-up of 22.5 ± 10.8 months: 12 (0.8%) had cardiac death, and 68 (4.3%) underwent coronary revascularization due to significant coronary artery disease. Independent predictors of MACEs included worsening post-stress ejection fraction (HR: 1.971; p = 0.008), and increased lung-to-heart ratio (HR: 2.207; p = 0.001). Kaplan-Meier analysis showed the highest MACEs' incidence in patients with two of these factors (p < 0.001). Among patients with normal resting ejection fraction, EF worsening (OR: 2.16; p = 0.004) and increased lung-to-heart ratio (OR: 1.91; p = 0.0013) both remained strong predictors.

CONCLUSIONS: Although normal myocardial perfusion typically indicates low risk for obstructive coronary artery disease, worsening post-stress ejection fraction and increased lung-to-heart ratio are crucial prognostic indicators. Importantly, these non-perfusion parameters retain their prognostic value even in patients without clinical heart failure, highlighting their relevance in comprehensive risk stratification beyond perfusion assessment alone.

PMID:40576735 | DOI:10.1007/s12149-025-02077-w

J Am Heart Assoc. 2025 Jun 27:e038770. doi: 10.1161/JAHA.124.038770. Online ahead of print.

ABSTRACT

BACKGROUND: In patients presenting with acute coronary syndromes (ACS), impaired coronary blood flow (CBF) after percutaneous coronary interventions (PCI) is linked to mortality. We developed a novel angiography-based approach for blood flow quantification using automatic contrast bolus tracking. Therefore, this study aimed to investigate the clinical impact of angiography-based blood flow quantification on major adverse cardiovascular events (MACE) after PCI in patients with ACS.

METHODS: Prospective, multicenter, nested case-control study of patients presenting ACS. A propensity score was used to match patients with and without MACE at 1 year of follow-up. MACE was defined as cardiovascular death, myocardial infarction, hospitalization for heart failure, or ischemia-driven revascularization. CBF was measured automatically from angiograms after PCI.

RESULTS: One hundred sixty-two patients were included. The mean age was 68.3±13.0 years, 83% were male, and 33% had diabetes. Overall, 66% of patients presented with ST-segment-elevation myocardial infarction. CBF after PCI was lower after ST-segment-elevation myocardial infarction compared with other clinical presentations (74.1±47.0 mL/min ST-segment-elevation myocardial infarction, 89.1±45.8 mL/min, non-ST-segment-elevation myocardial infarction, 95.7±48.8 mL/min, unstable angina, P=0.046). Patients with low post-PCI CBF (<54.3 mL/min) had an increased risk of MACE (hazard ratio, 2.11 [95% CI, 1.35-3.28], P=0.001).

CONCLUSIONS: After PCI, automatic quantification of CBF using angiography was associated with MACE in patients with ACS. Risk stratification using post-PCI CBF-derived angiography may enable tailored management strategies for individuals with ACS.

PMID:40576041 | DOI:10.1161/JAHA.124.038770

Catheter Cardiovasc Interv. 2025 Jun 27. doi: 10.1002/ccd.31724. Online ahead of print.

ABSTRACT

BACKGROUND: Coronary calcified nodules (CNs) are a challenging subset of calcific lesions associated with adverse procedural outcomes. While rotational atherectomy (RA) and balloon angioplasty (BA) have been traditionally used, orbital atherectomy (OA) offers a unique mechanism of plaque modification that may be advantageous in the treatment of CNs. Data on OA in CNs remains limited.

OBJECTIVES: To evaluate procedural success, periprocedural safety, in-hospital and long-term outcomes of retrograde OA in the treatment of CNs.

METHODS: We conducted a retrospective analysis of all patients who underwent OA for angiographically identified coronary calcification between January 1, 2022 and March 31, 2024. A total of 312 patient underwent OA during this period, of whom 57 had a CN identified. Baseline demographics, lesion characteristics, procedural details, and outcomes were assessed. CNs were defined by angiographic or intravascular ultrasound appearance.

