Cardiac Lesions Research Articles

OSDOKINA crush technique for the management of side branch ostial lesion ISTANBOL study

Abstract Background Isolated ostial bifurcation lesions (Medina type 0.0.1) represent <20% of coronary bifurcation lesions. Percutaneous coronary intervention (PCI) of this subset of lesions is challenging for the interventional cardiologist because of the technical difficulty and potential risk of serious complications. Purposes Recently, we devised a new technique, called the OSDOKINA crush technique, for the treatment of Medina type 0.0.1 coronary bifurcation lesions. The aim of this study was to evaluate the technical feasibility, safety and short-term and midterm procedural and clinical results achieved with OSDOKINA crush technique for Medina type 0.0.1 coronary bifurcation lesions. Materials and Methods Between September 2020 and January 2024, we included 49 patients who had Medina type 0,0,1 coronary bifurcation lesions. The vessel size had to be ≥2.5 mm by visual estimation on coronary angiography. Demographic, clinical and lesion characteristics of the cases were recorded. Quantitative coronary angiography analyses were performed using dedicated bifurcation angiographic software. Procedural success was defined as successful implantation of the stent into the target lesion, causing a final residual stenosis ≤30%. Major adverse cardiac events(MACE) were defined as cardiac death, myocard infarction and target lesion revascularisation. All patients were followed up to twelve months after the intervention. Results The lesion localisations were the ostium of diagonal branch in 19 (38.7%), ostium of the obtuse marginalis branch in 17 (34.6%), ostium of right posterior descending or right posterolateral branch in 13 (26.7%). SB RVD, SB lesion length and SB diameter stenosis by QCA were 2.65±0.35 mm, 9.4±3.9 mm, and 79.8±12.6, respectively. SB predilatation was applied in all cases. In 1 patient (2.1%), a stent had to be placed in the main branch using the double-kissing mini crush technique due to flow-limiting dissection that developed after the second kissing balloon inflation. Considering all cases, the angiographic success rate was 97.9% (n: 48). All patients had 12-month follow-up results. Acute myocardial infarction occurred in 1 patient (2.1%) due to side branch stent thrombosis. No patient had main branch revascularization. Cardiac or non-cardiac death was not observed. Cumulative MACE was 2.1%(n:1). Conclusion The OSDOKINA crush technique has excellent acute results and midterm clinical outcomes in the management of Medina type 0.0.1 coronary bifurcation lesions. Multicenter studies with large patient groups are needed.

Drug-coated balloon versus drug-eluting stent revascularization in the treatment of de novo acute myocardial infarction

Abstract Objective To assess the efficacy and safety of a drug-coated balloon (DCB) revascularization on percutaneous coronary intervention (PCI) in patients with de novo acute myocardial infarction (AMI). Background Data on DCB-only treatment in the context of AMI are limited. Methods A total of 96 patients with de novo AMI successfully treated with DCB alone were retrospectively enrolled. Visual residual stenosis ≤ 30% without flow-limiting dissection was considered a satisfactory pre-balloon angioplasty and followed by DCB treatment. We compared it with 96 propensity-matched patients treated with second-generation drug-eluting stent (DES) from the PTRG-DES registry (n = 13,160 patients). Major adverse cardiovascular events (MACE) comprised cardiac death, myocardial infarction, stroke, stent or target lesion thrombosis, target vessel revascularization, and major bleeding (Bleeding Academic Research Consortium bleeding type 3 or greater) at 1 year. Results Baseline clinical characteristics were comparable between the groups. The mean device diameter was larger in DES group (2.7 ± 0.3 mm vs. 3.1 ± 0.4 mm, P < 0.001). No abrupt vessel closure requiring treatment occurred after treatment with DCB. The MACE was comparable in both groups (6.2% in DCB group vs. 7.3% in DES group, P = 0.790) at 1-year follow-up. Conclusions In de novo AMI patients, DCB-only treatment approach had comparable clinical outcomes at 1-year follow-up. DCB-only treatment may be a safe and effective alternative to DES in carefully selected patients who had satisfactory pre-dilation results.

