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Biomedicines. 2025 Jun 13;13(6):1466. doi: 10.3390/biomedicines13061466.

ABSTRACT

Background: Estrogens play a protective role during the early stages of life. However, endogenous 17β-estradiol (E2) can accelerate atherosclerosis progression. Aim: The purpose of this study was to test for the significance of the sex-specific associations of gonadal hormones with the extent of the inflammatory response, myocardial damage, and ventricular arrhythmia risk in acute myocardial infarction (MI). Materials and Methods: Study design: single-center cohort study. Blood samples for the assessment of sex steroids (E2, total testosterone [T]), oxidized low-density lipoproteins, high-sensitivity C-reactive protein (CRP), white blood cell (WBC) counts, and cardiac enzymes were collected 48 h after the onset of symptoms (and within 6 h after PCI) from 111 patients (37% women) with acute MI. Coronary disease severity, left ventricular systolic function (LV), and indices of ventricular repolarization were assessed using coronary angiography, echocardiography, and a conventional electrocardiogram, respectively. Results: In men with acute MI, peak cardiac enzyme levels were predicted by post-percutaneous coronary intervention (PCI) E2 plasma levels, peak WBC count, and peak CRP plasma levels. T levels and the E2/T ratio were associated with post-PCI CRP in these men. For women, peak WBC count was a marker of highest testosterone, and only WBC count was a significant indicator of myocardial injury extent. The incidence of acute ventricular tachycardia detected in AMI was significantly associated with left ventricular ejection fraction and with peak WBC count (as a tendency) regardless of sex. A longer duration of cardiac repolarization prior to PCI was predicted by lower ejection fractions in men and by age, CRP, and testosterone levels in female patients. Conclusions: During acute MI, elevated endogenous estradiol levels in men and increased leukocytes in women indicate acute myocardial damage. Post-PCI plasma inflammatory markers are sex-specific confounding factors for acute endogenous E2 levels, T levels, and the E2/T ratio. LV systolic function in men and, characteristically, the acute inflammatory response and testosterone levels in women are predictors of longer ventricular repolarization and arrhythmia risk.

PMID:40564184 | PMC:PMC12190329 | DOI:10.3390/biomedicines13061466

Biomolecules. 2025 May 28;15(6):783. doi: 10.3390/biom15060783.

ABSTRACT

PURPOSE: Doxorubicin (DOX) is a broad-spectrum anti-tumor anthracycline drug. However, its clinical application is greatly limited due to the side effect of cardiotoxicity. Caffeic acid phenethyl ester (CAPE) is one of the major biologically active compounds isolated from propolis, which is effective in the treatment of cardiovascular diseases. The purpose of this study aimed to explore the possible mechanism of CAPE's protective effect on DOX-induced cardiotoxicity (DIC).

METHODS: In vivo, a DIC model was established by the intraperitoneal injection of 3 mg/kg DOX. The cardiac function of mice was monitored by electrocardiograms. Histopathological changes in myocardial tissue were detected by H&E staining. Serum samples were tested for the level of markers of myocardial injury. In vitro, transmission electron microscopy was used to assess the mitochondrial damage. Oxidative stress was measured by flow cytometry and mitochondrial respiration analysis. Necroptosis pathway changes were detected by Western blotting. Furthermore, the overexpression plasmid of a key necroptosis gene, necroptosis inhibitor or ROS inducer/inhibitor was applied to H9c2 and AC16 cells to explore whether CAPE exerted a protective effect against DIC through the cross-talk mediated by ROS and MLKL.

RESULTS: CAPE could improve the cardiac function and protect against myocardial tissue. CAPE pre-administration treatment attenuated the DOX-induced generation of ROS, protected mitochondrial functions and inhibited necroptosis. Moreover, there was cross-talk between the ROS and necroptosis. CAPE could protect against DIC by inhibiting the ROS-MLKL signaling that regulated the cross-talk.

CONCLUSIONS: CAPE alleviated the oxidative stress and necroptosis of DIC, indicating that the cross-talk mediated by ROS-MLKL signaling may be a potential therapeutic mechanism for clinical DIC.

