Background:Effective rate control is important in the management of atrial fibrillation (AF). However, the relationship between resting heart rate (RHR) and adverse outcomes in hospitalized patients remains uncertain. Objective:This study was to evaluate the association between RHR and in-hospital outcomes. Methods:Data from the Improving Care for Cardiovascular Disease in China-AF project from 2014 to 2019 were retrospectively analyzed. The primary outcome was the composite of in-hospital all-cause mortality and in-hospital acute heart failure (AHF). Secondary outcomes included stroke/transient ischemic attack (TIA) and bleeding during hospitalization. Logistic regression analyses were used to assess the association between RHR and outcomes. Results:Our study included 12,775 patients hospitalized for AF in 236 hospitals. Logistic regression analyses using different models showed a significant association between RHR exceeding 80 bpm and an increased risk of the primary outcome (adjusted OR: 1.79 [95% CI: 1.44-2.22]). A positive association between RHR and the primary outcome was identified with RHR ≥ 80 bpm. Marginal effect analyses showed that patients with advanced AF types were at higher risk across the range of RHR. Conversely, catheter ablation, but not antiarrhythmic drug use, was associated with a decreased risk. Conclusion:A significant association was identified between RHR and adverse outcomes in patients hospitalized for AF, where RHR exceeding 80 bpm was associated with an increased risk. Trial Registration: ClinicalTrials.gov identifier: NCT02309398.
Aim:This network meta-analysis (NMA) evaluated four novel proprotein convertase subtilisin/kexin type 9 (PCSK9) monoclonal antibodies for hypercholesterolemia management, comparing their lipid-lowering efficacy and safety. Methods:We systematically identified randomized controlled trials employing the frequentist NMA method to assess reductions in low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (ApoB), and lipoprotein (a) (Lp[a]), alongside treatment-emergent adverse events (TEAEs) and serious TEAEs. P-scores ranked therapeutic hierarchies, with meta-regression and subgroup analyses exploring heterogeneity. Trial sequential analysis determined the adequacy of cumulative evidence. Confidence in the network meta-analysis approach was used to evaluate the confidence in the findings from NMA. Results:A total of eight trials with 3,975 Chinese patients were included. Ongericimab 150 mg every 2 weeks (Q2W) ranked first in all efficacy outcomes, demonstrating pronounced effects in LDL-C, ApoB, and Lp(a) reduction versus placebo, with mean differences of -74.21% (95% confidence interval [CI]: -79.69% to -68.73%), -64.36% (95% CI: -68.58% to -60.13%), and -50.93% (95% CI: -56.24% to -45.61%), respectively. All interventions exhibited safety profiles comparable with placebo, with no significant differences in TEAEs or serious TEAEs incidence. The analyses suggested that a portion of the evidence base was robust and reliable. Conclusion:These findings positioned ongericimab 150 mg Q2W as a clinically optimal PCSK9 inhibitor with robust lipid-lowering capacity. The results highlight the potential of next-generation PCSK9 monoclonal antibodies, particularly in East Asian populations, while underscoring the need for large-scale multinational trials to validate ethnic-specific responses.