Comparison of Outcome After Percutaneous Coronary Intervention for De Novo and In-Stent Restenosis Indications.

In-stent restenosis (ISR) still occur after percutaneous coronary intervention (PCI). Few studies have compared outcomes after PCI for de novo stenosis and ISR and the results are conflicting. The aim of the present study is to compare outcomes after PCI for ISR and de novo coronary stenosis. Using patient level data from the randomized all-comer SORT OUT studies III-X, we included all patients with previous PCI and either an ISR or a de novo lesion as the study target lesion. Outcomes of interest were major adverse cardiac events (MACE) and target lesion revascularization (TLR) after 5 years. Of the 2928 patients with a previous PCI included in the SORT OUT studies, 491 (17%) were treated for ISR and 2437 (83%) for a de novo stenosis. Baseline characteristics did not differ significantly. At 5 years, MACE occurred in 148 patients (32%) in the ISR group and in 654 patients (28%) in the de novo stenosis group (Crude and adjusted HR 1.16 (0.97-1.38) and 1.16 (0.97-1.38)). The risk of TLR was higher in the ISR group when compared to the de novo stenosis group (Crude and adjusted HR 1.64 (95% CI, 1.24-2.17) and 1.71 (95% CI, 1.27-2.30)). In conclusion, the risk of MACE was similar after PCI of ISR and de novo lesions after 5 years. However, the risk of TLR was higher in the ISR group compared to the de novo stenosis group.

In vivo assessment of catheter-tissue contact using tissue proximity indication and its impact on cardiac lesion formation in pulsed field ablation

BackgroundNo evidence exists regarding whether tissue proximity indication (TPI), an impedance-based contact indicator, can improve in vivo lesion formation and durability during pulsed field ablation (PFA). ObjectiveThis in vivo study investigated the relationship between catheter-tissue contact and lesion formation. MethodsIn 5 porcine subjects, PFA applications were delivered at 35 atrial target sites using the VARIPULSE variable-loop circular catheter with the CARTO 3 mapping system. We compared acute ablative low-voltage zones (LVZs; <0.5 mV), chronic LVZs, and pathologic lesions between no/minimum contact (TPI-negative/flickering TPI-positive status) and consistent tissue contact (consistent TPI-positive status) for typical clinical scenarios and tissue tenting (TPI-positive status with electrodes extensively away from the 3-dimensional mapping surface) for safety margin. Ultrasound imaging also confirmed contact category assessments. ResultsAcute and chronic LVZs were significantly larger with consistent contact compared with no/minimum contact, including pathologic lesion length (36.0 ± 12.5 mm vs 17.4 ± 15.2 mm; P = .002) and maximum width (10.3 ± 2.7 mm vs 5.7 ± 5.1 mm; P = .035); results with tenting (length: 34.6 ± 11.7; width: 11.3 ± 1.9 mm) were comparable to consistent contact. Lesion transmurality was achieved in all lesions with consistent contact or tissue tenting but only in 54.5% with no/minimum contact (P = .001 for each). The TPI-based electrode contact distance, measured as the cumulative length of the multielectrode catheter tip positive for TPI, significantly correlated with lesion length, maximum width, and transmurality. ConclusionConsistent TPI-based contact during PFA was strongly associated with distinct chronic transmural lesions, emphasizing the importance of tissue contact in optimizing circumferential lesion formation with circular PFA catheters.