PMID:40563424 | PMC:PMC12190673 | DOI:10.3390/biom15060783

Antioxidants (Basel). 2025 May 31;14(6):671. doi: 10.3390/antiox14060671.

ABSTRACT

Ginnalin A (GA), a polyphenolic compound derived from amur maple trees, has been identified as a powerful scavenger of reactive oxygen species (ROS). Recognizing the pivotal role of ROS in exacerbating secondary damage during myocardial ischemia-reperfusion injury (MIRI), we fractionated GA-enriched extracts from the leaves of the amur maple tree, Acer tataricum L. subsp. ginnala (Maxim.) Wesm., using common solvents of dichloromethane (DCM) and ethyl acetate (EA). When co-administered for 30 min, the DCM- and EA-fractioned extracts effectively protected cardiomyocytes from H2O2-induced damage. ROS-sensitive probes indicated that treatment with ginnala extracts significantly reduced both intracellular and mitochondrial ROS levels. Instead of enhancing the activity of antioxidative enzymes, the ginnala extracts acted as natural antioxidases, directly scavenging various ROS such as superoxide, H2O2, hydroxyl radical, and Fe2+ within just 20 min. In a MIRI rat model, the in vivo administration of ginnala extracts provided significant cardioprotection by preserving viable myocardia and enhancing cardiac functions. Additionally, treatment with ginnala extracts significantly reduced cardiac fibrosis and denatured collagen. Our study suggests that the ultrafast ROS scavenging capability of ginnala extracts offers substantial heart protection during MIRI. Incorporating ginnala extracts as a pharmacological intervention during reperfusion could effectively mitigate ROS-induced cardiac injury.

PMID:40563305 | PMC:PMC12189229 | DOI:10.3390/antiox14060671

Br J Surg. 2025 May 31;112(6):znaf113. doi: 10.1093/bjs/znaf113.

NO ABSTRACT

PMID:40568914 | PMC:PMC12199258 | DOI:10.1093/bjs/znaf113

Autophagy. 2025 Jun 26. doi: 10.1080/15548627.2025.2524290. Online ahead of print.

ABSTRACT

Sunitinib is a receptor tyrosine kinase inhibitor used for the treatment of renal cell carcinoma and imatinib-resistant gastrointestinal stromal tumors. Clinical data have shown that patients receiving sunitinib develop reduced cardiac function, arrhythmia and heart failure, thereby largely limiting its clinical use. However, the molecular mechanisms underlying sunitinib-induced arrhythmogenesis remain unclear. Here, utilizing the human induced pluripotent stem cell-derived cardiomyocyte (iPSC-CM) model, we found that sunitinib caused a variety of deleterious phenotypes, including cardiomyocyte death, sarcomeric disorganization, irregular Ca2+ transients, impaired ATP2A2a/SERCA2a (ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 2a) activity, arrhythmia, and excessive macroautophagy/autophagy. Mechanistically, SQSTM1/p62 (sequestosome 1) interacts with MYLK3 (myosin light chain kinase 3) and drives excessive autophagic degradation of MYLK3 in sunitinib-treated iPSC-CMs. Downregulation of MYLK3 suppresses the phosphorylation of CAMK2/CAMKII (calcium/calmodulin dependent protein kinase II), thereby reducing the phosphorylation level of its downstream substrate PLN (phospholamban), leading to impaired ATP2A2a/SERCA2a activity and subsequent Ca2+ dyshomeostasis and arrhythmia. Moreover, pharmacological intervention of the cardiac myosin activator omecamtiv mecarbil (OM) or overexpression of MYLK3 significantly restored the expression of MYLK3 and reversed pathogenic phenotypes in sunitinib-treated iPSC-CMs. Nanoparticle delivery of OM effectively prevented sunitinib-induced cardiac dysfunction in mice. Our findings suggest that sunitinib-induced MYLK3 degradation causes the inhibition of the CAMK2-PLN-ATP2A2a signaling pathway and leads to sunitinib-induced arrhythmogenesis, and that MYLK3 can act as a novel cardioprotective target for sunitinib-induced cardiotoxicity.

PMID:40568844 | DOI:10.1080/15548627.2025.2524290

Haematologica. 2025 Jun 26. doi: 10.3324/haematol.2025.288067. Online ahead of print.