RESULTS: The mean age was 71, 71.9% were male, 71.9% had diabetes, 40.3% had CKD and 15.8% had prior coronary artery bypass. The majority of lesions involved the left anterior descending artery (49.1%). Retrograde treatment using a 1.25 mm burr at 80,000 rpms was exclusively used. Angiographic success was achieved in 100% of cases. No perforations or flow-limiting dissections were observed. During an average follow-up of 325.57 ± 233.45 days, there were no cases of early or late stent thrombosis, with one case of very late stent thrombosis. Major adverse cardiac events (MACE) occurred in 5.26% (three patients), comprising myocardial infarction in 3.51% (two patients) and target vessel revascularization in 1.75% (one patient).

CONCLUSIONS: In this real-world, single-center, retrospective analysis, OA was safe and effective in treating coronary CNs, achieving high angiographic success with minimal periprocedural complications. These findings support the use of OA as a viable strategy for CNs, though further studies are warranted.

PMID:40576015 | DOI:10.1002/ccd.31724

Zhongguo Yi Liao Qi Xie Za Zhi. 2025 May 30;49(3):269-275. doi: 10.12455/j.issn.1671-7104.240595.

ABSTRACT

This study investigated a novel coronary knobby scoring balloon through finite element analysis (FEA) and in vitro anti-slippage testing, evaluating its dilation process under various vascular conditions and comparing it with other balloons. The FEA results indicated that in the cases of healthy artery and diseased artery with different stenosis rates, the stress on the vessels caused by the knobby scoring balloon was significantly smaller than that of the scoring balloon, and was close to that of the plain balloon. In vitro anti-slippage testing showed that the slippage distance of a plain balloon was 0.11±0.06 mm, and there was no slippage for knobby scoring balloon under nominal pressure. Knobby scoring balloon can effectively expand calcified lesion while providing anti-slippage function, and has a lower risk of vascular injury.

PMID:40574436 | DOI:10.12455/j.issn.1671-7104.240595

Medicina (Kaunas). 2025 May 26;61(6):984. doi: 10.3390/medicina61060984.

ABSTRACT

Background and Objectives: Postoperative atrial fibrillation (AF) is a frequent complication after coronary artery bypass grafting (CABG), and is particularly associated with poor outcomes. Heart rate variability (HRV), a non-invasive marker of autonomic function, has been proposed as a tool to predict AF risk, but its utility in off-pump CABG remains unclear. This study aimed to evaluate the predictive value of preoperative HRV parameters, including nonlinear metrics, for postoperative AF in patients undergoing off-pump CABG. Materials and Methods: We prospectively enrolled 67 patients undergoing elective off-pump CABG. HRV was assessed using 15 min high-resolution ECGs. Linear and nonlinear HRV parameters were analyzed. Postoperative AF was monitored through continuous ECG (days 0-4), daily 12-lead ECGs (days 5-7), and a 24 h Holter ECG on day 7. Statistical comparisons between AF and non-AF groups were performed, and the predictive accuracy was evaluated using ROC analysis. Results: Postoperative AF occurred in 40.3% (n = 27) of patients. Standard HRV measures (total power, frequency components, LF/HF ratio) did not differ significantly between groups. However, preoperative DFA Alpha 1 was significantly lower in patients who developed AF (p = 0.010) and showed the highest predictive value (AUC = 0.725, specificity = 80%). Alpha 1 also remained significantly reduced postoperatively in the AF group. Other nonlinear parameters, such as low and average fractal dimension, were also lower postoperatively in the AF group. Conclusions: Traditional HRV parameters showed limited predictive value for postoperative AF following off-pump CABG. The nonlinear DFA Alpha 1 index demonstrated a moderate predictive performance and may serve as a useful marker of autonomic dysregulation. Incorporating nonlinear HRV measures into preoperative assessment may improve AF risk stratification.

PMID:40572672 | PMC:PMC12195077 | DOI:10.3390/medicina61060984

Medicina (Kaunas). 2025 May 25;61(6):975. doi: 10.3390/medicina61060975.