Impaired Cardiomyocytes Accelerate Cardiac Hypertrophy and Fibrosis by Delivering Exosomes Containing Shh/N-Shh/Gli1 in Angiotensin II Infused Mice

BackgroundsHeart failure (HF) is characterized by progressive cardiac hypertrophy and fibrosis, yet the underlying pathological mechanisms remain unclear. Exosomes are pivotal in cellular communication and are key signaling carriers in HFs. This study investigated the roles of exosomes in HF. MethodsEight-week-old male mice were divided into three groups: a control group, an Ang II group receiving angiotensin II (Ang II) infusion for 4 weeks, and an Ang II+DMA group receiving Ang II and dimethyl amiloride (DMA) infusion. This study examined the associations between cardiac injury, exosomes, and their substrate Shh. Furthermore, we conducted cellular experiments to assess the effects of Ang II-induced injury in primary cardiomyocytes on other cardiomyocytes and fibroblasts, and to test the therapeutic effects of the exosome inhibitor DMA and the Shh signaling inhibitor cyclopamine (CPN). ResultsAng II-induced cardiac hypertrophy and fibrosis, which were accompanied by exosome secretion and Shh upregulation in vivo. DMA relieved these cardiac lesions. Furthermore, cellular experiments revealed that Ang II-induced cardiomyocytes hypertrophy and activated cardiac fibroblasts by promoting the release of exosomes containing Shh/N-Shh/Gli1. Both DMA and CPN nullified fibroblast activation and proliferation. ConclusionsAng II-induced cardiomyocyte injury leads to cardiac hypertrophy and fibrosis through the release of exosomes carrying Shh signaling. The suppression of exosome secretion or the Shh pathway could offer new strategies for treating HF.

Transcriptomic and Multi-scale Network Analyses Reveal Key Drivers of Cardiovascular Disease.

Cardiovascular diseases (CVDs) and pathologies are often driven by changes in molecular signaling and communication, as well as in cellular and tissue components, particularly those involving the extracellular matrix (ECM), cytoskeleton, and immune response. The fine-wire vascular injury model is commonly used to study neointimal hyperplasia and vessel stiffening, but it is not typically considered a model for CVDs. In this paper, we hypothesize that vascular injury induces changes in gene expression, molecular communication, and biological processes similar to those observed in CVDs at both the transcriptome and protein levels. To investigate this, we analyzed gene expression in microarray datasets from injured and uninjured femoral arteries in mice two weeks post-injury, identifying 1,467 significantly and differentially expressed genes involved in several CVDs such as including vaso-occlusion, arrhythmia, and atherosclerosis. We further constructed a protein-protein interaction network with seven functionally distinct clusters, with notable enrichment in ECM, metabolic processes, actin-based process, and immune response. Significant molecular communications were observed between the clusters, most prominently among those involved in ECM and cytoskeleton organizations, inflammation, and cell cycle. Machine Learning Disease pathway analysis revealed that vascular injury-induced crosstalk between ECM remodeling and immune response clusters contributed to aortic aneurysm, neovascularization of choroid, and kidney failure. Additionally, we found that interactions between ECM and actin cytoskeletal reorganization clusters were linked to cardiac damage, carotid artery occlusion, and cardiac lesions. Overall, through multi-scale bioinformatic analyses, we demonstrated the robustness of the vascular injury model in eliciting transcriptomic and molecular network changes associated with CVDs, highlighting its potential for use in cardiovascular research.

The Abl1 tyrosine kinase is a key player in doxorubicin-induced cardiomyopathy and its p53/p73 cell death mediated signaling differs in atrial and ventricular cardiomyocytes