Background:The association between the atherogenic index of plasma (AIP) and different cardiovascular disease (CVD) outcomes remains insufficiently studied. Methods:Data from 16,302 US adults in NHANES 2005-2020 were analyzed. CVD outcomes included congestive heart failure, coronary heart disease, angina, heart attack, and stroke. Multivariable logistic regression models assessed the linear association between AIP and CVD. Restricted cubic splines were used to examine potential nonlinear relationships, whereas threshold effect analysis identified inflection points. Stratified analyses explored interactions between AIP and covariates. Results:Compared with the lowest quartile, the highest AIP quartile was associated with increased odds of overall CVD (OR = 1.73, 95% CI = 1.20-2.52, p for trend = 0.001), coronary heart disease (OR = 2.20, 95% CI = 1.20-4.25, p for trend = 0.013), and heart attack (OR = 2.53, 95% CI = 1.42-4.74, p for trend = 0.008). A U-shaped relationship was observed between AIP and congestive heart failure (p overall = 0.0004, p nonlinear = 0.002), with a sharp odds increase when AIP exceeded 0.22 (OR = 3.40, 95% CI = 1.81-6.38, p < 0.01). Subgroup analysis revealed a significant age interaction: Among adults younger than 55 years, each AIP increment was associated with higher odds of CVD (OR = 2.53, 95% CI = 1.60-3.98, p = 0.001), heart attack (OR = 2.58, 95% CI = 1.21-5.54, p = 0.014), and stroke (OR = 2.98, 95% CI = 1.44-6.17, p = 0.003). Conclusion:Elevated AIP is an independent predictor of CVD, coronary heart disease, and heart attack, particularly in younger adults (< 55 years). A U-shaped relationship was identified between AIP and congestive heart failure. These findings highlight AIP as a valuable biomarker for CVD risk assessment and emphasize the importance of age-specific intervention strategies targeting different CVD outcomes.
Objectives:The objectives of this study is to investigate the correlation between genotype polymorphism of aldehyde dehydrogenase 2 (ALDH2) and coronary artery disease (CAD) in atrial fibrillation patients. Methods:From November 2020 to December 2021, 80 patients with atrial fibrillation at a medical center in Chengdu were divided into two groups: CAD group (n = 25) and non-CAD group (n = 55). The genotype composition ratio of ALDH2 (mutant-type/wild-type), blood biochemical indexes, the proportion of the history of lipid-lowering drugs and time of taking lipid-lowering drug were compared between the two groups. Results:The CAD group showed significantly lower levels of total cholesterol and low-density lipoprotein cholesterol (LDL-C) compared with the non-CAD group (p < 0.05), and the proportion and time of taking lipid-lowering drugs in CAD group were significantly increased (p < 0.05). The frequency of the ALDH2 genotype (mutant-type/wild-type) in the CAD group was notably elevated compared with that in the non-CAD group (p < 0.05). In patients with atrial fibrillation, the risk of CAD in patients with ALDH2 mutant genotype (GA + AA) was 5.849 times that of ALDH2 wild-type genotype (GG) (95%CI = 1.437-23.795, p < 0.05). The area under ROC curve of ALDH2 mutant genotype (GA + AA) was 0.624 (SE = 0.069, 95%CI : 0.488-0.759). In patients with ALDH2 wild-type (GG), the levels of total cholesterol and LDL-C in CAD group were significantly lower than those in non-CAD group (p < 0.05). However, in patients with ALDH2 mutation genotype (GA + AA), the proportion of history of lipid-lowering drugs in CAD group was significantly higher than that in non-CAD group (p < 0.05). Conclusions:The polymorphism of ALDH2 gene is a high risk factor for CAD in patients with atrial fibrillation. The ALDH2 mutation genotype (GA + AA) may reduce the lipid-lowering efficacy of statins.
Background:This study is aimed at measuring the expression of serum cytokeratin 18 (CK18) in patients with nonalcoholic fatty liver disease (NAFLD) and at evaluating its ability to discriminate NAFLD patients with and without coronary heart disease (CHD), thereby elucidating its potential role in reflecting the link between NAFLD and increased cardiovascular involvement. Methods:A total of 127 patients diagnosed with NAFLD and treated between September 2022 and July 2024 were enrolled in this cross-sectional study. Based on the presence or absence of CHD, they were divided into two subgroups: a CHD-present group (n = 79) and a CHD-absent group (n = 48). In addition, a control group consisting of 100 age-matched and sex-matched healthy individuals undergoing routine physical examinations during the same period was included for comparison. Results:Compared with the control group, patients with NAFLD showed significantly higher levels of alanine aminotransferase (ALT), serum CK18-M65 and CK18-M30 levels, body mass index (BMI), homeostasis model assessment of insulin resistance index (HOMA-IR), triglyceride (TG), total cholesterol (TC), aspartate aminotransferase (AST), and waist-to-hip ratio (p < 0.05). Multivariate logistic regression analysis identified serum CK18-M65, CK18-M30, TC, ALT, AST, and HOMA-IR as independent factors in NAFLD patients (p < 0.05). The combination of CK18-M65 and CK18-M30 yielded an area under the curve of 0.843, with a sensitivity of 87.34% and a specificity of 75.00%. Functional enrichment analysis revealed that CK18-related genes were involved in inflammatory signaling and cardiovascular regulatory pathways, supporting a mechanistic role for CK18 in the liver-heart axis. Conclusion:Serum CK18 may serve as a useful biomarker for identifying NAFLD patients with concurrent CHD, offering diagnostic value in clinical assessment.