ABSTRACT

Background and Objectives: The aim of this study was to compare the effects of sevoflurane-based anesthesia and propofol-based total intravenous anesthesia (TIVA) on intraocular pressure (IOP) during coronary artery bypass graft surgery (CABG) with cardiopulmonary bypass (CPB). Materials and Methods: This prospective observational monocentric study included 68 patients scheduled for CABG with CPB, divided into two groups of propofol-based TIVA (Group P) and sevoflurane-based anesthesia (Group S). Intraocular pressure was measured and recorded at eight predefined time points using a tonometer: before anesthesia induction (T1), 10 min after induction (T2), immediately before the beginning of CPB (T3), 3 min after the beginning of CPB (T4), 3 min after cross-clamping (T5), 3 min after cross-clamp removal (T6), immediately before the weaning of CPB (T7), and at the end of the surgery (immediately after skin closure) (T8). The primary endpoint was to examine the effects of propofol-based TIVA and sevoflurane-based anesthesia methods on IOP during CABG operation. The secondary endpoints included a comparison of hemodynamic variables, blood gas values, and intensive care unit (ICU) and hospital stays. Results: Intraocular pressure values were similar for both groups at all time points. A statistically significant decrease was found in IOP in all measurements after induction compared to pre-induction values in both Group P and Group S (p < 0.05). Compared to IOP measured at 10 min after induction, no statistically significant difference was found at all subsequent time points in both groups. When the right and left IOP values were compared, no statistically significant difference was detected at all time points in both Group P and Group S. Conclusions: The results of the study indicated that propofol-based TIVA and sevoflurane-based anesthesia had similar effects on IOP in patients undergoing CABG with CPB.

PMID:40572662 | PMC:PMC12195263 | DOI:10.3390/medicina61060975

In Vivo. 2025 Jul-Aug;39(4):2066-2072. doi: 10.21873/invivo.14001.

ABSTRACT

BACKGROUND/AIM: The aim of the present study was to investigate on the repurposing of glatiramer acetate (GA), a drug traditionally used to treat multiple sclerosis, as well as explore GA potential to treat cardiac ischemia in rodent models. It has been shown that GA exerts immunomodulatory effects that reduced inflammation and increased repair of heart tissue following myocardial infarction (MI) in mice and rats. GA has been shown to enhance cardiac function by promoting angiogenesis, reducing scar tissue, and protecting cardiomyocytes from ischemic damage.

MATERIALS AND METHODS: Risteys/FinnGen and MedWatch/OpenVigil data were used to assess the effects of GA on the heart.

RESULTS: There was significantly less ischemic heart disease (p<0.001, Fisher's exact test) and cardiovascular disease (p<0.001) in 457 subjects with MS who used GA in Risteys/FinnGen. Analysis of MedWatch/OpenVigil data showed a significantly reduced risk of acute MI in individuals using GA, with a proportional reporting ratio (PRR) of 0.101, indicating statistical significance at the 95% confidence level. Additionally, analysis of MedWatch/OpenVigil data indicated a decreased risk of cardiovascular disease in GA users, with a PRR of 0.345, reaching statistical significance at the 95% confidence level.

CONCLUSION: Despite rare adverse cardiovascular side-effects and given its established safety profile, GA shows promise as a novel treatment option for heart disease. Further studies could lead to an important new use of GA especially in patients who do not receive tissue plasminogen activator within the first few hours following an MI.

PMID:40579010 | DOI:10.21873/invivo.14001

Anticancer Res. 2025 Jul;45(7):2905-2916. doi: 10.21873/anticanres.17658.

ABSTRACT

BACKGROUND/AIM: Doxorubicin (DOX) is the most impactful drug developed for osteosarcoma. However, despite its therapeutic effects, it also causes serious side effects, such as cardiotoxicity and hemotoxicity. To address this, we developed a novel DOX prodrug that exhibits high antitumor activity specifically in hypoxic regions while demonstrating low toxicity in normal organs. Based on these properties, we evaluated its efficacy against osteosarcoma with the aim of significantly reducing side effects while maintaining therapeutic efficacy.