BackgroundDoxorubicin is an important anticancer drug, however, elicits dose-dependently cardiomyopathy. Given its mode of action, i.e. topoisomerase inhibition and DNA damage, we investigated genetic events associated with cardiomyopathy and searched for mechanism-based possibilities to alleviate cardiotoxicity. We treated rats at clinically relevant doses of doxorubicin. Histopathology and transmission electron microscopy (TEM) defined cardiac lesions, and transcriptomics unveiled cardiomyopathy-associated gene regulations. Genomic-footprints revealed critical components of Abl1-p53-signaling, and EMSA-assays evidenced Abl1 DNA-binding activity. Gene reporter assays confirmed Abl1 activity on p53-targets while immunohistochemistry/immunofluorescence microscopy demonstrated Abl1, p53&p73 signaling.ResultsDoxorubicin treatment caused dose-dependently toxic cardiomyopathy, and TEM evidenced damaged mitochondria and myofibrillar disarray. Surviving cardiomyocytes repressed Parkin-1 and Bnip3-mediated mitophagy, stimulated dynamin-1-like dependent mitochondrial fission and induced anti-apoptotic Bag1 signaling. Thus, we observed induced mitochondrial biogenesis. Transcriptomics discovered heterogeneity in cellular responses with minimal overlap between treatments, and the data are highly suggestive for distinct cardiomyocyte (sub)populations which differed in their resilience and reparative capacity. Genome-wide footprints revealed Abl1 and p53 enriched binding sites in doxorubicin-regulated genes, and we confirmed Abl1 DNA-binding activity in EMSA-assays. Extraordinarily, Abl1 signaling differed in the heart with highly significant regulations of Abl1, p53 and p73 in atrial cardiomyocytes. Conversely, in ventricular cardiomyocytes, Abl1 solely-modulated p53-signaling that was BAX transcription-independent. Gene reporter assays established Abl1 cofactor activity for the p53-reporter PG13-luc, and ectopic Abl1 expression stimulated p53-mediated apoptosis.ConclusionsThe tyrosine kinase Abl1 is of critical importance in doxorubicin induced cardiomyopathy, and we propose its inhibition as means to diminish risk of cardiotoxicity.

Bioactive lipids are altered in the heart, kidney, and serum of male and female F344 rats sub-chronically exposed to dietary 2-MCPD

Chloropropanols have been identified as processing-induced food contaminants that occur as by-products of the manufacturing of refined food oils and hydrolyzed vegetable protein. There has been a paucity of research on the 2-monochloropropane-1,3-diol (2-MCPD) isomer, thus forming a data gap for regulatory risk assessment. Previous studies suggest 2-MCPD causes adverse cardiotoxic, nephrotoxic, and myotoxic effects, but were inconclusive for hazard identification; thus a dose-response OECD TG-408-compliant study was conducted by Health Canada. Our study profiled the effects of 2-MCPD on oxylipins and oxidized phosphatidylcholines, using HPLC-MS/MS, in heart, kidney, serum, and skeletal muscle of male and female F344 rats orally exposed to 2-MCPD (40 mg/kg BW/d) for 90 days. Cardiac n-3 polyunsaturated fatty acid-derived oxylipins, particularly DHA-derived oxylipins, were lower with 2-MCPD exposure, coincident with cardiac lesions. Lipoxygenase-derived oxylipins were decreased in the serum with a greater effect in the male 2-MCPD treatment group. Few oxylipin alterations were seen in the kidney and there was an absence of alterations in the tibialis anterior. Oxidized phosphatidylcholines and isoprostanes were not altered in this study, indicating that oxidative stress was not elevated by 2-MCPD. These findings add to the weight of the evidence for 2-MCPD toxicity and support the use of serum oxylipins as potential biomarkers of 2-MCPD exposure.

Clinical Impact of Intracoronary Imaging in the Management of Stent Thrombosis.

Objectives: Use of intracoronary imaging (ICI) in cases of stent thrombosis (ST) is recommended and tailored treatment appears reasonable. Nevertheless, data supporting such a strategy are lacking. The aim of this study was to evaluate the clinical impact of ICI in the management of ST. Methods: The unadjusted study population was consecutive patients with definite ST presenting in a single tertiary cardiac centre and undergoing percutaneous coronary intervention (PCI). The presumed major mechanism of ST was assigned according to the real-time ICI interpretation by the PCI operator. Propensity score matching was performed with regard to ICI use to form the adjusted population and Kaplan-Meier analysis was applied to compare survival free of cardiac death (CD) or target lesion revascularization (TLR). Results: The unadjusted population included 130 ST patients, with the majority presenting with ST-elevation myocardial infarction (STEMI) (88%) and very late ST (86%). ICI was performed in 45 patients, of whom optical coherence tomography (OCT) was performed in 30 cases. When the individual ST mechanisms were viewed as groups, there was an interaction observed between type of treatment (stent vs. non-stent) and ST mechanism, with non-stent treatment being more prevalent in cases of underexpansion, malapposition, in-stent restenosis and mechanism uncertainty. After application of matching, two groups of 30 patients were formed. ICI-guided management resulted in better survival free of CD-TLR at 2 years (93% vs. 73%, p = 0.037). Conclusions: Intracoronary imaging guidance during PCI for ST had a direct impact on management (stent vs. non-stent) and resulted in a lower event rate at mid-term follow-up when propensity matched analysis was applied.