Aims:To evaluate the real-world efficacy and safety of low-dose (2.5 mg) mavacamten initiation in Chinese patients with symptomatic obstructive hypertrophic cardiomyopathy (oHCM). Methods and Results:This single-center observational study (Zhongshan Hospital, China; Oct 2024-Apr 2025) enrolled 72 symptomatic oHCM patients (NYHA II/III, LVEF ≥ 55%, resting/Valsalva-provoked LVOT gradient [LVOTG] ≥ 30 mmHg). All patients initiated mavacamten 2.5 mg once daily. Doses were adjusted at Weeks 4, 8, and 12 based on LVEF and LVOTG. Primary outcomes were changes in resting/provoked LVOTG, NT-proBNP, and NYHA class at Week 12. Safety outcomes included LVEF < 50%, cardiac hospitalization, and death.Significant reductions from baseline to Week 12 were observed: Resting LVOTG (52.4 ± 28.7 to 32.1 ± 23.1 mmHg, p < 0.001), Valsalva-provoked LVOTG (74.1 ± 24.4 to 48.7 ± 25.4 mmHg, p < 0.001), NT-proBNP (1102.7 ± 1114.9 to 320.2 ± 406.2 pg/mL, p < 0.001). LVEF remained stable. NYHA class improved by ≥ 1 class in 83.3% (60/72) of patients.Subgroup analyses revealed significantly greater LVOTG reductions in patients with classic HCM (vs. apical HCM, p < 0.001) and high baseline resting LVOTG (≥ 50 mmHg vs. < 50 mmHg, p < 0.001/p = 0.04). NYHA improvement was consistent across subgroups.Twenty-two patients escalated to 5 mg at Week 12, achieving further significant LVOTG reductions (p < 0.001), particularly in apical HCM and high-baseline-gradient subgroups, with stable LVEF.No safety events occurred (LVEF < 50%, arrhythmias, hospitalization, and death). Four patients reported transient minor adverse events (dizziness, nausea, and fatigue). Conclusion:In this first Chinese real-world study, initiating mavacamten at 2.5 mg significantly improved haemodynamics (LVOTG), biomarkers (NT-proBNP), and functional status (NYHA) in oHCM patients over 12 weeks with an excellent safety profile. Greater haemodynamic efficacy was observed in classic HCM and high-baseline-gradient patients. Escalation to 5 mg provided additional benefit. Mavacamten is an effective and safe therapy for oHCM in this Asian population.