ABSTRACT

Not available.

PMID:40568731 | DOI:10.3324/haematol.2025.288067

medRxiv [Preprint]. 2025 Mar 5:2025.03.04.25323391. doi: 10.1101/2025.03.04.25323391.

ABSTRACT

BACKGROUND: Antibody-mediated rejection (AMR) remains the major risk factor for allograft loss across all solid organ transplantation. Unfortunately, its diagnosis relies on biopsy, an invasive gold standard that often sample unaffected allograft tissue leading to missed diagnosis. Plasma donor-derived cell-free DNA (dd-cfDNA) is noninvasive biomarker that has high sensitivity but low specificity for AMR diagnosis. This proof-of-concept study assessed the utility of cell-free chromatin immunoprecipitation (cfChIP) as a surrogate for gene expression to detect cardiac AMR and the associated pathobiology.

METHODS: The discovery GRAfT multicenter cohort of heart transplant patients ( NCT02423070 ) identified AMR, acute cellular rejection (ACR), and stable controls based on biopsy and dd-cfDNA results. Plasma cfChIP-sequencing was performed to identify peaks, associated genes and pathobiological pathways. Plasma from an external cohort (GTD, NCT01985412 ) was also analyzed to verify pathways identified. Digital droplet PCR (ddPCR) assays targeting differential regions were constructed to test the diagnostic performance of cfDNA to detect AMR/ACR from stable controls (rejection-specific assays) or AMR from ACR (AMR-specific assays).

RESULTS: The cohort included 21 AMR, 28 ACR, and 45 stable controls from GRAfT and GTD, and 23 healthy controls. cfChIP detected expected active genes, including housekeeping genes and gene targets of transplant immunosuppressive drugs but not inactive genes. Unsupervised clustering of the discovery GRAfT cohort assigned 95% of samples correctly as AMR, ACR or stable control. Differential analysis identified pathobiological pathways of AMR such as neutrophil degranulation and complement activation. The pathways were consistent in GTD samples. Rejection-specific assays detected AMR/ACR from controls with AUC of 0.78 - 0.95. AMR-specific assays detected AMR from ACR with AUC of 0.71 - 0.85, sensitivities of 0.73 - 0.94 and specificities of 0.73 - 0.80.

CONCLUSION: This study provides valuable preliminary data supporting the use of cfChIP to detect AMR and the associated pathobiological pathways.

PMID:40568656 | PMC:PMC12191110 | DOI:10.1101/2025.03.04.25323391

Cardiovasc Ther. 2025 Jun 18;2025:9910333. doi: 10.1155/cdr/9910333. eCollection 2025.

ABSTRACT

Background and Aims: Trimethylamine-N-oxide (TMAO) is recognized as a novel marker and mediator of atherosclerotic cardiovascular disease (ASCVD). Endothelial progenitor cells (EPCs) are crucial for maintaining vascular homeostasis. Impaired EPC numbers and function correlate with increased adverse cardiovascular events. The aim of this study was to decipher the effect of TMAO on late EPCs (LEPCs) and its underlying molecular mechanism. Methods and Results: In vitro migration and tubulogenic capacities of LEPCs were attenuated by TMAO in a dose-dependent manner, accompanied by inhibition of manganese superoxide dismutase (MnSOD) and mitochondrial damage. TMAO-induced mitochondrial damage provoked proinflammatory responses (increased levels of IL-6, IL-1b, ICAM-1, E-sel, and TNF-α) and autophagic cell death (confirmed by western blot immunofluorescent staining and transmission electron microscopy) in LEPCs. Overexpression of MnSOD through adenovirus transfection reversed TMAO-related LEPCs dysfunction. To study the effect of TMAO on LEPC-mediated vascular repair in vivo, a hind limb ischemia model was established in nude mice, and LEPCs were injected in the ischemic hind limb. Laser Doppler imaging of mouse ischemic hindlimbs at 21 days indicated that TMAO treatment inhibited LEPCs-mediated blood flow recovery, which was restored by MnSOD overexpression. Immunohistology analyses further revealed consistent alterations in capillary density determined by CD31 staining. Conclusions: TMAO induces mitochondrial damage in LEPCs via MnSOD suppression, which leads to cell dysfunction, proinflammatory activation, and autophagic cell death in vitro and impaired LEPCs-mediated revascularization in vivo. Overexpression of MnSOD restores TMAO-induced LEPCs dysfunction and further enhances LEPC-mediated revascularization in the ischemic hind limbs in nude mice.

