Background Transcatheter aortic valve replacement (TAVR) for native aortic regurgitation (AR) remains technically challenging due to the absence of annular calcification and difficulties in achieving stable anchoring. Mechanical complications such as anchoring strut fracture are rare but may have implications for long-term valve durability.Case summary A 64-year-old man with severe symptomatic native AR underwent transapical TAVR using a 29-mm self-expanding J-Valve system. Routine echocardiography and gated CT on postoperative day 7 identified an isolated fracture of the right coronary sinus anchoring strut without migration, leaflet dysfunction, or haemodynamic compromise. No balloon post-dilatation was performed. Serial multimodal imaging over nearly 3 years demonstrated persistent structural stability, preserved valve function, and marked left-ventricular reverse remodelling.Discussion This case provides long-term multimodal imaging follow-up of isolated anchoring strut fracture after TAVR for native AR. Early fracture detection and absence of calcification support a deployment-related stress mechanism rather than late cyclic fatigue. Although this favourable evolution suggests that isolated fracture does not necessarily result in immediate structural valve dysfunction, prognostic conclusions cannot be generalized. Careful, individualized imaging surveillance remains essential.

BACKGROUND:For patients undergoing surgical valve procedures with concomitant coronary artery disease, current guidelines recommend that coronary artery bypass grafting (CABG) should be anatomically guided on the basis of stenosis severity, as assessed by coronary angiography. We aimed to test whether a physiologically guided strategy using angiography-derived fractional flow reserve (FFR) could improve clinical outcomes in this population. METHODS:FAVOR IV-QVAS is an investigator-initiated, multicentre, randomised, triple-blind trial done at 12 tertiary hospitals in China. Eligible patients were aged 18 years or older and were scheduled for valve surgery, with at least one clinically significant stenosis in a major coronary artery. Patients were randomly assigned (1:1) to undergo physiologically guided CABG (for lesions with an angiography-derived FFR value ≤0·80) or anatomically guided CABG (for lesions with a stenosis diameter ≥50% on coronary angiography). Randomisation was done using a web-based program and stratified by site with fixed blocks of four. Patients, surgeons, follow-up physicians, and outcome assessors were masked to treatment allocation. The primary outcome was a composite of death, myocardial infarction, stroke, unplanned coronary revascularisation, and new renal failure requiring dialysis within 30 days after surgery. The key secondary outcome was a composite of death, myocardial infarction, stroke, unplanned coronary revascularisation, and hospitalisation for unstable angina or heart failure at a minimum follow-up of 1 year. The primary analysis of the primary and key secondary outcomes was done in a modified intention-to-treat population that included all randomly assigned patients who underwent surgery and had available data for the primary outcome. Missing data for the primary outcome were planned to be analysed using complete-case analysis or multiple imputation, with a proportion of missing data of 2% as the threshold. This trial is registered at ClinicalTrials.gov (NCT03977129); extended follow-up is ongoing. FINDINGS:Between Aug 4, 2019, and Aug 13, 2024, 793 patients were enrolled. 396 were randomly assigned to the angiography-derived FFR group and 397 to the coronary angiography group; one patient in the coronary angiography group declined surgery and was excluded from the modified intention-to-treat population. The median age was 65 years (IQR 59-70), 221 (28%) patients were female, and 571 (72%) were male. Concomitant CABG was done in 223 (56%) patients in the angiography-derived FFR group and in 388 (98%) patients in the coronary angiography group. The primary outcome occurred in 31 (7·8%) patients in the angiography-derived FFR group and 53 (13·4%) in the coronary angiography group (absolute difference -5·6 percentage points [95% CI -9·9 to -1·3]; risk ratio 0·58 [95% CI 0·38 to 0·89]; p=0·011). Death within 30 days occurred in 11 (2·8%) patients in the angiography-derived FFR group and 17 (4·3%) patients in the coronary angiography group. At a median follow-up of 27 months (28 months [IQR 18-44] in the angiography-derived FFR group and 27 months [18-42] in the coronary angiography group), the key secondary outcome occurred in 82 (20·7%) patients in the angiography-derived FFR group and in 106 (26·8%) patients in the coronary angiography group (hazard ratio 0·74 [95% CI 0·55-0·98]; p=0·036). INTERPRETATION:Among patients undergoing valve surgery with concomitant coronary artery disease, physiologically guided CABG using angiography-derived FFR reduced the incidence of the composite perioperative outcome compared with anatomically guided CABG. These findings support a selective approach to surgical coronary revascularisation guided by physiological assessment in patients undergoing valve procedures. FUNDING:Shanghai Hospital Development Center, Shanghai Municipal Science and Technology Commission, and Ministry of Science and Technology of the People's Republic of China.