Biological Evaluation of Thermosensitive Hydrogels of Chitosan/Hydrolyzed Collagen/β-GP in an In Vitro Model of Induced Cardiac Ischemia.

Ischemic events can culminate in acute myocardial infarction, which is generated by irreversible cardiac lesions that cannot be restored due to the limited regenerative capacity of the heart. Cardiac cell therapy aims to replace injured or necrotic cells with healthy and functional cells. Tissue engineering and cardiovascular regenerative medicine propose therapeutic alternatives using biomaterials that mimic the native extracellular environment and improve cellular and tissue functionality. This investigation evaluates the effect of thermosensitive hydrogels, and murine fetal ventricular cardiomyocytes encapsulated in thermosensitive hydrogels, on the contractile function of cardiomyocyte regeneration during an ischemic event. Chitosan and hydrolyzed collagen thermosensitive hydrogels were developed, and they were physically and chemically characterized. Likewise, their biocompatibility was evaluated through cytotoxicity assays by MTT, LDH, and their hemolytic capacity. The hydrogels, and cells inside the hydrogels, were used as an intervention for primary cardiomyocytes under hypoxic conditions to determine the restoration of the contractile capacity by measuring intracellular calcium levels and the expressions of binding proteins, such as a-actinin and connexin 43. These results evidence the potential of natural thermosensitive hydrogels to restore the bioelectrical functionality of ischemic cardiomyocytes.

Enhancing the Classification of Congenital Heart Defects for Outcome Association Studies in Birth Defects Registries.

Traditional strategies for grouping congenital heart defects (CHDs) using birth defect registry data do not adequately address differences in expected clinical consequences between different combinations of CHDs. We report a lesion-specific classification system for birth defect registry-based outcome studies. For Core Cardiac Lesion Outcome Classifications (C-CLOC) groups, common CHDs expected to have reasonable clinical homogeneity were defined. Criteria based on combinations of Centers for Disease and Control-modified British Pediatric Association (BPA) codes were defined for each C-CLOC group. To demonstrate proof of concept and retention of reasonable case counts within C-CLOC groups, Texas Birth Defect Registry data (1999-2017 deliveries) were used to compare case counts and neonatal mortality between traditional vs. C-CLOC classification approaches. C-CLOC defined 59 CHD groups among 62,262 infants with CHDs. Classifying cases into the single, mutually exclusive C-CLOC group reflecting the highest complexity CHD present reduced case counts among lower complexity lesions (e.g., 86.5% of cases with a common atrium BPA code were reclassified to a higher complexity group for a co-occurring CHD). As expected, C-CLOC groups had retained larger sample sizes (i.e., representing presumably better-powered analytic groups) compared to cases with only one CHD code and no occurring CHDs. This new CHD classification system for investigators using birth defect registry data, C-CLOC, is expected to balance clinical outcome homogeneity in analytic groups while maintaining sufficiently large case counts within categories, thus improving power for CHD-specific outcome association comparisons. Future outcome studies utilizing C-CLOC-based classifications are planned.

Somatostatin receptors in fibrotic myocardium.