PMID:40568449 | PMC:PMC12197513 | DOI:10.1155/cdr/9910333

JHLT Open. 2025 May 26;9:100289. doi: 10.1016/j.jhlto.2025.100289. eCollection 2025 Aug.

ABSTRACT

INTRODUCTION: Donation after circulatory death (DCD) with thoracoabdominal normothermic regional perfusion (TA-NRP) has been increasingly used to procure cardiac allografts; however, concerns persist regarding its impact on lung allografts. We present our institution's experience with DCD TA-NRP and donation after brain death (DBD) lung transplants, comparing outcomes between the two techniques.

METHODS: All lung transplants recovered with DBD or DCD TA-NRP performed between October 2022 and December 2024 were included. DCD TA-NRP procured lungs were retrieved using a lung protective strategy including early reintubation and pulmonary venting as previously described. The primary outcome was survival, with secondary outcomes of primary graft dysfunction (PGD) and pulmonary-related mortality.

RESULTS: There were 85 DBD and 23 DCD TA-NRP lung transplants performed in the study period. Overall survival was not significantly different by Kaplan-Meier curve (p = 0.49), with 1-year absolute survival of 81.6% for DCD TA-NRP, with only one pulmonary-related mortality, and 89.4% for DBD, with six pulmonary-related mortalities. PGD grade 3 rates were not statistically different at postoperative day (POD) 0 (47.8% DCD TA-NRP vs 35.2% DBD, p = 0.27), POD 1 (21.7% vs 10.6%, p = 0.16), POD2 (8.7% vs 11.7%, p = 0.68), and POD3 (13.0% vs 11.8%, p = 0.87). Other intraoperative and postoperative outcomes were not significantly different.

CONCLUSION: Lung transplantation outcomes were not significantly different between lung grafts recovered by DCD TA-NRP and DBD. This early data suggests TA-NRP may not adversely impact DCD lung allografts during procurement.

PMID:40568346 | PMC:PMC12192336 | DOI:10.1016/j.jhlto.2025.100289

Mayo Clin Proc Innov Qual Outcomes. 2025 Jun 11;9(4):100634. doi: 10.1016/j.mayocpiqo.2025.100634. eCollection 2025 Aug.

ABSTRACT

OBJECTIVE: To evaluate temporal associations of cancer with subsequent incident atrial fibrillation (AF) and temporal associations of AF with subsequent incident cancer, within 3, 3 to 12, and >12 months after index diagnosis.

PATIENTS AND METHODS: We included 13,748 community-dwelling adults (mean age, 54 years) in the Atherosclerosis Risk in Communities study without cancer or AF histories at baseline (follow-up between January 1, 1987, and December 31, 2019). Atrial fibrillation was ascertained from electrocardiograms at study visits and health records. Cancer was ascertained via linkage with state registries and health records. We estimated associations of cancer with AF risk and AF with cancer risk by time since diagnosis using Cox regression, adjusting for shared risk factors and other cardiovascular diseases.

RESULTS: In 3909 adults, cancer was diagnosed before AF. Atrial fibrillation risk was the highest within 3 months after cancer diagnosis (hazard ratio [HR], 11.71; 95% CI, 9.52-14.41), followed by 3 to 12 months (HR, 2.07; 95% CI, 1.54-2.80) and >12 months (HR, 1.46; 95% CI, 1.29-1.64). In 1973 adults, AF was diagnosed before cancer. Cancer risk was the highest within 3 months of AF diagnosis (HR, 2.24; 95% CI, 1.47-3.41), followed by 3 to 12 months (HR, 1.28; 95% CI, 0.91-1.80) and >12 months (HR, 1.09; 95% CI, 0.91-1.29).

CONCLUSION: In adult cancer patients, AF risk is the highest within 3 months after diagnosis and remains significantly elevated throughout survivorship but could be due to detection bias. Cancer risk is strongest within 3 months of AF diagnosis but significantly attenuated over time, suggesting detection bias and reverse causation.