Background After percutaneous coronary intervention (PCI), patients with acute coronary syndrome (ACS) require long-term medication, risk-factor control, rehabilitation, and symptom recognition. Large language models (LLMs) are increasingly used for health consultation, but their quality, safety, and stability in post-PCI discharge education remain unclear. Methods Twenty-five standardized Chinese discharge questions were submitted to ChatGPT 5.5 Instant and DeepSeek V3. Each model generated three responses per question (150 total). Three cardiovascular experts rated the original Chinese responses across five Likert domains and two binary safety judgments. Comparisons used exact paired permutation tests, question-clustered bootstrap confidence intervals, and Holm adjustment for six quality-score comparisons. Results Overall, 149/150 responses (99.3%; 95% CI, 96.3%–100.0%) met the primary safety criterion: 75/75 for ChatGPT (100.0%; 95% CI, 95.2%–100.0%) and 74/75 for DeepSeek (98.7%; 95% CI, 92.8%–100.0%). The paired risk difference was 1.3 percentage points (95% CI, −1.3 to 2.7; P=1.000). One DeepSeek response contained both a major error and a potentially harmful recommendation. After pairing and Holm adjustment, ChatGPT scored higher in accuracy, guideline concordance, completeness, and total quality (adjusted P=0.015, 0.015, 0.019, and 0.005). Five-domain satisfactory response rates did not differ significantly (100.0% vs 90.7%; P=0.125). Conclusions Both models produced few expert-adjudicated safety flags in this limited question set. ChatGPT received higher ratings in selected quality domains, but sparse safety events and restricted question coverage preclude conclusions of equivalence or clinical safety. LLM-generated discharge information should supplement, not replace, individualized clinical advice.

PIWI-interacting RNAs (piRNAs) are widely expressed in cardiac tissues and play important roles in cardiac pathophysiology. However, their functions and molecular mechanisms in cardiac remodeling following myocardial infarction (MI) and cardiomyocyte ferroptosis remain largely unknown. Here, we identified a ferroptosis-related piRNA (FERPIR), which inhibits ischemia/reperfusion (I/R) induced myocardial injury, cardiac remodeling and ferroptosis by targeting HNRNPA2B1-dependent regulation of Fis1. FERPIR levels were decreased in hypoxia/reoxygenation (H/R)-exposed cardiomyocytes and I/R-injured mouse hearts. FERPIR prevented I/R-induced acute injury and pathological cardiac remodeling. In vitro, overexpression of FERPIR inhibits H/R-induced ferroptosis. Mechanistically, FERPIR directly bound to HNRNPA2B1 and promoted its stability, which exhibited decreased ferroptosis and improved cardiac function upon I/R injury. Fis1 acted as a downstream regulator of HNRNPA2B1, and FERPIR recruited HNRNPA2B1 to bind to Fis1 mRNA and decreased its stability, thereby inhibiting mitochondrial fission and ferroptosis, which improves cardiac remodeling after myocardial infarction. Our findings reveal that FERPIR prevents myocardial I/R induced injury and pathological cardiac remodeling through the HNPA2B1/Fis1 axis, which provides potential therapeutic targets against cardiac injury caused by cardiomyocyte ferroptosis.