Aims:Novel drugs that target apoC-III in lipoprotein metabolism to reduce plasma triglycerides are currently under development. Olezarsen, a drug similar to its predecessor, volanesorsen, is in Phase 3 trials. A meta-analysis of RCTs was done to study its effect on hypertriglyceridemia. Material and Methods:Screening was done on PubMed, Embase, Scopus, and the Cochrane Library from inception to August 2024. We used Review Manager (Version 5.4) for statistical analysis. Subgroups of olezarsen at doses of 10, 50, and 80 mg were made. Continuous outcomes were reported as mean differences with 95% CIs. Adverse events were reported using risk ratios and 95% CIs. The risk of bias was analyzed using the Cochrane risk of bias tool. Results:Four RCTs with 374 participants, 278 in intervention and 96 placebo controls, were included. At all doses of olezarsen, a significant reduction in fasting triglyceride levels (MD: 45.69; 95% CI: 35.84, 55.54; p < 0.00001) was seen. This was most pronounced at 80 mg dose (MD: 51.98 95% CI: 43.06, 60.90; p < 0.00001). A reduction in apoC-III (MD: 58.77; 95% CI: 35.94, 81.61; p < 0.00001) and an increase in HDL (MD: 0.21; 95% CI: 0.04, 0.37; p = 0.01) were also observed. No significant effect was observed on LDL levels (MD: -0.13; 95% CI: -0.40, 0.14; p = 0.34). Overall, no significant adverse effects were seen compared to placebo (RR: 1.42; 95% CI: 0.66, 3.05; p = 0.37). Conclusion:Olezarsen showed remarkable efficacy in lowering triglycerides, with a dose-dependent effect, while significantly increasing HDL levels and reducing apoC-III. Its safety profile is commendable. Although it performed well compared to volanesorsen, inconsistencies in LDL reduction and heterogeneity in some groups warrant further large-scale RCTs to better assess its safety and efficacy. Clinical decisions should be tailored to individual patient profiles, as hypertriglyceridemia management may vary on a case-to-case basis.
Purpose:The purpose of this study is to investigate the role of aldehyde dehydrogenase-2 (ALDH2) in septic myocardial injury, focusing on noncanonical pyroptosis. Methods:In vivo, C57BL/6J mice were divided into five groups: Sham, cecal ligation and puncture (CLP), CLP + Alda-1 (ALDH2 agonist), Sham + dimethyl sulfoxide (DMSO, solvent control), and CLP + DMSO. Cardiac function and histological/ultrastructural changes were assessed via echocardiography, hematoxylin-eosin (HE) staining, and transmission electron microscopy (TEM). Tumor necrosis factor-α (TNF-α) and noncanonical pyroptosis-related proteins (caspase-11, gasdermin-D [GSDMD], high mobility group box 1 [HMGB1], and receptor for advanced glycation end products [RAGE]) were measured by enzyme-linked immunosorbent assay (ELISA) and western blotting. Coimmunoprecipitation (CO-IP) explored molecular mechanisms. In vitro, H9C2 cells were divided into six groups: Control, lipopolysaccharide (LPS)-treated, ALDH2-green fluorescent protein (GFP), LPS + ALDH2-GFP, GFP, and GFP + LPS. Cell viability, lactate dehydrogenase (LDH) release, creatine kinase isoenzymes (CK-MB), and target protein levels were detected via spectrophotometry, western blotting, and immunofluorescence (IF). Results:In vivo, Alda-1 significantly attenuated CLP-induced cardiac dysfunction and reduced myocardial histological damage and ultrastructural impairment. In vitro, ALDH2 overexpression lowered LPS-induced H9C2 cell viability, CK-MB, and LDH release. Upregulating ALDH2 significantly reduced caspase-11, HMGB1, and RAGE expression. CO-IP showed ALDH2 interacted with HMGB1, RAGE, and GSDMD. Conclusion:ALDH2 protects the myocardium from septic injury by inhibiting caspase-11-mediated noncanonical pyroptosis, possibly via direct interactions with GSDMD, HMGB1, and RAGE.