MATERIALS AND METHODS: To evaluate antitumor effects, tumor diameter changes were measured in osteosarcoma cell line-bearing mice divided into the following groups: control, DOX 8 mg/kg, DOX prodrug 8 mg/kg, and 5 doses of DOX prodrug 16 mg/kg every other day. To evaluate side effects, blood samples were collected 2 weeks after treatment in all groups to determine the complete blood count and aspartate aminotransferase, alanine aminotransferase, creatinine, and blood urea nitrogen levels. After the mice were sacrificed, sections of the liver, kidney, heart, and testes were prepared for histological evaluation.

RESULTS: Regarding antitumor effects, the DOX and DOX prodrug groups showed comparable reductions in tumor size when compared to the control group. Blood test results showed that mice in the DOX prodrug group had no leukopenia or liver dysfunction. Histological evaluation revealed that the DOX prodrug group showed significantly less myocardial damage and gonadal toxicity compared to the DOX group.

CONCLUSION: The DOX prodrug developed by our group showed tumor-suppressive effects comparable to those of DOX while being able to suppress blood toxicity, cardiotoxicity, as well as liver and testicular dysfunction.

PMID:40578960 | DOI:10.21873/anticanres.17658

Eur J Med Chem. 2025 Jun 10;296:117802. doi: 10.1016/j.ejmech.2025.117802. Online ahead of print.

ABSTRACT

Heart failure (HF) is a progressive disease characterized by persistent or episodic worsening of symptoms, leading to functional deterioration. Clinically, guidelines recommend the use of SGLT2 inhibitors for the treatment of heart failure. However, the SGLT2 inhibitors exist potential risks including weight loss and euglycemic diabetic ketoacidosis. We designed and synthesized a series of O-glucoside derivatives by introducing nitrogen-containing heterocyclic fragments. Among them, compound E9 showed the most protective effect on the glucose-free DMEM-induced injured cardiomyocytes, and the structure-activity relationships (SAR) of these compounds were preliminarily evaluated in cardiomyocyte injury model. Furthermore, compound E9 significantly enhanced the inhibition of SGLT2, NHE1, and SOD enzyme activity, increased ATP levels in damaged cardiomyocytes, and suppressed Ang II-induced myocardial fibrosis, the autophagy receptor protein P62 and the expression of cell injury markers. Additionally, compound E9 significantly improved cardiac function in TAC-induced HF mice, inhibited cardiomyocyte hypertrophy and collagen deposition, ameliorated myocardial tissue damage, enhanced mitochondrial autophagy in injured cardiomyocytes, and ultimately increased survival rates in HF mice. In conclusion, this study reveals that the novel O-glucoside derivative E9 was a promising compound for the treatment of heart failure.

PMID:40578252 | DOI:10.1016/j.ejmech.2025.117802

Environ Int. 2025 Jun 24;202:109617. doi: 10.1016/j.envint.2025.109617. Online ahead of print.

ABSTRACT

BACKGROUND: Air pollution has been linked to cardiovascular diseases (CVDs). In this study, we assess whether exposure to air pollutants and ambient temperature is associated with repeated admissions with adverse cardiovascular outcomes.

METHODS: We used data from Medicare beneficiaries between 2000 and 2016 to look at the effects of intermediate and long-term exposure to ambient PM2.5, NO2, O3, and temperature on second admissions with myocardial infarction (MI) and ischemic stroke. We derived exposure levels from high-resolution spatiotemporal models. We adjusted for demographic, socioeconomic, and access-to-care characteristics. Cox proportional hazards models were used to assess these relationships. We further looked at the effects of exposure at lower air pollution concentrations defined as PM2.5 < 9 µg/m3, NO2 < 25 ppb, and O3 < 50 ppb.

