Background:Left ventricular pseudoaneurysm (LVPA) is a rare but life-threatening complication of myocardial infarction (MI). We pooled clinical and imaging findings of post-MI LVPA reported in case reports/series and compared them with findings in post-MI left ventricular aneurysm (LVA). Method:We comprehensively searched the literature published since 1991 on online databases. Individual-level patient data (IPD) and aggregated-level data (AD) studies were combined through a two-stage meta-analysis method. Results:We identified 379 eligible articles on LVPA (N = 504 patients). LVPA patients were predominantly male (70.4%) with a mean age of 65.4 years (95% CI: 62.4, 68.4). The time interval between the last MI and the diagnosis of LVPA varied from one day to 20 years; 54.5% fell into the acute/subacute category. On echocardiography, the most frequent locations of LVPA were posterior (34.5%) and inferior (21.2%). The average dimensions were 5.7 and 7.3 cm. On MRI, late gadolinium enhancement, primarily pericardial, was observed in 84% of patients. Arrhythmia was more frequently observed in LVA than LVPA (33.8% vs. 1%). Echocardiography showed a lower diagnostic value in LVPA than LVA (sensitivity: 81.4% vs. 97.5%). A higher percentage of LVPA than the LVA group died during hospitalization (13.8% vs. 4.7%) or after discharge (17.5% vs. 9.0%). Conclusion:LVPA is probably located on the posterior and inferior segments in most patients, contrary to LVA, which mainly involves the anterior and apical segments. Arrhythmia is likely a common clinical finding in LVA but not LVPA. Echocardiography may not always detect LVPA in 20% of patients.
Chemotherapy-induced cardiotoxicity remains a major barrier to durable cancer control and survivor well-being, arising from oxidative stress, mitochondrial injury, inflammation, and emerging pyroptotic pathways. This updated narrative review integrates mechanistic and clinical data on nutraceuticals, including amino acids, fatty acids, vitamins, minerals, and polyphenols. Consistent clinical signals include omega-3 fatty acids, alpha-lipoic acid, vitamin D, coenzyme Q10, black seed oil, and vitamin E with levocarnitine, which primarily reduce oxidative stress to protect against cardiotoxicity. Additional preclinical and early clinical work highlights vitamin C-, taurine-, zingerone-, and rosemary-derived phenolics as candidates that target oxidative and inflammatory injury without compromising antitumor activity. Translation to care should be prevention-focused, pairing baseline risk assessment with surveillance that utilizes high-sensitivity troponin, natriuretic peptides, and advanced echocardiography, such as global longitudinal strain. Nutraceuticals should complement rather than replace established oncologic therapy and cardioprotection, with integration guided by individual risk and ongoing monitoring.
Myocarditis is an inflammatory disease of the myocardium with diverse aetiologies, ranging from infections and autoimmune processes to drug-induced reactions. Clinical manifestations vary widely from mild chest discomfort to life-threatening complications such as acute heart failure, cardiogenic shock and sudden cardiac death. Although the diagnosis of myocarditis historically relied heavily on invasive biopsy, recent advances in noninvasive imaging modalities, notably cardiac magnetic resonance (CMR) imaging, have transformed clinical practice. The Lake Louise Criteria (LLC), supplemented by parametric imaging techniques, have significantly enhanced diagnostic accuracy. Furthermore, the emergence of COVID-19 has renewed interest in myocarditis due to its association with viral-induced myocardial injury. This review synthesises the current understanding of myocarditis, including epidemiological insights, its diverse aetiologies, diagnostic innovations including the importance of viral load quantification and contemporary management strategies.