Background:The relationship between hypothyroidism and cardiovascular disease is well established. However, data on subclinical hypothyroidism (SH) and its impact on major adverse cardiovascular events (MACEs) and postoperative complications following coronary artery bypass grafting (CABG) remain limited. This study was aimed at evaluating whether SH is associated with an increased risk of these outcomes. Methods:From 2010 to 2019, 863 patients who underwent CABG for cardiovascular diseases at a reference center were included. The primary outcomes included MACE (composite and individual events: all-cause death, cardiovascular death, stroke, acute myocardial infarction [AMI], and new revascularization) and postoperative complications, including atrial fibrillation (AF), pleural effusion (PLE), pericardial effusion (PCE), infections at any site (IASs), and mediastinitis. Results:SH patients had higher rates of MACE (20.3% vs. 8.2%, p = 0.001), MACE 4p (22.0% vs. 12.9%, p = 0.002), and stroke (10.2% vs. 3.0%, p = 0.013) than those of euthyroid patients. No significant differences were observed in all-cause death, cardiovascular death, AMI, or new revascularization. Postoperative complications were also more frequent in the SH group: AF (18.6% vs. 9.7%, p = 0.043), PLE (52.6% vs. 19.2%, p < 0.0001), PCE (20.3% vs. 7.8%, p = 0.03), and IAS (28.8% vs. 16.9%, p = 0.032). However, no significant difference was noted in the incidence of mediastinitis. Conclusions:SH patients who underwent CABG had a higher frequency of MACE and postoperative complications than those of euthyroid patients.
Background:Coronary heart disease (CHD) is a leading cause of cardiovascular mortality worldwide, with its pathogenesis being complex and not yet fully understood. The rapid development of genomics, especially in epigenetic research, has provided essential tools for identifying new pathogenic targets. This study is aimed at systematically exploring the molecular mechanisms of CHD using protein quantitative trait locus (pQTL) data and multiomics Mendelian randomization (MR) approaches, with a specific focus on the epigenetic regulation of the key gene ITGB7. Methods:The study first integrated 1812 cis-pQTL data with CHD GWAS data to perform a two-sample MR analysis, identifying protein-coding genes significantly associated with CHD. Transcriptomic data were then used to validate the differential expression of these genes. Subsequently, a two-step MR mediation analysis was conducted to explore the upstream regulatory effect of DNA methylation on the key gene ITGB7, as well as the potential mediating roles of ITGB7 on downstream immune cells and plasma metabolites. Results:MR analysis identified 17 genes significantly positively associated with CHD, with PCSK9 and ITGB7 showing significant upregulation in the peripheral blood of CHD patients. Mediation analysis revealed that the DNA methylation site cg14524975 (beta_p = 45.64%) significantly increased the risk of CHD by positively regulating the expression of ITGB7. In downstream mechanisms, ITGB7 significantly promoted CHD progression by regulating immune cells, such as CD4+ CD8dim AC (beta_p = 12.04%), and plasma metabolites, including N,N-dimethylalanine (beta_p = 18.96%), benzoate-to-oleoyl-linoleoyl-glycerol (18:1 to 18:2) ratio (beta_p = 34.63%), and serine-to-threonine ratio (beta_p = 12.58%). Conclusion:This study identifies ITGB7 as a novel pathogenic gene for CHD and reveals its multiomics mechanisms in promoting CHD development through DNA methylation regulation, immune response activation, and metabolic pathway disruption. The findings provide valuable theoretical insights and potential biomarkers for the pathogenesis and targeted intervention of CHD.
Background:Elderly patients with heart disease face elevated mortality risk, yet predictive models specifically tailored for this population across different global regions remain limited. Current mortality prediction tools often lack cross-cultural validation and interpretability, hindering their clinical application in diverse healthcare settings. Methods:We developed and validated machine learning models for predicting mortality in elderly heart disease patients using data from three major aging cohorts: the China Health and Retirement Longitudinal Study (CHARLS, n = 2130), the Survey of Health, Ageing and Retirement in Europe (SHARE, n = 10,928), and the Health and Retirement Study (HRS) from the United States (n = 4835). Boruta feature selection identified 27 common predictors across cohorts. Eleven machine learning algorithms were trained on the SHARE cohort (70% training and 30% testing) and externally validated on CHARLS and HRS cohorts. Model performance was assessed using area under the receiver operating characteristic curve (AUC), sensitivity, specificity, and calibration metrics. SHapley Additive exPlanations (SHAP) analysis was employed to interpret model predictions. Results:XGBoost demonstrated superior performance with the highest average AUC (0.798) across all datasets, showing excellent generalizability from the SHARE training set (AUC: 0.805) to internal validation (AUC: 0.799) and external validation in HRS (AUC: 0.821) and CHARLS (AUC: 0.770) cohorts. Age consistently emerged as the most influential predictor across all cohorts (SHAP values: 0.056-0.102), followed by gender, moderate physical activity, and self-rated health, though their relative importance varied by cohort. Feature dependence analysis revealed important nonlinear relationships, including U-shaped associations between grip strength and mortality risk. Conclusion:Our multicohort machine learning approach successfully developed a robust, interpretable model for predicting mortality in elderly heart disease patients across diverse global populations. The model's strong performance in external validation demonstrates its potential for cross-cultural clinical application, while SHAP analysis provides valuable insights into population-specific risk factors that could guide targeted interventions.