PMID:40568232 | PMC:PMC12192571 | DOI:10.1016/j.mayocpiqo.2025.100634

SAGE Open Med. 2025 Jun 24;13:20503121251348420. doi: 10.1177/20503121251348420. eCollection 2025.

ABSTRACT

OBJECTIVES: Ruxolitinib is used to treat myelofibrosis, polycythemia vera, and steroid-refractory graft-versus-host disease following allogeneic stem cell transplantation. This study aimed to determine the association between ruxolitinib and adverse events by evaluating case reports published between January 2014 and March 2024 in the Japanese Adverse Drug Event Report database.

METHODS: The signals for the ruxolitinib-adverse event association were identified using propensity score-adjusted reporting odds ratio analysis. Data obtained from the drug-gene interaction, drug signature, search tool for chemical interactions, and interaction reference index databases were used to construct a drug-gene interaction network. Functional and pathway enrichment analyses were performed using the Disease Ontology Semantic and Enrichment and ReactomePA R packages.

RESULTS: The propensity score-adjusted reporting odds ratio for ruxolitinib-associated adverse events was as follows: anemia, 18.49 (95% confidence interval (CI): 16.15-21.16); myelosuppression, 4.70 (95% CI: 3.54-6.24); pancytopenia, 1.97 (95% CI: 1.23-3.16); cardiac failure, 2.29 (95% CI: 1.60-3.28); hepatic function abnormal, 1.60 (95% CI: 1.15-2.23); herpes zoster, 6.40 (95% CI: 4.35-9.41); pneumonia, 2.96 (95% CI: 2.35-3.73); renal impairment, 1.34 (95% CI: 0.94-1.90); sepsis, 5.14 (95% CI: 3.75-7.05); interstitial lung disease, 0.33 (95% CI: 0.21-0.52); deep vein thrombosis, 0.32 (95% CI: 0.07-1.44); hemorrhage, 1.99 (95% CI: 1.05-3.75). We also assessed 3015 human genes that directly or indirectly interact with ruxolitinib. The molecular complex detection plug-in of Cytoscape was used to detect 24 clusters. Several genes were enriched in the biological processes of "anemia" and "bacterial infections," identified as significant ruxolitinib-related disease terms.

CONCLUSIONS: This retrospective analysis using the Japanese Adverse Drug Event Report database indicated potential associations between ruxolitinib and adverse events, including anemia and bacterial infections. Future research should explore the underlying pharmacological mechanisms using functional enrichment analysis of ruxolitinib-associated genes related to blood toxicity and bacterial infections.

PMID:40567936 | PMC:PMC12188073 | DOI:10.1177/20503121251348420

Plast Reconstr Surg Glob Open. 2025 Jun 25;13(6):e6916. doi: 10.1097/GOX.0000000000006916. eCollection 2025 Jun.

ABSTRACT

Pediatric heart transplantation can present with many obstacles, including size mismatch of the donor heart with the thoracic cavity of the recipient. For the patient to have vitality, they may need to have surgical interventions to address these conditions. We investigate the case of a 23-month-old infant who underwent orthotopic heart transplantation for nonischemic dilated cardiomyopathy. Given the large size of the donor heart relative to the infant, a subsequent modified thoracoplasty was performed to allow for chest wall closure. This report provides potential surgical techniques that can be taken and follows the patient for a 25-year time span.

PMID:40567426 | PMC:PMC12190079 | DOI:10.1097/GOX.0000000000006916

Circ Res. 2025 Jun 26. doi: 10.1161/CIRCRESAHA.124.326030. Online ahead of print.

ABSTRACT

BACKGROUND: Sipa1 (signal-induced proliferation-associated gene 1) is known as a specific Rap1 GTPase-activating protein that negatively regulates Rap1 signaling. Although Sipa1 has been extensively studied in cancer research, its role in the wound-healing response after myocardial infarction (MI) remains unexplored.

METHODS: To investigate the role of endogenous Sipa1 in MI, we performed permanent left anterior descending artery ligation in both Sipa1 knockout mice and their control littermates. Bone marrow transplantation, flow cytometry, cell sorting, and transcriptomic analysis were conducted to identify the cellular source of Sipa1 in the infarcted heart. The role of cardiac fibroblast-derived Sipa1 during MI was examined using Sipa1 deletion approaches, specifically in cardiac fibroblasts, in vivo and in vitro.