Heart failure (HF) is a syndrome of global concern with high morbidity and mortality, whose complex molecular regulatory mechanisms are not yet fully understood. Moving beyond the traditional research framework focused on microRNAs, long non-coding RNAs (ncRNAs), and circular RNAs, this review concentrates on the pivotal roles of emerging ncRNAs - specifically Piwi-interacting RNAs (piRNAs), transfer RNA-derived small RNAs (tsRNAs), and small nucleolar RNAs (snoRNAs) - in the pathological progression of HF. In the acute phase of HF, these molecules rapidly respond to stressors such as ischemia and hypoxia. They directly influence cardiomyocyte fate and acute injury outcomes by regulating processes including apoptosis, necroptosis, autophagy, and inflammatory responses. During the chronic phase, they are deeply involved in pathological myocardial remodeling. They precisely regulate cardiomyocyte hypertrophy, cardiac fibroblast activation, and interstitial fibrosis in a cell-specific manner, maintaining a fine-tuned balance between pro-pathological and protective functions. These discoveries significantly enrich the molecular regulatory map of HF and reveal the considerable potential of these ncRNAs as novel non-invasive biomarkers and promising therapeutic targets. Of particular note, strategies employing engineered exosomes to deliver specific snoRNAs have demonstrated therapeutic effects in preclinical models, such as reversing fibrosis and improving cardiac function. This marks a shift in the treatment paradigm for HF toward precise RNA-level regulation.

tRNA-derived small RNAs (tsRNAs) or tRNA-derived fragments (tRFs) are an important class of regulatory molecules whose role in cardiac hypertrophy remains largely unknown. Here, we identified a novel tRF contributing to the regulation of cardiac hypertrophy that we termed CHAtRF (cardiac hypertrophy-associated tRF). The CHAtRF level was increased in mice and in patients with cardiac hypertrophy. CHAtRF deficiency attenuated angiotensin II (AngII)-induced cardiac hypertrophy and restored the heart function, while CHAtRF overexpression enhanced hypertrophic responses. Mechanistically, CHAtRF directly interacts with SRSF5 and blocks SRSF5 to bind with Psmg4 pre-mRNA, which mediates alternative splicing of Psmg4 pre-mRNA and promotes exon 2 skipping of Psmg4. CHAtRF-dependent alternative splicing of Psmg4 inhibits the expression of Psmg4 full-length isoform, resulting in progression of pathological hypertrophy. The ability of CHAtRF to regulate hypertrophy was confirmed in hiPSC-CMs, and CHAtRF serum levels are higher in individuals with myocardial hypertrophy or heart failure. Our findings reveal new insights into the previously unrecognized role of tsRNAs during cardiac hypertrophy, which provide potential novel therapeutic targets for pathological hypertrophy and might serve as potential biomarkers for diagnosing cardiac hypertrophy and heart failure.

Introduction:This study aimed to compare echocardiographic outcomes and analyze the changes in ventricular remodeling at different time points after surgery in patients with severe aortic stenosis (AS) undergoing either surgical aortic valve replacement (SAVR) or transcatheter aortic valve replacement (TAVR). Methods:This retrospective study consecutively enrolled 175 patients with severe AS who underwent either SAVR or TAVR. Transthoracic echocardiograms obtained at baseline, 30 days, and 1 year after the procedure were analyzed by multiple echocardiographers at our institution. Results:At baseline, the TAVR group was significantly older (74 ± 7 years vs. 62 ± 9 years, p < 0.001) and had a higher prevalence of hypertension (53.5% vs. 31.0%, p = 0.003), coronary artery disease (38.4% vs. 23.0%, p = 0.028), and atrial fibrillation (16.3% vs. 2.3%, p = 0.002). Additionally, the TAVR cohort demonstrated significantly worse cardiac functional status (p < 0.001). Compared to TAVR patients, SAVR patients (N = 87) exhibited a more pronounced reduction in left ventricular end-systolic dimension (-0.5 ± 0.65 cm vs. -0.2 ± 0.47 cm, p < 0.001) and left ventricular end-diastolic dimension (-0.6 ± 0.64 cm vs. -0.3 ± 0.55 cm, p < 0.001) at the 1-month follow-up. A decrease in left ventricular mass was observed in both groups from baseline to 1 month postoperatively, with the SAVR group showing a significantly greater reduction (LV mass: -67.3 ± 59.31 g vs. -38.2 ± 46.49 g, p = 0.003; LVMI: -39.1 ± 33.93 g/m2 vs. -22.5 ± 27.08 g/m2, p = 0.005). However, these differences were not sustained at the 1-year follow-up. SAVR patients experienced a transient decline in right ventricular function at 1 month, which recovered by 1 year postoperatively. At the 1-year follow-up, the TAVR group experienced a higher incidence of Major Adverse Cardiac Events (MACE) (p = 0.01), despite showing significant improvement in the severity of both mitral and tricuspid regurgitation compared to baseline (p < 0.001). Although pulmonary artery pressure improved in both groups after AVR, the SAVR group demonstrated significantly lower pressure at 1 year (p < 0.001). Conclusion:In patients with severe aortic stenosis, SAVR was associated with more significant regression of left ventricular dimensions and mass at 1 month compared to TAVR, alongside a transient impairment of right ventricular function. By 1 year postoperatively, however, no significant differences in ventricular remodeling were observed between the two groups.