Background:Drug-coated balloons (DCBs) present a viable option distinct from drug-eluting stents (DESs) in addressing coronary artery disease (CAD), particularly when it comes to in-stent restenosis (ISR) scenarios. The utilization of DCBs marks a significant deviation from traditional DES applications. For CAD patients experiencing ISR, DCBs offer an innovative pathway to treatment. However, their efficacy and safety in de novo CAD lesions remain uncertain. This meta-analysis evaluates DCB versus other percutaneous coronary intervention (PCI) strategies, including DES, bare-metal stents (BMSs), and plain old balloon angioplasty (POBA), in de novo CAD. Methods:A comprehensive search was conducted across PubMed, Embase, Web of Science, and the Cochrane Central Register of Controlled Trials (CENTRAL), spanning from their inception up until November 14, 2024. Studies included were randomized controlled trials (RCTs) and cohort studies, which assessed DCB against alternative PCI strategies in patients with de novo CAD. The key outcome measures focused on major adverse cardiac events (MACEs) as well as late lumen loss (LLL). Trial sequential analysis (TSA) assessed the robustness of findings. Results:Fifty studies (19 RCTs, 31 cohort studies) involving 28,292 patients were analyzed. DCB showed a lower MACE incidence compared to noncoated devices (RR = 0.52, 95% CI: 0.40-0.69) but no significant difference versus DES (RR = 0.96, 95% CI: 0.84-1.10). DCB significantly reduced LLL compared to all controls (MD = -0.22, 95% CI: -0.29 to -0.14). Subgroup analyses confirmed DCB's safety across indications, ethnicities, comorbidities, and dual antiplatelet therapy (DAPT) durations, with reduced LLL in small vessel disease and shorter DAPT. TSA supported LLL findings but indicated inconclusive MACE results in RCTs, necessitating further research. Conclusion:DCB is a safe and effective alternative to DES in de novo CAD, with comparable safety and superior LLL reduction. However, MACE results in RCTs require further validation. Future studies should explore long-term outcomes and integrate newer-generation DCB and DES technologies to optimize clinical practice.
Background:Atherosclerotic cardiovascular disease (ASCVD) pathogenesis is closely associated with macrophages. This study sought to explore the role of phagocytosis by monocyte-derived macrophages (MDMs) in the blood in the context of coronary heart disease (CHD) and acute coronary syndromes (ACSs). Methods:This study employed a matched case-control design. Individuals with suspected CHD were recruited and allocated to a control cohort or a CHD cohort, with the latter further stratified into stable angina pectoris and ACS subgroups according to clinical diagnoses. Clinical data were collected, MDMs were isolated, and macrophage phagocytic activity was evaluated using fluorescent-labeled latex microspheres. Results:Macrophage phagocytic rates were significantly reduced in the CHD group relative to the control group, with further decreases observed in the ACS subgroup. Multivariable linear regression revealed that age, low-density lipoprotein cholesterol (LDL-C), high-sensitivity C-reactive protein (hs-CRP), and fibrinogen were independently and negatively correlated with macrophage phagocytic rates. Multivariable analyses suggested that diminished macrophage phagocytic rates were linked to an elevated risk of both CHD and ACS. Receiver operating characteristic (ROC) curve analysis identified the optimal cutoff values of macrophage phagocytic rates for predicting CHD and ACS as 62.6% and 63.4%, respectively, with the area under the curves (AUCs) measured at 0.679 and 0.669. Conclusions:Macrophage phagocytic activity is reduced in CHD patients, particularly in those with ACS. Diminished macrophage phagocytic function is linked to CHD and ACS. Macrophage phagocytosis could act as a protective biomarker in CHD and ACS, providing new insights into the pathophysiology of ASCVD.