RESULTS: Mice deficient in Sipa1 exhibited improved post-MI survival and cardiac function, along with attenuated expression of inflammatory mediators and diminished accumulation of Ly6Chigh monocytes and CCR (C-C chemokine receptor) 2+ macrophages in the infarcted heart. Although Sipa1 was broadly expressed in the heart, cardiac fibroblasts were responsible for the Sipa1-induced deleterious phenotype as demonstrated by cardiac fibroblast-specific Sipa1 conditional knockout mice, which averted excessive inflammation and adverse cardiac remodeling following MI. Mechanistically, Sipa1 promotes the production of CCL (C-C chemokine ligand) 2, CCL7, and GM-CSF (granulocyte/macrophage colony-stimulating factor) in the cardiac fibroblasts early after MI via a noncanonical RasGRP2-Ras-JNK signaling pathway, irrespective of canonical Rap1, thereby facilitating the accumulation and activation of inflammatory monocytes and macrophages.

CONCLUSIONS: These results identify a previously unknown fibroblast-myeloid axis characterized by Sipa1, which initiates excessive inflammation and leads to poor outcomes after MI. Targeting Sipa1 offers a potential novel therapeutic strategy to optimize post-MI wound-healing response, thereby preventing the development of chronic ischemic heart failure.

PMID:40567222 | DOI:10.1161/CIRCRESAHA.124.326030

Circ Heart Fail. 2025 Jun 26:e012835. doi: 10.1161/CIRCHEARTFAILURE.125.012835. Online ahead of print.

ABSTRACT

BACKGROUND: The use of donation after circulatory death (DCD) donors for heart transplantation (HT) is increasing in the United States. Whether sex differences exist in DCD HT utilization and outcomes is unknown.

METHODS: Adults listed for HT at DCD centers between January 1, 2019 (first US DCD HT) and September 15, 2023, in the Organ Procurement and Transplantation Network Registry were included. Differences in listing for DCD HT by sex were investigated using multivariable logistic regression. The impact of listing for DCD HT (modeled as a time-varying covariate) on waitlist outcomes including the rate of HT waitlist removal for death or clinical deterioration was assessed using multivariable competing risk analyses. Annual trends in DCD HT and 2-year survival after DCD HT by sex were also investigated.

RESULTS: A total of 9807 individuals were listed at DCD centers during the study period. Listing for DCD HT was less common among women after multivariable adjustment (odds ratio, 0.84 [95% CI, 0.76-0.92]; P<0.001). Listing for DCD HT was associated with an adjusted increased rate of HT (hazard ratio, 1.85 [95% CI, 1.75-1.95]; P<0.001) and a lower risk of waitlist removal for death or clinical deterioration (hazard ratio, 0.57 [95% CI, 0.45-0.73]; P<0.001) for both men and women; these protective effects were not different between sexes (interaction terms: transplant, P=0.55; delisting, P=0.91). During the study period, women made up 26% to 29% of donation after brain death transplants, but only 18% to 20% of DCD transplants. Survival at 2 years after DCD HT was similar between sexes (87% for women and 88% for men; log-rank P=0.37).

CONCLUSIONS: Women were less likely to be listed for DCD HT and makeup proportionally less DCD transplants compared with men. Being listed for DCD HT improved waitlist outcomes in both sexes. One-year survival after DCD HT was similar by sex. As DCD HT expands, additional measures to ensure equitable access are imperative.

PMID:40567220 | DOI:10.1161/CIRCHEARTFAILURE.125.012835

World J Pediatr Congenit Heart Surg. 2025 Jun 26:21501351251345790. doi: 10.1177/21501351251345790. Online ahead of print.

ABSTRACT

Congenital sinus of Valsalva aneurysm (SVA) is a rare cardiac anomaly with an incidence ranging from 0.1% to 3.5% of all congenital heart disease. Sinus of Valsalva aneurysm involving more than one sinus of Valsalva is very rare and dangerous. Valve-sparing root replacement is a safe and effective procedure that preserves growth potential for the aortic valve and has some benefits compared with valve replacement. There are limited data on valve-sparing operations in neonates and young children. In this case report, we present the surgical correction of an isolated, unruptured, multiple SVA in a 1.4-year-old child using the Yacoub II valve-sparing procedure.