Aims The adult mammalian heart possesses severely limited regenerative capacity. Cardiomyocyte loss during cardiac injury, coupled with this restricted regenerative potential, represents a fundamental cause of heart failure and associated mortality. While PIWI-interacting RNAs (piRNAs) are abundantly expressed in cardiac tissue, their functional roles and molecular mechanisms in cardiomyocyte proliferation and heart regeneration remain largely undefined. In this study, we systematically investigated piRNA-mediated regulation of cardiomyocyte proliferation and cardiac repair processes. Methods and results Using piRNA microarray analysis, we identified a novel piRNA regulating cardiomyocyte proliferation, which we named MCPPIR (myocardial cell proliferation-promoting piRNA). Genetic ablation of MCPPIR in mice attenuated cardiomyocyte proliferation and impaired neonatal heart regeneration, while MCPPIR overexpression enhanced proliferation, reduced fibrosis, and improved cardiac function post-myocardial infarction. Through mass spectrometry and RNA pull-down assays, we identified HNRNPH1 as a key binding partner. Cardiomyocyte-specific HNRNPH1 knockout mice displayed enhanced proliferative capacity. o(8)G-RNA immunoprecipitation sequencing revealed POC1B as the downstream target, with MCPPIR preventing HNRNPH1-mediated repression of POC1B mRNA. Mechanistically, the MCPPIR-HNRNPH1-POC1B axis maintains centrosome integrity, thereby promoting cardiomyocyte proliferation and cardiac repair. Conclusion Our study reveals a previously unrecognized role of piRNAs in regulating cardiomyocyte proliferation. We demonstrate that MCPPIR drives cardiomyocyte proliferation and promotes cardiac repair in adult hearts through o(8)G-mediated post-transcriptional regulation of POC1B mRNA. These findings establish the MCPPIR/POC1B axis as a promising therapeutic target for ischaemic heart diseases and a novel paradigm for developing regenerative therapies against myocardial injury.

This study aims to investigate the impacts of various body mass index (BMI) classifications on perioperative parameters and short-term outcomes in patients undergoing Da Vinci robot-assisted atrial septal defect (ASD) repair providing evidence for personalized perioperative management. A retrospective analysis was conducted on 100 patients who underwent Da Vinci robot-assisted ASD repair at Qingdao University Affiliated Hospital between November 2014 and December 2025. Based on the Chinese adult BMI classification criteria, the patients were categorized into four groups: underweight group (BMI < 18.5 kg/m², n = 9), normal weight group (18.5 ≤ BMI < 24.9 kg/m², n = 52), overweight group (25.0 ≤ BMI < 29.9 kg/m², n = 26), and obese group (BMI ≥ 30.0 kg/m², n = 13). This study compared baseline characteristics, intraoperative indicators, postoperative recovery, and short-term prognosis across these groups. Furthermore, multivariate logistic regression analyzed the independent associations of BMI classification and age with postoperative surgical site infection and hospital readmission. No significant differences were observed among the four groups concerning baseline echocardiographic parameters, key intraoperative metrics (e.g., operation duration, cardiopulmonary bypass time), or most postoperative recovery measures (e.g., mechanical ventilation duration, length of intensive care unit stay), with all P > 0.05. No sternotomy conversion or early mortality occurred. Univariate analysis showed the obese group had significantly higher rates of surgical site infection (15.4