RESULTS: PM2.5 and NO2 increased the hazard of second admissions with both MI and stroke. For PM2.5, the effects were more pronounced for longer exposure time windows. Each µg/m3 increase in one-year PM2.5 levels before the first admission increased the hazard of a second admission with MI by 1.1% (95% CI: 1.0%-1.2%) and stroke by 0.9% (95% CI: 0.8%-1.1%). O3 exhibited a slight protective effect for both outcomes. Higher temperatures were associated with a higher hazard of second admissions with stroke. These results persisted at lower concentrations.

CONCLUSION: Our study demonstrates that exposures to PM2.5 and NO2 are associated with increased rates of second admissions with MIs and strokes. Higher temperatures were also further associated with an increase in the rate of second admissions with stroke.

PMID:40578117 | DOI:10.1016/j.envint.2025.109617

J Mol Histol. 2025 Jun 27;56(4):207. doi: 10.1007/s10735-025-10453-z.

ABSTRACT

Myocardial ischemia followed by reperfusion triggers a range of pathological events, among which excessive autophagy plays a key role. Theaflavin-3,3'-digallate (TF3) is a functional polyphenol of black tea and is beneficial in the prevention or/and treatment of various diseases. Here, we explored the therapeutic effect of TF3 on myocardial ischemia/reperfusion (I/R) injury. I/R injury was induced in rats through ischemia (30 min) followed by reperfusion (24 h). TF3 was administered seven days before the I/R. Cardiac function was determined by echocardiography. Infarct size and apoptosis were assessed using TTC and TUNEL, respectively. H9C2 cardiomyocytes were treated with TF3 or/and PI3K inhibitor (LY294002) and then exposed to hypoxia/reoxygenation (H/R). Content levels of myocardial injury indicators in rat hearts and H9C2 cardiomyocytes were detected using corresponding kits. H9C2 cardiomyocyte apoptosis was evaluated by flow cytometry. Protein levels of autophagy, apoptosis, and PI3K/Akt/mTOR signaling in vivo and in vitro were detected using western blotting. TF3 reduced myocardial infarct size and decreased serum CK-MB, cTnT, and LDH content levels in rat model of myocardial I/R. TF3 reduced apoptosis and autophagy in I/R rat hearts and H9C2 cardiomyocytes by reducing Bax, cleaved caspase-3, Beclin-1, and LC3B levels, and elevating Bcl-2 and p62 levels. TF3 administration activated PI3K/Akt/mTOR signaling in I/R rat hearts and H9C2 cells. PI3K inhibitor LY294002 reversed the inhibitory effect of TF3 on H/R-induced apoptosis and autophagy in H9C2 cells. Overall, TF3 alleviates I/R-induced myocardial injury by reducing autophagy and apoptosis by activating PI3K/Akt/mTOR signaling.

PMID:40576913 | DOI:10.1007/s10735-025-10453-z

Ann Nucl Med. 2025 Jun 27. doi: 10.1007/s12149-025-02077-w. Online ahead of print.

ABSTRACT

PURPOSE: The study aimed to assess the prognostic value of non-perfusion parameters for gated myocardial perfusion imaging (MPI) performed using Cadmium-Zinc-Telluride (CZT) single-photon emission computed tomography (SPECT) for individuals with normal myocardial perfusion.

METHODS: We analyzed data from consecutive patients who underwent thallium-201 MPI SPECT with normal perfusion. Major adverse cardiovascular events (MACEs) were recorded during a 2-year follow-up. Non-perfusion parameters were evaluated as predictors of MACEs.

RESULTS: Among 1570 patients with normal SPECT perfusion, 80 (5.1%) experienced MACEs over a mean follow-up of 22.5 ± 10.8 months: 12 (0.8%) had cardiac death, and 68 (4.3%) underwent coronary revascularization due to significant coronary artery disease. Independent predictors of MACEs included worsening post-stress ejection fraction (HR: 1.971; p = 0.008), and increased lung-to-heart ratio (HR: 2.207; p = 0.001). Kaplan-Meier analysis showed the highest MACEs' incidence in patients with two of these factors (p < 0.001). Among patients with normal resting ejection fraction, EF worsening (OR: 2.16; p = 0.004) and increased lung-to-heart ratio (OR: 1.91; p = 0.0013) both remained strong predictors.