PMID:40567013 | DOI:10.1177/21501351251345790

Perm J. 2025 Jun 26:1-9. doi: 10.7812/TPP/25.041. Online ahead of print.

ABSTRACT

INTRODUCTION: Chagas disease (CD) is caused by the protozoan parasite Trypanosoma cruzi and can remain clinically silent for decades. The objectives of this study were to quantify the prevalence of CD within the membership of Kaiser Permanente Northern California, to describe the demographic and clinical characteristics of patients with CD, and to report their adverse cardiovascular outcomes.

METHODS: In this cohort study from 2006 to 2022, the authors identified patients with CD by screening the electronic medical record for International Classification of Diseases, 9th Revision and 10th Revision codes. The authors obtained demographic, medical history, electrocardiographic, echocardiographic, and pharmacy data. Adverse outcomes, including all-cause mortality, heart failure hospitalization, and heart transplantation, were identified by database programming and confirmed by manual chart review.

RESULTS: There were 53 cases of CD in total, and 75% of patients self-identified as Hispanic. The mean age was 49 years old, and 45% were female. Dyslipidemia (45%) and hypertension (32%) were common comorbidities. A total of 7 patients (13%) had a left ventricular ejection fraction < 45%. During the follow-up period, adverse outcomes included 4 cardiovascular deaths, 5 heart failure hospitalizations, and 4 heart transplantations. The prevalence of diagnosed CD in the Kaiser Permanente Northern California population has risen from 0.22 per 100,000 persons from 2006 to 2010 to 0.70 per 100,000 persons from 2018 to 2022.

DISCUSSION: The prevalence of diagnosed CD in Kaiser Permanente Northern California increased during the study period, and patients with CD frequently had poor cardiovascular outcomes, likely due to the patients presenting with advanced disease.

CONCLUSION: Systematic screening and awareness are likely to facilitate early diagnosis and improve treatment to avoid chronic complications of CD.

PMID:40566857 | DOI:10.7812/TPP/25.041

J Clin Med. 2025 Jun 12;14(12):4195. doi: 10.3390/jcm14124195.

ABSTRACT

Objectives: This study aims to describe the experience of using ECMO on various patients who require ECMO support during the entire perioperative period of lung transplantation. ECMO has several roles: it can bridge patients to transplantation, improve lung graft function in case of primary graft dysfunction after transplantation, improve left ventricle function after transplantation in patients with primary pulmonary hypertension, and manage COVID-19 patients who are awaiting LuTx or undergoing LTx. Methods: We present 6-year results from a high-volume lung transplant center (219 cases/6 years, >50 cases/2022). We used ECMO in 56 cases (25.6%) of all lung transplants between 2018 and 2023. Results: The one-year survival rate of patients transplanted on ECMO was 85.7%. We applied all advanced ECMO techniques, such as bridging to transplantation on ECMO (n = 15, early survival 66.7%) and left ventricular conditioning after LuTx with VA-ECMO (n = 12, 60-day and one-year survival 85.1% and 53%, respectively). We also bridged patients with COVID-19 to transplantation and transplanted them from ECMO (n = 9, early survival 55%). Conclusions: This article shows possible applications of ECMO therapy for various indications in lung transplant patients and, along with data from other publications, it demonstrates that ECMO can improve survival and outcomes for patients with respiratory failure, primary pulmonary hypertension, and COVID-19. The COVID-19 pandemic highlighted new utilization of ECMO, demonstrating its usefulness and importance in critical care medicine. Further research into capabilities of the ECMO system may expand the knowledge about its role in lung transplantation and future treatments.

PMID:40565939 | PMC:PMC12194707 | DOI:10.3390/jcm14124195

J Clin Med. 2025 Jun 9;14(12):4083. doi: 10.3390/jcm14124083.