Background:Coronary artery disease (CAD) is the leading cause of death worldwide. Among women, CAD is often underestimated, resulting in underdiagnosis and undertreatment. This study aimed to assess the prevalence of CAD and its risk factors in adult women, using data from the Tehran Cohort Study (TeCS). Methods:We analyzed data from 4478 women with complete CAD information collected during the TeCS recruitment phase. The age-weighted prevalence of CAD was estimated using the 2016 national census data and previous CAD diagnoses. Logistic regression models were applied to identify factors independently associated with CAD in women. Results:The overall prevalence of CAD was 4.48% (mean age: 53.0 ± 12.37 years), with an age-weighted prevalence of 4.1% (95% CI: 3.1%-5.4%). Increasing age was strongly associated with CAD, with women aged ≥ 75 years showing markedly higher odds (OR: 11.94, 95% CI: 3.93-36.31, p < 0.001). Hypertension (OR: 2.58, 95% CI: 1.75-3.80, p < 0.001), hyperlipidemia (OR: 2.25, 95% CI: 1.55-3.24, p < 0.001), and diabetes mellitus (OR: 2.07, 95% CI: 1.49-2.88, p < 0.001) were also significant determinants of CAD. Older age groups exhibited a higher prevalence of CAD risk factors. Within the CAD group, a greater proportion of women had multiple comorbid risk factors compared with their non-CAD counterparts in the same age categories. Conclusion:The prevalence of CAD and its associated risk factors among women in Tehran is substantial. These findings highlight the need for targeted preventive strategies to reduce CAD incidence in vulnerable female populations.
Mavacamten is a cardiac myosin inhibitor used in adults with symptomatic obstructive hypertrophic cardiomyopathy (HCM). Echocardiography is central to selecting suitable patients, confirming left ventricular outflow tract (LVOT) obstruction, excluding inappropriate use when left ventricular ejection fraction (LVEF) is < 55% and guiding dose titration during treatment. This narrative review summarises the practical echocardiographic approach to mavacamten therapy, with emphasis on reproducible LVOT gradient assessment, goal-directed Valsalva manoeuvres, LVEF monitoring, mitral valve and systolic anterior motion assessment, mitral regurgitation, diastolic function and left atrial size. Current regulatory monitoring requires echocardiographic assessment during early titration and permits 6-monthly maintenance surveillance only in stable patients meeting defined criteria, including LVEF ≥ 55% and Valsalva LVOT gradient < 30 mmHg, or a decision not to uptitrate. The review also discusses unresolved issues, including exercise echocardiography, global longitudinal strain, atrial fibrillation, reverse remodelling, implementation variability and the broader emergence of cardiac myosin inhibitors such as aficamten. Standardised acquisition and reporting are essential to ensure that treatment decisions reflect true physiological response rather than technical variability.
Background:Accurate prediction of left atrial appendage thrombus (LAAT) is critical for stroke prevention in patients with nonvalvular atrial fibrillation (AF). We investigated the incremental value of epicardial fat tissue (EFT) metrics derived from cardiac computed tomography angiography (CCTA) beyond conventional risk factors. Methods:In this retrospective study of 287 AF patients prior to ablation, CCTA was used to measure left atrial appendage volume (LAAV) and EFT volume within 1 mm of the left atrium (EFT1). Multivariate logistic regression analysis identified predictors of LAAT or prethrombotic state (thrombus/spontaneous echo contrast), which were incorporated into a nomogram. Model performance was evaluated using the area under the curve (AUC), calibration plots, and decision curve analysis. Results:The thrombus group exhibited significantly larger LAAV (15.07 ± 2.7 mL vs. 11.94 ± 2.55 mL, p < 0.001) and EFT1 volume (6.39 ± 1.38 mL vs. 5.36 ± 1.47 mL, p < 0.001) compared to the normal/SEC group. Multivariate analysis identified EFT1 (odds ratio [OR] = 1.57 per mL), LAAV (OR = 1.56 per mL), and the CHA2DS2-VA score (OR = 1.34 per point) as independent predictors. The resulting nomogram demonstrated excellent discrimination for LAAT (AUC = 0.851) and for thrombus/SEC (AUC = 0.819), with good calibration and clinical utility. Conclusion:EFT1, the EFT volume immediately adjacent to the left atrium, is strongly associated with LAAT. The novel nomogram integrating EFT1, LAAV, and the CHA2DS2-VA score provides enhanced risk stratification for thrombotic and prethrombotic states in patients with AF.