Postoperative atrial fibrillation (POAF) is a prevalent complication following cardiac surgery, which has been associated with inflammatory activity in epicardial adipose tissue. There is a lack of effective means for its prediction and prevention. The fat attenuation index (FAI) serves as a non-invasive imaging biomarker capable of quantifying pericoronary adipose tissue inflammation. In this retrospective study, patients who underwent off-pump coronary artery bypass grafting (OPCABG) and had preoperative coronary computed tomography angiography (CCTA) were included. The pericoronary FAI was measured from CCTA images. POAF was identified based on ECG monitoring within 7 days after surgery. A multivariate logistic regression model incorporating variables significant in univariate analysis and clinically relevant factors was constructed. Model performance with and without FAI was compared using the area under the curve (AUC) with DeLong’s test. A total of 140 patients were finally included, including 41 patients (29.2

Aortic aneurysm and dissection (AAD) represent catastrophic vascular conditions with high mortality rates. Currently, non-surgical therapeutic options remain limited, while surgical intervention entails significant risk. As the second most common aortic disease after atherosclerosis and the ninth leading cause of death worldwide, aortic dissection involves separation of the parietal layer caused by intimal tear or intramural hemorrhage. Endothelial dysfunction is an important participant and amplifier in the early onset of AAD. Most cases begin with intimal injury in which endothelial injury plays a contributing role and are characterized by increased permeability, inflammatory infiltration, and disrupted intercellular junctions. This process compromises vessel wall integrity and initiates a complex cascade of reactions that ultimately lead to AAD. Therefore, discussing the localization of the role of endothelial cells in the early stage of aortic disease, and based on this analysis of possible therapeutic targets and directions, is of great significance for understanding the initial events associated with AAD.

Cardiac myxoma is a benign primary cardiac tumor, but its clinical impact varies with tumor size, mobility, valvular obstruction, pulmonary arterial pressure, and preoperative functional status. Whether an integrated myxoma-related preoperative clinical burden is associated with postoperative recovery remains unclear. We conducted a single-center retrospective cohort study of patients with preoperatively suspected and pathologically confirmed cardiac myxoma between 2020 and 2025. A seven-item composite myxoma-related clinical burden index was used as an exploratory descriptive measure. Index values of 0–2 and ≥ 3 were used for descriptive group comparisons. To reduce bias from undocumented components, the primary continuous association analysis used an index standardized to the number of evaluable components among patients with at least five of seven components available. Recovery outcomes were postoperative hospital stay and postoperative ICU stay. Associations were assessed using Spearman correlation and log-linear models, with the latter adjusted for age, sex, and albumin. The cohort included 79 patients, of whom 62 had index values of 0–2 and 17 had values ≥ 3. No clinically documented major postoperative event was identified during the index hospitalization. Median postoperative hospital stay was 14.5 (10, 18.75) days and 12 (10, 15) days in the two descriptive groups, respectively (P = 0.243); median ICU stay was 3 (2, 4) days in both groups (P = 0.963). In the primary standardized-index analysis, correlations with hospital stay (rho = − 0.178, P = 0.190; N = 56) and ICU stay (rho = 0.230, P = 0.086; N = 57) were not statistically significant. Adjusted geometric mean ratios per 1-point increase were 0.953 (95

Neonatal mouse heart apical resection (AR) can induce cardiac tissue regeneration. However, conventional AR models lack precise parameters for cryoanesthesia duration, thoracotomy site, and ambient temperature. We varied cryoanesthesia time, ambient temperature, and thoracotomy location to quantify blood loss, and survival rate. After surgery, RT-qPCR, immunofluorescence, and Masson staining were used to track AR model. Iterative testing showed that 4 min 30 s of cryoanesthesia followed by a 10-min delay at 24-28°C maintained complete cardiac arrest, providing a stable operative window. A fifth-intercostal thoracotomy, performed by gently compressing the lactating pup's back and dilating the thorax with blunt forceps, minimized bleeding and markedly improved survival. The refined AR protocol reproducibly elicits structural injury, transient functional impairment, and subsequent regenerative repair in P1 neonatal mouse hearts.