ABSTRACT

This review provides an in-depth analysis of argatroban as an alternative anticoagulant in cardiac surgery, with a focus on its use in patients with heparin-induced thrombocytopenia (HIT). We examine argatroban's pharmacokinetics and dosing regimens and the challenges associated with cosnventional monitoring methods-such as activated clotting time (ACT) and activated partial thromboplastin time (aPTT)-to evaluate its safety and effectiveness in high-risk surgical settings. Drawing on data from multiple case reports and series, our review highlights both the potential benefits and limitations of argatroban, including complications such as clot formation in extracorporeal circulation systems and prolonged postoperative coagulopathy. In addition to the literature review, we present a detailed clinical case of urgent HeartMate 3 left ventricular assist device implantation in a patient with advanced heart failure and active HIT. In this case, despite targeting an ACT above 400 s, intraoperative complications such as clot formation in the heart-lung machine and difficulty achieving hemostasis highlight the need for improved monitoring and dosing protocols. Our findings call for refined anticoagulation strategies and advanced monitoring techniques to optimize argatroban use in cardiac surgery, offering valuable insights for clinicians managing complex scenarios where conventional heparin therapy is contraindicated.

PMID:40565829 | PMC:PMC12194504 | DOI:10.3390/jcm14124083

Bioengineering (Basel). 2025 Jun 16;12(6):657. doi: 10.3390/bioengineering12060657.

ABSTRACT

Stem-cell-based therapies rely on the transplantation of stem cells or stem-cell-derived organotypic cells into injured tissues in order to improve or restore tissue function that has been impaired by various diseases. The potential of induced pluripotent stem cells has created many applications in the field of cell therapy, for example. Some applications, for example, those in cardiac cell therapy, suffer from low or very low efficiencies of cell engraftment. Therefore, magnetic cell targeting can be discussed as a method for capturing superparamagnetic nanoparticle-labelled cells in the tissue. Here, we employ superparamagnetic iron oxide nanoparticles (SPIONs) for the intracellular magnetic loading of mesenchymal stem cells (MSCs). In addition, we test a novel strategy of labelling MSCs with ferromagnetic particles. The adhesion assays demonstrate a faster adhesion kinetic of SPIONs-loaded MSC spheroids when a magnetic field was applied, resulting in >50% spheroid adhesion after 30 min. Clustering of cells inside the magnetic field is a second potential mechanism of magnetic cell retention and >80% of cells were found to be aggregated in clusters when placed in a magnetic field for 10 min. SPIONs-loaded and ferromagnetic-particle-loaded cells performed equally in the cell clustering assay. In conclusion, the clustering of SPION-labelled cells explains the observation that magnetic targeting reaches maximal efficiency in vivo after only 10 min of magnetic field application. This has significant implications for magnetic-targeting-assisted stem cell and cell replacement therapies.

PMID:40564473 | PMC:PMC12189464 | DOI:10.3390/bioengineering12060657

Biomedicines. 2025 May 29;13(6):1335. doi: 10.3390/biomedicines13061335.

ABSTRACT

Background: Right ventricular primary graft dysfunction (RV-PGD) is a rare but serious complication following heart transplantation, associated with a high morbidity and mortality. Temporary mechanical circulatory support is indicated when patients fail to respond to pharmacological therapy. This study aimed to evaluate the outcomes of patients with RV-PGD who received RV mechanical support with the Impella RP Flex device at our institution. Methods: Medical records of patients with RV-PGD supported by the Impella RP Flex device between December 2022 and March 2024 were reviewed retrospectively to assess survival, procedural complications, duration of support, and end organ dysfunction. Results: Of the 20 patients reviewed, 5 met the inclusion criteria. All five patients demonstrated recovery of RV function after a mean support duration of 8.6 ± 3.05 days. One pump showed transient evidence of biologic material ingestion during a weaning trial. No cases of tricuspid valve injury were observed. The most common complications were hemolysis, bleeding, and acute kidney dysfunction, with all patients requiring hemodialysis. Conclusions: Impella RP Flex support is safe and effective for managing primary and isolated RV-PGD without the need for additional blood oxygenation. However, bleeding complications requiring intervention remain a significant concern, and further evaluation of renal recovery is warranted.

PMID:40564056 | PMC:PMC12190657 | DOI:10.3390/biomedicines13061335