CONCLUSIONS: Although normal myocardial perfusion typically indicates low risk for obstructive coronary artery disease, worsening post-stress ejection fraction and increased lung-to-heart ratio are crucial prognostic indicators. Importantly, these non-perfusion parameters retain their prognostic value even in patients without clinical heart failure, highlighting their relevance in comprehensive risk stratification beyond perfusion assessment alone.

PMID:40576735 | DOI:10.1007/s12149-025-02077-w

Mol Med Rep. 2025 Sep;32(3):237. doi: 10.3892/mmr.2025.13602. Epub 2025 Jun 27.

ABSTRACT

The specific mechanisms of doxorubicin (Dox)‑induced cardiotoxicity (DIC) remain unclear. In the present study, H9c2 cardiomyocytes were treated with Dox, and it was revealed that DEAD‑box RNA helicase 3 X‑linked (DDX3X), mitochondrial antiviral signaling (MAVS) and stress granules (SGs) were present at lower levels in the treated H9c2 cardiomyocytes compared with those in the control cells. The present study further investigated the mechanisms through which DIC occurs. Pretreatment with arsenite, which pharmacologically accelerates SGs, alleviated the myocardial injury caused by Dox. By contrast, anisomycin, an SG inhibitor, increased cardiomyocyte apoptosis induced by Dox. In addition, both DDX3X knockdown and pretreatment with RK‑33 (a DDX3X pharmacological inhibitor) decreased SG expression, whereas DDX3X overexpression promoted SG generation. These results indicated that DDX3X mitigated DIC through the regulation of SGs. In addition, MAVS knockdown inhibited SG assembly and reduced the expression of the anti‑apoptotic inhibitor Bcl2, and MAVS was influenced by DDX3X, thereby serving as a connector between DDX3X and SGs. The results from western blotting, reverse transcription‑quantitative PCR, immunofluorescence and flow cytometry analysis demonstrated that DDX3X, MAVS, and SGs may serve as key protective factors in DIC.

PMID:40576139 | DOI:10.3892/mmr.2025.13602

World J Cardiol. 2025 Jun 26;17(6):104832. doi: 10.4330/wjc.v17.i6.104832.

ABSTRACT

BACKGROUND: Right ventricular hypertrophy (RVH) occurs because of volume or pressure overload within the right ventricular (RV) system. RVH is associated with complex pathological changes, including myocardial cell injury, apoptosis, myocardial fibrosis, neuroendocrine disturbances, and abnormal water and liquid metabolism. Ferroptosis, a novel type of iron-dependent cell death characterized by lipid peroxide accumulation, is an important mechanism of cardiomyocyte death. However, the role of ferroptosis in RVH has rarely been studied. We hypothesize that hydrogen (H2), an experimental medical gas with superior distribution characteristics, inhibits ferroptosis.

AIM: To explore the protective effect of H2 on RVH and the mechanism by which H2 regulates ferroptosis.

METHODS: An in vivo RVH rat model was induced by monocrotaline (MCT) in 30 male Sprague-Dawley rats. An H9C2 cell model was treated with angiotensin II to simulate pressure overload in the RV system in vitro. H2 was administered to rats by inhalation (2% for 3 hours daily for 21 days) and added to the cell culture medium. The Nrf2 inhibitor ML385 (1 μM) was used to investigate anti-ferroptotic mechanisms.

RESULTS: In MCT-treated rats, H2 inhalation decreased RVH; the RV wall thickness decreased from 3.5 ± 0.3 mm to 2.8 ± 0.2 mm (P < 0.05) and the RV ejection fraction increased from 45 ± 3% to 52 ± 4% (P < 0.05). In H9C2 cells, H2 alleviated hypertrophy. H2 inhibited ferroptosis by modulating the iron content, oxidative stress, and ferroptosis-related proteins, thereby restoring the Nrf2/HO-1 signaling pathway.