A patient with a neuroendocrine tumor and history of coronary artery disease underwent PET with 68Ga-DOTATATE PET tracer for tumor visualization. Analysis of the scan showed uptake of 68Ga-DOTATATE in the left ventricle corresponding to previous myocardial infarct. 68Ga-DOTATATE binds by somatostatin receptors (SSTR) and it has been proposed that it may be useful for the detection of cardiac inflammatory lesions. We aimed to test whether SSTR could be upregulated in cardiac fibrotic scar. We analyzed SSTR in cardiac samples from patients with end-stage ischemic cardiomyopathy (ICM, n = 8) and control hearts (n = 5). In mature ICM tissue, SSTR1 and SSTR2 expression was unchanged and SSTR5 expression was significantly decreased in ICM samples vs. control. Immunohistochemistry showed increased SSTR1 and SSTR2 in ICM. Areas with SSTR1 or SSTR2 staining were often adjacent to fibrotic areas. The majority of SSTR1 and SSTR2 staining localized in cardiomyocytes in fibrotic scar-rich areas where CD68 macrophage staining was not present. SSTR are occasionally upregulated in cardiac fibrotic areas. When using 68Ga-DOTATATE PET tracer to detect cardiac sarcoidosis or atherosclerotic plaque, the possibility of tracer uptake in fibrotic areas should be considered.

The 2023 new European guidelines on infective endocarditis: main novelties and implications for clinical practice.

The 2023 European Society of Cardiology (ESC) guidelines for the management of infective endocarditis update the previous 2015 guidelines with main novelties in five areas: (1) antibiotic prevention for high-risk patients, and prevention measures for intermediate-risk and high-risk patients; (2) diagnosis with emphasis on multimodality imaging to assess cardiac lesions of infective endocarditis' (3) antibiotic therapy allowing an outpatient antibiotic treatment for stabilized, uncomplicated cases; (4) cardiac surgery with an emphasis on early intervention without delay for complicated cases; and (5) shared management decision by the endocarditis team. Most evidence came from observational studies and expert opinions. The guidelines strongly support a patient-centred approach with a shared decision process by a multidisciplinary team that should be implemented either in tertiary referral centres, becoming heart valve centres, and referral centres. A continuous sharing of data is warranted in the hospitals' network between heart valve centres, which are used for referrals for complicated cases of infective endocarditis, and referral centres, which should be able to manage uncomplicated cases of infective endocarditis.

Evidence for enduring cardiac and multiorgan toxicity after repeated exposure to the synthetic cannabinoid JWH-018 in male rats

The use of synthetic cannabinoid receptor agonists (SCRAs) represents a public health concern. Besides abuse liability and cognitive impairments, SCRAs consumption is associated with serious medical consequences in humans, including cardiotoxicity. The precise mechanisms underlying cardiac or other toxicities induced by SCRAs are not well understood. Here, we used in silico, in vivo, and ex vivo approaches to investigate the toxicological consequences induced by exposure to the SCRA JWH-018. Along with in silico predictive toxicological screening of 36 SCRAs by MC4PC software, adult male Sprague-Dawley rats were repeatedly exposed to JWH-018 (0.25 mg/kg ip) for 14 consecutive days, with body temperature and cardiovascular parameters measured over the course of treatment. At 1 and 7 days after JWH-018 discontinuation, multiorgan tissue pathologies and heart mitochondria bioenergetics were assessed. The in silico findings predicted risk of cardiac adverse effects specifically for JWH-018 and other aminoalkylindole SCRAs (i.e., electrocardiogram abnormality and QT prolongation). The results from rats revealed that repeated, but not single, JWH-018 exposure induced hypothermia and cardiovascular stimulation (e.g., increased blood pressure and heart rate) which persisted throughout treatment. Post-mortem findings demonstrated cardiac lesions (i.e., vacuolization, waving, edema) 1 day after JWH-018 discontinuation, which may contribute to lung, kidney, and liver tissue degeneration observed 7 days later. Importantly, repeated JWH-018 exposure induced mitochondrial dysfunction in cardiomyocytes, i.e., defective lipid OXPHOS, which may represent one mechanism of JWH-018-induced toxicity. Our results demonstrate that repeated administration of even a relatively low dose of JWH-018 is sufficient to affect cardiovascular function and induce enduring toxicological consequences, pointing to risks associated with SCRA consumption.