Circular RNAs (circRNAs) are a distinct class of endogenous RNAs characterized by their covalently closed circular structure. CircRNAs play crucial regulatory roles in various biological processes and pathogenesis. In this study we investigated the role of circRNAs in cardiomyocyte pyroptosis and underlying mechanisms. Ischemia/reperfusion (I/R)-induced myocardial injury was induced in mice by ligation of the left anterior descending coronary artery (LAD). Neonatal mouse cardiomyocytes were subjected to hypoxia/reoxygenation (H/R) assault. By using circRNA microarray, we found that the expression levels of a pyroptosis-related circRNA (designated PYRCR) were markedly decreased in H/R-exposed cardiomyocytes and I/R-injured mouse hearts. Overexpression of PYRCR inhibited cardiomyocyte pyroptosis, attenuated I/R-induced myocardial infarction and ameliorated cardiac function in mice. By RNA pull-down assays coupled with MS analysis followed by molecular validation, we identified developmental regulated GTP-binding protein 2 (DRG2) as the direct downstream target of PYRCR. Cardiac-specific DRG2 knockout mice displayed attenuated pyroptosis and enhanced cardiac function following I/R injury compared to DRG2fl/fl controls. DRG2 directly bound to dynamin-related protein 1 (Drp1), the master regulator of mitochondrial fission, and enhanced its protein stability and expression. Importantly, PYRCR competitively disrupted the DRG2-Drp1 interaction, thereby suppressing DRG2-mediated Drp1 expression and subsequently reducing mitochondrial fission, cardiomyocyte pyroptosis, and myocardial damage. In conclusion, we demonstrate that PYRCR, a novel pyroptosis-related circRNA, protects against I/R-induced myocardial injury through the DRG2-mediated modulation of Drp1 activity, offering promising new therapeutic strategies for preventing cardiac damage mediated by cardiomyocyte pyroptosis.

BACKGROUND:Vascular smooth muscle cell (VSMC) proliferation and migration contribute to vascular remodelling in thoracic aortic aneurysms (TAA). An increase in cytosolic Ca2+ concentration triggers VSMC proliferation and migration. Piezo1, a mechanosensitive cation channel, may be involved in the proliferation and migration of VSMCs, and potentially in the development of TAA. METHOD:This study analysed Piezo1 and its potential downstream protein extracellular signal-regulated kinases (ERK) in aortic surgical specimens from six patients with TAA and six controls. In in vitro experiments, Yoda1, a Piezo1 agonist, SCH772984, an ERK inhibitor, si-Piezo1, used for silencing the piezo1 gene, and LM22B-10, an ERK activator, were used to regulate the expression of Piezo1 and ERK in rat thoracic aortic VSMCs. The effects of these treatments on cell proliferation, migration, apoptosis, and phenotypic switch were measured. RESULTS:Through the comparison of human samples, it was discovered that the expressions of Piezo1 and ERK in the aortic media of TAA were higher than in normal samples. Additionally, the levels of VSMC proliferation and apoptosis were higher in TAA samples. This confirmed that upregulation of Piezo1 can induce cell proliferation and migration by activating the ERK pathway. It was also found that Piezo1/ERK signalling does not affect cell apoptosis. Additionally, it was discovered that inhibiting Piezo1/ERK signalling can induce a phenotypical switch in cells. CONCLUSIONS:These data indicate that Piezo1 is significantly activated in aortic VSMCs from patients with TAA, which may be involved in TAA by promoting VSMC proliferation and migration through the ERK signalling pathway. This study provides a new insight into the biological action of the Piezo1/ERK signalling pathway in the pathogenesis of TAA.

Background Da Vinci robot-assisted cardiac surgery has emerged as an indispensable modality in minimally invasive cardiac surgery. This study aimed to compare the clinical outcomes of Da Vinci robot-assisted atrial septal defect (ASD) repair under beating-heart versus cardioplegic arrest conditions. Methods A retrospective cohort study was conducted on consecutive patients who underwent Da Vinci robot-assisted ASD repair at our institution from November 2014 to April 2024. Patients were stratified into two groups on the basis of the surgical approach: the cardioplegia arrest group ( n = 23) and the beating-heart group ( n = 75). General clinical data, perioperative parameters, postoperative recovery metrics, and early clinical outcomes were compared between the groups. Results A total of 114 patients underwent successful Da Vinci robot-assisted ASD repair, with no perioperative or 30-day mortality. Compared with the cardioplegic arrest group (n = 23), the beating-heart group (n = 75) presented a significantly shorter cardiopulmonary bypass (CPB) time (81.07 ± 20.95 min vs. 149.87 ± 50.50 min, P < 0.001), and eliminated aortic cross-clamping (0 ± 0 min vs. 71.43 ± 24.45 min, P < 0.001). The operative time was significantly shorter in the beating-heart group [200 (180–240) min vs. 260 (230–300) min, P < 0.001]. Postoperatively, the beating-heart group required less mechanical ventilation [11 (8–14) h vs. 15 (12–20) h, P = 0.001], had a lower 24-hour drainage volume [120 (70–200) mL vs. 230 (160–330) mL, P < 0.001], and had a shorter intensive care unit (ICU) stay [66 (42–80) h vs. 87 (63–94) h, P = 0.018]. Complication rates were comparable between the groups, with no residual shunts or severe arrhythmias. Conclusion Da Vinci robot-assisted beating-heart ASD repair is safe and feasible, avoids aortic cross-clamping-related risks, significantly reduces the CPB time, and offers postoperative recovery advantages.