CONCLUSION: H2 retards RVH by inhibiting ferroptosis via Nrf2/HO-1 restoration, suggesting a new treatment strategy.

PMID:40575431 | PMC:PMC12186143 | DOI:10.4330/wjc.v17.i6.104832

Front Physiol. 2025 Jun 12;16:1641580. doi: 10.3389/fphys.2025.1641580. eCollection 2025.

ABSTRACT

[This retracts the article DOI: 10.3389/fphys.2020.551318.].

PMID:40574900 | PMC:PMC12198966 | DOI:10.3389/fphys.2025.1641580

Medicina (Kaunas). 2025 May 30;61(6):1020. doi: 10.3390/medicina61061020.

ABSTRACT

Galectin-1 (Gal-1), a β-galactoside-binding lectin, plays a complex role in cardiovascular diseases (CVDs), exerting both protective and pathological effects depending on the context. This review synthesizes findings from the past decade to explore Gal-1's involvement in key aspects of CVD pathogenesis, including vascular homeostasis, inflammation regulation, atherosclerosis progression, myocardial remodeling, and heart failure. While Gal-1 supports endothelial integrity and immune modulation, its dysregulation contributes to disease progression through pro-inflammatory signaling, fibrosis, and adverse cardiac remodeling. Emerging evidence suggests that Gal-1 holds potential as both a biomarker for risk assessment and a therapeutic target. However, critical knowledge gaps remain, particularly regarding its context-dependent effects, the limited scope of clinical trials, and unresolved mechanistic insights. Addressing these challenges will be essential to fully harness Gal-1's therapeutic potential in cardiovascular medicine, guiding future research efforts toward precision interventions and clinical applications.

PMID:40572708 | PMC:PMC12195248 | DOI:10.3390/medicina61061020

Molecules. 2025 Jun 10;30(12):2527. doi: 10.3390/molecules30122527.

ABSTRACT

Anthracyclines play an irreplaceable role in cancer treatment, although their clinical application is limited due to severe side effects such as arrhythmia, cardiomyopathy, and myocardial infarction. The currently available clinical drugs for treating anthracycline-induced cardiotoxicity (AIC) are limited by numerous drawbacks, including the side effects of the therapeutic agents, single treatment mechanisms, and individual patient variations. Therefore, novel drugs with broader applicability and multitarget synergistic protective effects are, therefore, urgently needed. Ginsenosides, the primary bioactive constituents of plants belonging to the genus Panax (family Araliaceae), exhibit a wide range of pharmacological activities, including anti-inflammatory, antioxidative, and antitumor effects, and have demonstrated cardioprotective properties against AIC. This article examines the mechanisms of AIC and the modulatory effects of ginsenosides on these mechanisms. This review highlights the potential molecular targets and signaling pathways through which ginsenosides exert therapeutic effects on AIC, including the regulation of oxidative-stress-related pathways such as Keap1/Nrf2, MAPK, STAT, PI3K/Akt, and AMPK; the restoration of mitochondrial function; the modulation of autophagy; and the inhibition of pyroptosis, ferroptosis, and apoptosis. Therefore, this review serves as a theoretical basis and provides a research direction for future investigation regarding the prevention and treatment of AIC with ginsenosides, as well as clinical translation studies.

PMID:40572494 | PMC:PMC12196387 | DOI:10.3390/molecules30122527

Open Heart. 2025 Jun 27;12(1):e003301. doi: 10.1136/openhrt-2025-003301.

ABSTRACT

INTRODUCTION: The current standard treatment for ST-segment elevation myocardial infarction is prompt reperfusion through primary percutaneous coronary intervention. However, myocardial infarction remains the leading cause of heart failure, contributing to prolonged hospital stay and a 30% rehospitalisation rate within 6 months. Stem cell therapy has emerged as a potential approach to repair myocardial damage.