Identifying novel data-driven subgroups in congenital heart disease using multi-modal measures of brain structure

Individuals with congenital heart disease (CHD) have an increased risk of neurodevelopmental impairments. Given the hypothesized complexity linking genomics, atypical brain structure, cardiac diagnoses and their management, and neurodevelopmental outcomes, unsupervised methods may provide unique insight into neurodevelopmental variability in CHD. Using data from the Pediatric Cardiac Genomics Consortium Brain and Genes study, we identified data-driven subgroups of individuals with CHD from measures of brain structure. Using structural magnetic resonance imaging (MRI; N = 93; cortical thickness, cortical volume, and subcortical volume), we identified subgroups that differed primarily on cardiac anatomic lesion and language ability. In contrast, using diffusion MRI (N = 88; white matter connectivity strength), we identified subgroups that were characterized by differences in associations with rare genetic variants and visual-motor function. This work provides insight into the differential impacts of cardiac lesions and genomic variation on brain growth and architecture in patients with CHD, with potentially distinct effects on neurodevelopmental outcomes.

Electrophysiological and biochemical effect of zinc oxide nanoparticles on heart functions of male Wistar rats

Zinc oxide nanoparticles (ZnO NPs) are one of the most abundantly used nanomaterials in cosmetics and topical products, and nowadays, they are explored in drug delivery and tissue engineering. Some recent data evidenced that they are responsible for cardiotoxic effects and systemic toxicity. The present study aimed to investigate the toxic effect of ZnO NPs (39 nm) on the heart of Wistar rats and to perform a dose–response relationship using three different dose levels (25, 50, 100 mg/kg bw) of ZnO NPs on the electrocardiogram (ECG) readings, the levels of biochemical function parameters of heart, and the oxidative stress and antioxidant biomarkers. Furthermore, zinc concentration level and histopathological examination of heart tissues were determined. ZnO NPs showed a dose-dependent effect, as the 100 mg/kg bw ZnO NPs treated group showed the most significant changes in ECGs parameters: R–R distance, P–R interval, R and T amplitudes, and increased levels of heart enzymes Creatine Kinase- MB (CK-MB) and Lactate dehydrogenase (LDH). On the other hand, elevated zinc concentration levels, oxidative stress biomarkers MDA and NO, and decreased GSH levels were found also in a dose-dependent manner, the results were supported by impairment in the histopathological structure of heart tissues. While the dose of 100 mg/kg bw of ZnO bulk group showed no significant effects on heart function. The present study concluded that ZnO NPs could induce cardiac dysfunctions and pathological lesions mainly in the high dose.

Impact of antiphospholipid antibodies on cardiac valve lesions in systemic lupus erythematosus: a systematic review and meta-analysis

This meta-analysis assesses antiphospholipid antibodies’ (aPLs) impact on heart valve disease in Systemic Lupus Erythematosus (SLE) patients. We searched PubMed, Embase, Cochrane, and Web of Science up to January 2024 for comparative studies of heart valve disease in aPL-positive versus aPL-negative SLE patients. Fixed-effect or random-effect models were used to synthesize data, with I2 and sensitivity analyses for heterogeneity and the trim-and-fill method for publication bias. Including 25 studies with 8089 patients, of which 919 had valvular changes, aPLs significantly increased the risk of heart valve disease (OR = 2.24, 95% CI: 1.58–3.18, p < 0.001). Lupus anticoagulant (LA) indicated the highest risk (OR = 4.90, 95% CI: 2.26–10.60, p < 0.001), anticardiolipin antibodies (aCL) doubled the risk (OR = 2.69, 95% CI: 1.47–4.93, p = 0.001), and anti-β2 glycoprotein I (aβ2GPI) showed a 70% increase (OR = 1.70, 95% CI: 1.17–2.45, p = 0.005). Valve-specific analysis indicated the mitral valve was most commonly involved (26.89%), with higher occurrences in aPL-positive patients (33.34% vs. 15.92%, p = 0.053). Aortic and tricuspid valve involvements were 13.11% vs. 5.42% (p = 0.147) and 12.03% vs. 8.52% (p = 0.039), respectively. Pulmonary valve disease was rare and similar across groups (1.01% in aPL-positive vs. 1.52% in aPL-negative). Significantly, only tricuspid valve disease showed increased risk in aPL-positive patients (OR = 2.66, 95% CI: 1.05–6.75, p = 0.039). APLs notably increase the risk of heart valve disease in SLE patients, with a pronounced effect on tricuspid valve involvement. Regular cardiac assessments for aPL-positive SLE patients are crucial for timely intervention and improved prognosis.