Ferroptosis has recently been identified as a critical mechanism underlying arsenic trioxide (ATO)-induced cardiotoxicity. This study aimed to determine whether Honokiol (HKL) protects against ATO-induced cardiac injury by inhibiting ferroptosis and to investigate the role of the SIRT3 signaling pathway in this process. Using 129S1/SvImJ wild-type (WT) and SIRT3-knockout (SIRT3-/-) mice, we demonstrated that HKL attenuates ATO-induced myocardial injury and hypertrophy in a SIRT3-dependent manner. Mechanistically, HKL reduced oxidative stress through the SIRT3/SOD2 pathway, as evidenced by decreased mitochondrial ROS production and SOD2 acetylation, along with preserved mitochondrial ATP generation capacity. Furthermore, HKL inhibited ferroptosis, indicated by reduced iron content, MDA levels, and 4-HNE expression, along with restored GPX4 and GSH levels. Notably, HKL restored autophagic flux impaired by ATO, and this effect was associated with its antiferroptotic and cardioprotective actions. Pharmacological or genetic inhibition of SIRT3 or autophagic flux abolished the protective effects of HKL. Autophagic flux is closely associated with the protective effect of Honokiol on ATO-induced ferroptosis. These findings reveal that HKL protects against ATO-induced cardiomyopathy by restoring autophagic flux and inhibiting ferroptosis via the SIRT3 signaling pathway.
Background:Acute decompensated heart failure (ADHF) is a major cause of morbidity and mortality, with congestion being the primary reason for hospitalization. Despite treatment, many patients are discharged with residual congestion, hence the growing interest in utilizing biomarkers as objective tools to guide decongestion therapy. Carbohydrate Antigen 125 (CA125) has emerged as a promising biomarker of systemic congestion, with potential advantages over routine markers. This study evaluated the relationship between CA125 changes and clinical congestion score (CCS) at discharge and assessed its association with 30-day outcomes. Methods:This was a prospective cohort study conducted over seven months at Moi Teaching and Referral Hospital, a tertiary hospital in Western Kenya. Patients with ADHF were enrolled. CA125 levels were measured at admission and discharge using an automated immunoassay. In addition, other markers of congestion, i.e., CCS, NT-proBNP levels, body weight, and inferior vena cava (IVC) diameter, were assessed at both admission and discharge. The 30-day outcomes, which included all-cause mortality and heart failure (HF) rehospitalizations, were recorded. Statistical analyses included correlation and generalized linear models. Results:A total of 213 patients were included, with an in-hospital mortality rate of 23.5%. There was a significant correlation between changes in CA125 levels and improvements in CCS at discharge (p = 0.018). Patients with in-hospital CA125 reductions had lower rates of the composite 30-day outcome (all-cause mortality or HF rehospitalization) at 15%, compared to 40% in those with rising CA125 levels. Conclusion:A reduction in CA125 levels during hospitalization is associated with better clinical decongestion and improved short-term outcomes.
Background:Blood pressure variability (BPV) is recognized as an independent risk factor for cardiovascular morbidity and mortality. However, findings regarding the association between the coefficient of variation (CV) of 24-h blood pressure and mortality in patients with acute myocardial infarction (AMI) remain inconsistent. The aim of this study was to examine the association between 24-h CV and the risk of in-hospital, 30-day, 1-year, and 3-year mortality in AMI patients. Methods:This retrospective cohort study included AMI patients who were admitted to the intensive care unit (ICU) from the MIMIC-IV 2.0 database. The CV was calculated from blood pressure measurements taken during the first 24 h. Patients were divided into three groups according to tertiles of 24-h blood pressure CV. The relationship between 24-h CV and the risk of all-cause mortality in AMI patients was analyzed using logistic regression, Cox proportional hazards regression, and Kaplan-Meier survival analyses. Results:A total of 1291 eligible AMI patients were included. Compared with Q1 (lowest CV), Q3 (highest 24-h systolic blood pressure [SBP]-CV) was significantly associated with an increased risk of in-hospital (odds ratio [OR]: 3.333, 95% confidence interval [CI]: 1.725-6.439), 30-day (hazard ratio [HR]: 1.868, 95% CI: 1.201-2.904), and 1-year (HR: 1.420, 95% CI: 1.058-1.907) mortality. Both Q2 and Q3 of 24-h diastolic blood pressure (DBP)-CV were significantly associated with an increased risk of in-hospital, 30-day, 1-year, and 3-year mortality. Kaplan-Meier survival curves demonstrated that patients in Q3 had significantly lower 30-day, 1-year, and 3-year survival probabilities than those in other tertiles for both SBP and DBP. Conclusions:Our findings suggest that 24-h SBP-CV and DBP-CV are significantly associated with both short- and long-term outcomes in AMI patients. BPV may serve as a prognostic marker for all-cause mortality in AMI patients.