Purpose:The purpose of the study is to analyze the clinicopathological characteristics of essential hypertension (EH) in high-altitude regions of China and provide evidence-based guidance for rational diagnosis and treatment strategies in these areas. Methods:This cross-sectional retrospective study enrolled two cohorts of EH patients from Qinghai (high altitude, ≥ 2500 m) and Chengdu (low altitude, 500 m) between 2020 and 2022. Participants were stratified based on their residential altitude. Clinical parameters, biochemical markers, cardiac imaging data, and antihypertensive regimens were systematically compared. Statistical analyses were conducted using SPSS software (Version 26.0). Results:Compared with patients with EH at low altitude, high-altitude EH patients had a higher mean systolic/diastolic blood pressure and a lower percentage of compliance with blood pressure lowering and were more likely to have hyperuricemia (HUA) and abnormally elevated metabolic function (p = 0.03). Significant cardiac structural changes occurred in patients with high-altitude EH: increased pulmonary artery internal diameter (p < 0.001). In addition, the proportion of angiotensin-converting enzyme inhibitor, angiotensin II receptor blocker, β-blocker, and diuretic use was lower in patients with high-altitude EH, while the proportion of SPC combination use was higher; conversely, the proportion of diuretic use was higher in patients with high-altitude EH with comorbid HUA. Conclusion:EH in high-altitude populations demonstrates distinct clinicopathological manifestations, including right ventricular overload and compensatory left cardiac adaptation. These findings underscore the necessity for altitude-specific clinical guidelines to optimize hypertension management in these regions.
Background/Objectives:Dual antiplatelet therapy (DAPT), which combines aspirin with a P2Y12 receptor inhibitor for platelets, is crucial for the prevention of cardiac and systemic ischemic events in patients with coronary artery disease who have undergone revascularization procedures. Although indobufen is suggested as an alternative for individuals who exhibit intolerance to aspirin, the long-term safety and efficacy of indobufen-based DAPT treatment for the prevention of cardiac and systemic ischemic events in these patients remain ambiguous. This meta-analysis seeks to examine the long-term safety and efficacy of DAPT based on indobufen in the context of revascularization procedures for patients. Methods:A thorough search was performed across PubMed, Embase, the Cochrane Library, Web of Science, ClinicalTrials.gov, and CNKI, covering all records from each database's inception to October 10, 2024. Included were randomized trials analyzing oral DAPT antiplatelet agents for coronary artery disease patients who received revascularization. Two reviewers independently handled the selection process: screening articles, overview, extracting data, and assessing study quality in accordance with PRISMA guidelines. The pooled data were later subjected to analysis using a random-effects model meta-analysis. Results:The final analysis included three randomized controlled trials, which yielded the following findings regarding major adverse cardiovascular and cerebrovascular events (MACCEs): The relative risk (RR) was 1.58 (95% CI, 0.72-3.38); for BARC Type 2, 3, or 5 bleeding events, the RR was 0.35 (95% CI, 0.18-0.67); and for gastrointestinal intolerance events, the RR was 0.06 (95% CI, 0.03-0.18). Conclusions:Indobufen-based DAPT may potentially increase the risk of ischemic events without compromising safety for revascularization, as its upper RR limit exceeds 1 for MACCEs.