Predictors of target lesion failure after percutaneous coronary intervention with a drug-coated balloon for de novo lesions.

There are limited data about determinant factors of target lesion failure (TLF) in lesions after percutaneous coronary intervention (PCI) using a drug-coated balloon (DCB) for de novo coronary artery lesions, including optical coherence tomography (OCT) findings. The present study aims to investigate the associated factors of TLF in de novo coronary artery lesions with DCB treatment. We retrospectively enrolled 328 de novo coronary artery lesions in 328 patients who had undergone PCI with a DCB. All lesions had been treated without a stent, and both pre- and post-PCI OCT had been carried out. Patients were divided into two groups, with or without TLF, which was defined as a composite of culprit lesion-related cardiac death, myocardial infarction, and target lesion revascularisation, and the associated factors of TLF were assessed. At the median follow-up period of 460 days, TLF events occurred in 31 patients (9.5%) and were associated with patients requiring haemodialysis (HD; 29.0% vs 10.8%), with a severely calcified lesion (median maximum calcium arc 215° vs 104°), and with the absence of OCT medial dissection (16.1% vs 60.9%) as opposed to those without TLF events. In Cox multivariable logistic regression analysis, HD (hazard ratio [HR]: 2.26, 95% confidence interval [CI]: 1.00-5.11; p=0.049), maximum calcium arc (per 90°, HR: 1.34, 95% CI: 1.05-1.72; p=0.02), and the absence of post-PCI medial dissection on OCT (HR: 8.24, 95% CI: 3.15-21.6; p<0.001) were independently associated with TLF. In de novo coronary artery lesions that received DCB treatment, factors associated with TLF were being on HD, the presence of a severely calcified lesion, and the absence of post-PCI medial dissection.

Fetal single ventricle journey to first postnatal procedure: a multicentre UK cohort study

ObjectivesUK single ventricle (SV) palliation outcomes after first postnatal procedure (FPP) are well documented. However, survival determinants from fetal diagnosis to FPP are lacking. To better inform parental-fetal counselling, we...

Impact of long lasting pulmonary arterial hypertension on the surgery of congenital heart defect

BackgroundLittle is known about the management of this high-risk subgroup of patients because only a few small retrospective studies were available in the literature. ObjectivesThis study was designed to identify the determinants of post operative mortality and to assess during 10 years follow-up functional and hemodynamic variables for children presenting at surgery with pulmonary vascular disease associated with congenital heart defect. MethodsThis is a prospective study that enrolled children with pulmonary arterial hypertension associated with congenital heart disease and presenting beyond the optimal time frame for surgery. Inclusion criteria were late presentation for surgery and severe pulmonary arterial hypertension, defined as mean pulmonary arterial pressure > 50 mmhg. An univariable analysis, receiver operating characteristic curves, and Kaplan-Meier curves were used for survival analysis. Results75 patients underwent repair of their cardiac lesions. The operative mortality rate was 16%(12 patients); 43 patients (57 %) had right heart catheterization, and all of them were positive for acute vasodilatatory challenge (NO, oxygen). In the postoperative period, 32 % of patients had pulmonary hypertensive crisis, and 72 % had right heart failure. During follow-up, pulmonary arterial hypertension subclass 4 was present in 5% of our patients. ConclusionOur study indicated that for operable patients but beyond the optimal time frame the surgical mortality remained high despite using iNO. However, for those who survived they achieved good results in functional exercise, their PAP dropped to normal level and small proportion had persistent pulmonary arterial hypertension encouraging surgical closure of the defect.