Timely assessment of Low cardiac output syndrome (LCOS) risk after off-pump coronary artery bypass grafting (OPCAB) is crucial, yet hindered by the lack of standardized diagnostic criteria beyond symptoms, therapy response, and ultrasound. This study aims to develop, construct, and internally validate a predictive model to predict low cardiac output syndrome (LCOS) in patients undergoing off-pump coronary artery bypass grafting (OPCAB). Using a clinical dataset of 765 OPCAB patients treated between May 2018 and July 2020, encompassing admission, surgical, and postoperative data, a predictive model was developed. Feature selection was performed using Least Absolute Shrinkage and Selection Operator (LASSO) regression. The selected features were then incorporated into a multivariate logistic regression model to establish the final predictor. Model performance was evaluated using the C-index (discrimination), calibration plots (calibration), and decision curve analysis (clinical validity). Internal validation via bootstrap resampling assessed model robustness. The final prediction model incorporated the following predictors: age, smoking history, ejection fraction, left ventricular end-diastolic diameter, lactic acid levels, room-air pre-operative PaO₂, room-air pre-operative oxygen saturation, carotid artery stenosis, myocardial enzyme levels, internal mammary artery condition, intra-operative blood transfusion volume, intra-operative blood loss, ICU stay duration, ventilator time, and IABP implantation. The model demonstrated excellent discrimination, with a C-index of 0.943 (95

DNA molecules are susceptible to reactive oxygen species (ROS) attack leading to oxidative damage, of which 8-oxoguanine (8-oxoG) is a core oxidative marker. OGG1 acts as a DNA repair enzyme and maintains genomic stability by specifically repairing 8-oxoG through the base excision repair (BER) pathway. The Ser326Cys polymorphism significantly reduces enzyme activity and potentially impacts phosphorylation-mediated subcellular localization dynamics and epigenetic regulatory networks, thereby potentially exacerbating genomic instability. In this review, we analyzed the association between the OGG1 Ser326Cys polymorphism and different diseases, such as risk, platinum-based chemotherapy sensitivity, and radiotherapy toxicity in cancer. In neurodegenerative disorders, the Cys326 type leads to the accumulation of 8-oxoG in neurons and accelerates CAG triplet repeat amplification. In metabolic disorders, its insufficient repair may trigger β-cell dysfunction, which increases the risk of type 2 diabetes mellitus. Finally, we integrated multiomics data and proposed a genotype-based precision intervention strategy to provide a theoretical basis for disease risk prediction, personalized therapy, and novel targeted drug development.

Transfer RNA is a class of non-coding RNA that plays a role in amino acid translocation during protein synthesis. After specific modification, the cleaved fragment is called tRNA-derived small RNA. The advancement of bioinformatics technology has led to an increase in the visibility of small RNA derived from tRNA, and their functions in biological processes are being revealed. These include gene silencing, transcription and translation, epigenetics, and cell death. These properties have led to the implication of tsRNAs in various diseases. Although the current research mainly focuses on the role of tRNA-derived small RNA in cancer, there is mounting evidence that they are also strongly associated with cardiovascular disease, including cardiac hypertrophy, atrial fibrillation, heart failure, and myocarditis. Therefore, the regulatory role of tRNA-derived small RNA in cardiovascular disease will become an emerging therapeutic strategy. This review succinctly summarizes the characteristics, classification, and regulatory effect of tsRNA. By exploring the mechanism of tsRNA, it will provide a new tool for the diagnosis and prognosis of cardiovascular disease.