Purpose:To systematically review the efficacy and safety of dapagliflozin and sacubitril/valsartan (SV) in patients with heart failure (HF) following percutaneous coronary intervention (PCI)-treated acute myocardial infarction (AMI) and to provide evidence for clinical practice. Methods:Seven electronic databases were systematically searched from their inception to July 25, 2024. Following literature screening, data extraction, and risk of bias assessment, 14 randomized controlled trials involving 1310 patients were included. A meta-analysis was subsequently conducted using RevMan 5.4 and Stata 18. Results:Meta-analysis results showed that dapagliflozin combined with SV was superior to the control in improving left ventricular ejection fraction (LVEF) (WMD = 3.79, 95% CI: 2.70∼4.87; p < 0.001) and reducing N-terminal pro-brain natriuretic peptide (NT-proBNP) levels (WMD = -83.49, 95% CI: -129.33∼-37.65; p = 0.0004). This combination also significantly reduced left ventricular end-diastolic diameter (LVEDD) (WMD = -2.27, 95% CI: -3.64∼-0.90; p = 0.001), left ventricular end-systolic diameter (LVESD) (WMD = -3.29, 95% CI: -3.98∼-2.59; p < 0.001), left ventricular remodeling index (LVRI) (WMD = -0.08, 95% CI: -0.10∼-0.06; p < 0.001), and left ventricular mass index (LVMI) (WMD = -8.84, 95% CI: -12.25∼-5.43; p < 0.001), while increasing the 6-min walking distance (6MWD) (WMD = 51.74, 95% CI: 32.33∼71.14; p < 0.001). Compared with SV monotherapy, adding dapagliflozin reduced major adverse cardiovascular event (MACE) incidence (OR = 0.24, 95% CI: 0.15∼0.39; p < 0.001). However, no significant difference in adverse drug events (ADEs) was observed. Subgroup analyses revealed no significant differences in NT-proBNP (WMD = -194.85, 95% CI: -396.53∼6.82; p = 0.06), LVEDD (WMD = -1.50, 95% CI: -3.90∼0.89; p = 0.22), or the incidence of ADE (OR = 1.26, 95% CI: 0.74∼2.14; p = 0.39) when the follow-up duration was short (≤ 12 w). Additionally, significant heterogeneity was observed across studies for most outcomes. However, this heterogeneity was markedly reduced in the long-term follow-up subgroup (≥ 24 w), and the results were consistent with those of previous meta-analyses. Conclusion:Current evidence suggests that early initiation of dapagliflozin combined with SV offers superior efficacy and cardiovascular benefits for patients with HF following PCI-treated AMI. These benefits become increasingly evident with sustained treatment. Nevertheless, these conclusions warrant validation through more high-quality evidence.
Background:Hypertrophic cardiomyopathy (HCM) is a common genetic cardiac disease primarily affecting the left ventricle. While the disease is traditionally associated with myocardial hypertrophy and left ventricular outflow tract (LVOT) obstruction, aortic dilation has emerged as a potentially serious but underrecognized complication. This study aimed to determine the prevalence of aortic dilation in HCM patients and to identify associated clinical and echocardiographic factors. Methods:In this cross-sectional, retrospective study, 216 adult patients diagnosed with HCM at Rajaie Cardiovascular Institute (Tehran, Iran) from 2016 to 2021 were evaluated. Patients with significant valvular disease, congenital aortic anomalies, prior aortic surgery, or other cardiomyopathies were excluded. Clinical data and echocardiographic measurements, including aortic dimensions indexed to body surface area (BSA), were collected. Cardiac magnetic resonance imaging (MRI) data of myocardial fibrosis were also assessed in a subset of patients. Logistic regression was used to identify factors independently associated with aortic dilation. Results:Dilated ascending aorta was present in 56 patients (26.3%), while 12 patients (5.6%) had dilation of the sinus of Valsalva (SOV). Dilated ascending aorta was significantly associated with older age (p = 0.001), hypertension (p = 0.001), and increased BSA (p = 0.002). LV end-systolic diameter (LVESD) also showed a significant correlation (p = 0.002). Multivariate analysis identified age (OR = 1.063), hypertension (OR = 5.49), LVESD (OR = 3.25), and right ventricular hypertrophy (OR = 4.99) as independent predictors of ascending aorta dilation. SOV dilation was similarly associated with age (OR = 1.117) and lower weight (OR = 0.915). Although myocardial fibrosis was more common in patients with ascending aorta dilation, this did not reach statistical significance (p = 0.006). Conclusion:Aortic dilation is a relatively common finding in patients with HCM and is significantly associated with age, hypertension, and structural cardiac remodeling. Routine evaluation of the ascending aorta and SOV in HCM patients may aid in the early detection and management of this potential complication.