METHODS: This study is a meta-analysis of randomised clinical trials available online. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines were followed, and the study was conducted according to the Cochrane Handbook for Systematic Reviews of Interventions.

RESULTS: 21 articles from 15 trials (21 clinical trial interventions) with a total of 1218 participants were included. Stem cell therapy was associated with fewer adverse events than controls (OR 0.66, 95% CI 0.44 to 0.99, p=0.05), supporting its short-term to mid-term safety. No cardiac-related cancer cases were reported in any group, but longer follow-up is needed to assess potential oncogenic risks. Efficacy analyses showed no significant effect on infarct size (absolute or relative) or left ventricular ejection fraction (LVEF) in short-term follow-up. In long-term follow-up, relative infarct size became statistically significant in favour of stem cell therapy only after exclusion of an outlier study (standardised mean difference -0.63, 95% CI -0.94 to -0.32, p<0.0001). Long-term LVEF improvement was also significant (mean difference 2.63%, 95% CI 0.50% to 4.76%, p=0.02), although substantial heterogeneity remained unexplained despite sensitivity analyses, including the removal of low-correlation studies.

CONCLUSION: Stem cell therapy for acute myocardial infarction demonstrates a favourable safety profile. While overall efficacy remains uncertain, long-term benefits may exist, particularly for relative infarct size and LVEF. However, interpretation is limited by study heterogeneity. Future trials with standardised protocols and longer follow-up are warranted.

PMID:40579230 | DOI:10.1136/openhrt-2025-003301

Eur J Prev Cardiol. 2025 Jun 20:zwaf352. doi: 10.1093/eurjpc/zwaf352. Online ahead of print.

ABSTRACT

BACKGROUND AND AIMS: Familial hypercholesterolemia (FH) significantly increases cardiovascular risk from childhood yet remains widely underdiagnosed. This cross-sectional study aimed to evaluate existing pediatric FH diagnostic criteria in real-world cohorts and to develop two novel diagnostic tools: a semi-quantitative scoring system (FH-PeDS) and a machine learning model (ML-FH-PeDS) to enhance early FH detection.

METHODS: Five established FH diagnostic criteria were assesed (Dutch Lipid Clinics Network [DLCN], Simon Broome, EAS, Simplified Canadian, and Japanese Atherosclerosis Society) in Slovenian (N=1,360) and Portuguese (N=340) pediatric hypercholesterolemia cohorts, using FH-causing variants as the reference standard. FH-PeDS was developed from the Slovenian cohort, and ML-FH-PeDS was trained and tested using a 60%/40% split before external validation in the Portuguese cohort.

RESULTS: Only 47.4% of genetically confirmed FH cases were identified by all established criteria, while 10.9% were missed entirely. FH-PeDS outperformed DLCN in the combined cohort (AUC 0.897 vs. 0.857; p<0.01). ML-FH-PeDS showed superior predictive power (AUC 0.932 in training, 0.904 in testing vs. 0.852 for DLCN; p<0.01) and performed best as a confirmatory test in the testing subgroup (39.7% sensitivity, 87.7% PPV at 98% specificity). In the Portuguese cohort, ML-FH-PeDS maintained strong predictive performance (AUC 0.867 vs. 0.815 for DLCN; p<0.01) despite population differences.

CONCLUSIONS: Current FH diagnostic criteria perform suboptimally in children. FH-PeDS and ML-FH-PeDS provide tools to improve FH detection, particularly where genetic testing is limited. They also help guide genetic testing decisions for hypercholesterolemic children. By enabling earlier diagnosis and intervention, these tools may reduce long-term cardiovascular risk and improve outcomes.

PMID:40578816 | DOI:10.1093/eurjpc/zwaf352

J Heart Lung Transplant. 2025 Jun 25:S1053-2498(25)02061-3. doi: 10.1016/j.healun.2025.06.023. Online ahead of print.

NO ABSTRACT

PMID:40578718 | DOI:10.1016/j.healun.2025.06.023