Background:The association between thyroid hormones and cardiovascular disease (CVD) has been widely examined; however, the role of biological aging in this relationship remains unclear. This study systematically investigates the mediating role of phenotypic age acceleration (PhenoAgeAccel) in the relationship between thyroid hormones and CVD. Methods:The data were sourced from the 2007-2010 cycles of the National Health and Nutrition Examination Survey (NHANES). Analyses included logistic regression, linear regression, restricted cubic splines, subgroup analyses, and mediation analysis to assess the role of PhenoAgeAccel. Results:Among participants aged ≥ 60 years, elevated free triiodothyronine (FT3) concentrations were linked to a reduced risk of CVD (adjusted odds ratio [aOR] = 0.483; 95% CI: 0.273-0.856; p = 0.013). Similarly, total triiodothyronine (TT3) levels were associated with a decreased CVD risk in those aged 60 and above (aOR = 0.988; 95% CI: 0.980-0.995; p = 0.013). Mediation analysis showed that PhenoAgeAccel mediated 21.13% of the FT3-CVD association and 23.41% of the TT3-CVD association in older adults. Conclusion:This study identifies an age-dependent relationship between FT3, TT3, and CVD and reveals that PhenoAgeAccel partially mediates this association. These findings suggest that interventions targeting thyroid function and biological aging may offer novel strategies for CVD prevention and management in older populations.
Several randomized controlled trials (RCTs), animal studies, and observational studies have demonstrated the cardioprotective effects of statins, though their effectiveness varies. The observed variability may be attributed to individual differences, patient ages, disparities in statin type and dosage of anthracyclines (ANT) administered, and variations in cancer conditions among patients. Overall, statins play a beneficial role in reducing oxidative stress and inflammation, enhancing tumor sensitivity to chemotherapeutic drugs, improving mitochondrial function in cardiac cells, exerting antiapoptotic effects, and preserving left ventricular ejection fraction (LVEF). Despite these promising findings, the long-term effects of statins remain unclear due to the lack of a standardized protocol. Statins may also cause side effects by depleting essential substances in the body. This limitation underscores the need for further research to assess their long-term impact and establish standardized guidelines for dosing, duration, and potential side effects. The implications of this review highlight the importance of understanding the pleiotropic effects of statins to develop targeted therapies for chemotherapy-induced cardiotoxicity. Additionally, integrating ongoing research into clinical guidelines is essential, ensuring that clinicians carefully consider patient-specific factors when prescribing statins alongside ANT. This present review explores the potential role of statins in mitigating ANT-induced cardiotoxicity, a major complication of chemotherapy that reduces LVEF and leads to heart failure (HF).
Purpose:The utilization of stress perfusion cardiac magnetic resonance (CMR) in patients with cardiac implantable electronic devices (CIEDs) is still limited. Methods:The study was registered in the Prospective Register of Systematic Reviews (PROSPERO) with ID CRD42023457308. PubMed, Scopus, Embase, Web of Science, ProQuest, and CINAHL databases were searched using the Mesh and related terms of CMR imaging, stress, and CIEDs. Results:Out of the 1695 papers we found, eight met our inclusion criteria. We reviewed the included studies and provided a concluding remark concerning (a) image quality; (b) CMR compatibility, scanner, and safety; (c) device protocols and exclusion criteria; (d) vasodilator choices, effects, and safety; and (e) clinical outcomes. Conclusion:This study has demonstrated a positive trend in the utilization of stress CMR in MR-conditional devices. However, the review has identified multiple research gaps that warrant further investigation.
Background:Peak heart rate (HR peak) and first ventilatory threshold heart rate (HR VT1) guide exercise prescription formulation, but existing formulas lack accuracy in coronary heart disease (CHD) patients due to unaccounted pathophysiological differences. This study aimed to construct prediction equation for HR peak and HR VT1 in CHD patients. Methods:This was a multicenter retrospective study that included 14,465 cases of cardiopulmonary exercise test (CPET) data from CHD patients in 20 hospitals in China. Seventy percent of the cohort was divided into a development group (n = 10,125), and the remaining 30% served as a validation group (n = 4340). Stepwise multiple backward regression established HR peak and HR VT1 equations, with accuracy compared to traditional formulas. Results:Age, weight, resting heart rate (HR rest), CHD diagnostic category, and β-blockers were included in the equation. The mean absolute percentage error (MAPE) of China-CPET-HR peak is 9.04%, with an adjusted coefficient of determination (R 2) of 0.399. For the China-CPET-HR VT1 formula, the MAPE is 7.32% and the adjusted R 2 is 0.509. The %HR peaks of the FOX, TANAKA, KETEYIAN, and China-CPET-HR peak formulas are 82 ± 11%, 79 ± 11%, 105 ± 13%, and 100 ± 11%, respectively. Conclusion:Based on CPET data from CHD patients, we developed prediction equations for HR peak and HR VT1. The prediction accuracy of these equations is significantly higher than others, which helps to formulate accurate individualized exercise prescriptions and rehabilitation training guidance for CHD patients.
Objective:This study investigated whether electroacupuncture (EA) at Neiguan (PC6) acupoint alleviates adverse myocardial remodeling in post-myocardial infarction (MI) heart failure (HF) by activating the vagus nerve-mediated cholinergic pathway and its downstream α7nAChR-Akt-HIF-1α-VEGF signaling cascade. Methods:Male Sprague Dawley (SD) rats were randomized into sham, MI model, and EA groups (n = 6 per group). MI was induced by ligation of the left anterior descending coronary artery. EA was applied at PC6 for 14 days starting 1 week after MI induction. Cardiac function and structure were evaluated using echocardiography and histological examination. The expression levels of choline acetyltransferase (ChAT), α7-nicotinic acetylcholine receptor (α7nAChR), phosphorylated Akt (p-Akt), hypoxia-inducible factor-1α (HIF-1α), and vascular endothelial growth factor (VEGF) were analyzed by real-time quantitative PCR, Western blotting, and immunohistochemistry. Results:EA intervention significantly attenuated pathological myocardial remodeling and improved cardiac function. Compared with the model group, EA treatment markedly enhanced cardiac function, increased contractility, reduced ventricular dilation, restored autonomic balance, and alleviated myocardial necrosis and fibrosis. Molecular studies revealed that EA treatment increased the expression of ChAT and α7nAChR, elevated p-Akt levels, and upregulated the expression of HIF-1α and VEGF. These findings suggest the activation of the vagus nerve-cholinergic signaling pathway and its downstream prosurvival and pro-angiogenic pathways. Conclusions:EA attenuated maladaptive ventricular remodeling and improved cardiac performance. These effects were associated with modulation of autonomic function and engagement of the α7nAChR/Akt/HIF-1α/VEGF signaling axis, supporting a potential neuro-immune-angiogenic mechanism underlying EA-mediated myocardial repair during the subacute post-MI phase.
Objective:To explore the predictive value of the controlling nutritional status (CONUT) score combined with the systemic immune-inflammation index (SII) for frailty and prognosis in chronic heart failure (CHF) patients with atrial fibrillation (AF). Methods:This retrospective study included 264 patients with CHF and AF who were admitted to and treated at the inpatient and outpatient departments of Nanjing Integrated Traditional Chinese and Western Medicine Hospital from January 2016 to July 2019. Follow-up ended upon patient death, with the final follow-up deadline set for September 2024. Binary logistic regression and Cox regression were used to identify factors influencing frailty and all-cause mortality. The cutoff values for the CONUT score and SII are determined by the ROC diagnostic threshold for mortality. Cutoff values for the CONUT score and SII were 6.5 and 990.2, respectively, categorizing patients into four groups: G1 (high CONUT ≥ 6.5 and high SII ≥ 990.2), G2 (high CONUT ≥ 6.5 and low SII < 990.2), G3 (low CONUT < 6.5 and high SII ≥ 990.2), and G4 (low CONUT < 6.5 and low SII < 990.2). Results:Frailty was present in 165 patients (165/264). Multivariate logistic regression identified disease duration, CONUT score, and SII as significant factors for frailty. A positive correlation between CONUT and SII was observed (r = 0.648, p < 0.001). Cox regression analysis found smoking, CONUT, and SII as risk factors for mortality. Survival analysis showed lower survival rates in high CONUT and high SII groups (p < 0.001), with the G1 group having the lowest survival rate compared to G2, G3, and G4 (p < 0.001). Conclusion:The CONUT score and SII are useful predictors of frailty and mortality in CHF patients with AF. Their combined use may improve the assessment of frailty and prognosis in this population.
Objective To explore the research course, hotspots, and development trends of mitochondrial DNA (mtDNA) and atherosclerosis (AS) based on knowledge graph technology, providing references for clinical and basic research in this field. Methods Publications themed on mtDNA and AS published between 2004 and 2025 were retrieved from the Web of Science Core Collection (WOSCC) database. CiteSpace 6.4. R1 Advanced software was used to construct and visually analyze knowledge graphs of authors, institutions, keywords, etc. Results A total of 341 publications were included, with the annual publication volume showing an overall upward trend. Research methods for mtDNA and AS are diversifying, with mechanistic investigations showing a trending focus toward specific molecular pathways. A total of 241 authors and 353 publishing institutions were analyzed. Ten keyword clusters were identified, including Cluster #0 oxidative stress, Cluster #1 mitochondrial DNA, Cluster #2 degradation, Cluster #3 atherosclerosis, Cluster #4 hydrogen peroxide, Cluster #5 roles, Cluster #6 MAPK pathway, Cluster #7 epigallocatechin gallate, Cluster #8 mitochondrial DNA copy number, and Cluster #9 vascular disease. Conclusion Research has evolved from foundational mechanistic studies to a focus on translational and clinical applications. Moving forward, efforts should be intensified to enhance collaboration among research teams and deepen mechanistic investigations, thereby laying a solid foundation for clinical translation.
Background:Patients with chronic kidney disease (CKD) undergoing dialysis who also suffer from severe aortic stenosis (AS) present a complex management challenge. Both transcatheter aortic valve replacement (TAVR) and surgical aortic valve replacement (SAVR) are treatment options, but comparative outcomes in this specific, high-risk population continue to remain unclear. Aim:This study aims to compare TAVR and SAVR postoperative clinical outcomes in patients with severe AS and CKD undergoing dialysis. Methods:According to PRISMA guidelines, a comprehensive search was conducted across various databases such as PubMed, EMBASE, Scopus, and Google Scholar. Original studies that compared the clinical outcomes between TAVR and SAVR in patients with severe AS and CKD undergoing dialysis were included in the study. Results:Ten studies, all retrospective, involving 28,625 (14,625 TAVR and 14,000 SAVR) patients with severe AS and CKD undergoing dialysis who underwent TAVR or SAVR were included in this study. Patients who underwent TAVR had significantly lower odds of in-hospital mortality (OR 0.49; 0.29, 0.84; p = 0.01) and shorter length of stay (LOS) (SMD -2.59; 95% CI -5.04, -0.14; p ≤ 0.04). However, the TAVR group had significantly higher odds of permanent pacemaker implantation (OR 2.25; 95% CI 1.71-2.94; p < 0.00001). Conclusion:In patients with severe AS and CKD undergoing dialysis, TAVR is associated with lower in-hospital mortality and shorter LOS, suggesting a favorable early safety profile and recovery in this population.
Despite considerable progress in managing ST-elevation myocardial infarction (STEMI), sudden cardiac death (SCD) remains a major clinical challenge. Although implantable cardioverter-defibrillator (ICD) therapy, guided primarily by left ventricular ejection fraction (LVEF), has been proven to reduce mortality in landmark trials (e.g., MADIT, MUSTT, and MADIT-II), the modest sensitivity and specificity of LVEF limit its utility as a sole risk stratifier. Emerging clinical trends highlight the progression from traditional LVEF-based models to more comprehensive risk assessment strategies. This review critically examines additional modalities, including advanced cardiac magnetic resonance imaging, echocardiography, myocardial biomarkers, detailed electrocardiographic parameters, and assessments of myocardial tissue heterogeneity, as well as patient-specific factors such as age, sex, and prehospital cardiac arrest history. Furthermore, we discuss recent advances, particularly the integration of artificial intelligence and machine learning algorithms, that help to enhance risk prediction and optimize ICD therapy decisions. By combining these novel approaches into a comprehensive risk assessment framework, our review promotes a more personalized strategy to identify STEMI patients most likely to benefit from ICD implantation, improve survival outcomes, and reduce unnecessary interventions. Future research should focus on validating these integrative models in large prospective cohorts and refining current guidelines for ICD therapy post-STEMI.