Objective:This study is aimed at comparing the efficacy and safety of dronedarone, amiodarone, and propafenone in preventing early recurrence of atrial arrhythmias during the blanking period following catheter ablation in patients with nonparoxysmal atrial fibrillation. Methods:We retrospectively analyzed 408 patients with nonparoxysmal atrial fibrillation who underwent their first catheter ablation. Patients were divided into three groups based on the postoperative antiarrhythmic drug prescribed: dronedarone, amiodarone, or propafenone. A propensity score matching (PSM) analysis was performed as the primary analysis to compare early recurrence rates and drug-related adverse events. An inverse probability of treatment weighting (IPW) analysis was conducted as a sensitivity analysis. Results:Of the 408 patients, 65 (15.9%) experienced early recurrence. The early recurrence rate was significantly lower in the dronedarone group (9.2%) compared to propafenone (27.2%), but not significantly different from amiodarone (14.0%). The dronedarone group showed a lower recurrence rate of atrial flutter compared to both the propafenone and amiodarone groups (p < 0.05). After PSM, the recurrence rate of atrial flutter remained significantly lower in the dronedarone group compared to propafenone and amiodarone. Regarding drug-related adverse events, 73 patients (17.9%) experienced adverse reactions, with the amiodarone group showing a significantly higher incidence (24.2%) compared to the propafenone (13.6%) and dronedarone (11.8%) groups. Conclusion:In this retrospective study of patients with nonparoxysmal atrial fibrillation after catheter ablation, dronedarone and amiodarone showed a trend toward better efficacy than propafenone in preventing overall early recurrence. Dronedarone demonstrated a specific advantage in preventing early recurrence of atrial flutter.
Purpose:The purpose of this study is to analyze clinical characteristics of patients with Kawasaki disease (KD) aged below 1 year and identify risk factors for coronary aneurysm (CA) and its associated prognosis. Methods:A retrospective study enrolling infants (under 1 year of age) with KD admitted to a children's hospital between January 1, 2012, and August 30, 2024, was conducted. Patients were divided into two groups based on CA presence. Clinical records, including demographics, clinical manifestations, treatments, laboratory parameters, and cardiac ultrasound examination, were collected and analyzed. Results:Of 381 infants with KD, 96 developed CA. Male sex (adjusted odds ratio [aOR] = 1.982, p = 0.04), duration of fever (aOR = 1.143, p = 0.03), illness days of initial intravenous immunoglobulin (IVIG) (aOR = 1.319, p < 0.01), and higher C-reactive protein (CRP) (aOR = 1.007, p = 0.02) were associated with CA development in infants with KD in multivariable analysis. Specifically, an increase of 10 mg/L in CRP is associated with a 7.2% elevation in risk of CA development. Among patients diagnosed with CA, 30, 42, and 24 had small aneurysm (sAN), medium aneurysm (mAN), and giant aneurysm (gAN), respectively. The complete regression proportion and regression times of sAN, mAN, and gAN were 86.7%, 76.2%, and 33.3% and 3.9 ± 9.2, 12.8 ± 17.2, and 20.7 ± 11.2 months, respectively. Conclusions:CA incidence was higher in infants with KD and was associated with male sex, fever duration, days of initial IVIG, and higher CRP. The ability and time of regression depend on the size of the CA; however, giant CA in infant patients has a greater tendency to regress than those in older patients with KD.
Backgrounds:Anemia is associated with poor prognosis in heart failure patients. Erythropoiesis-stimulating agents have been used for the treatment of renal anemia, but they increase the risk of thrombotic events. Hypoxia-inducible factor prolyl hydroxylase inhibitors (HIF-PHIs) have emerged as a new treatment for renal anemia. HIF-PHIs are expected to have pleiotropic effects beyond correcting anemia. Evidence regarding the effects of HIF-PHIs in cardiorenal anemia syndrome has not been established. Methods and Results:The present study is a single-center, retrospective analysis of patients with heart failure and renal anemia who were treated with HIF-PHIs or oral iron supplementation at Kyushu University Hospital (n = 39 and n = 26). Both treatments significantly raised hemoglobin levels (HIF-PHIs 9.1 [8.6-9.6] vs. 10.3 [9.5-11.8], p < 0.001; oral iron 10.1 [9.3-11.0] vs. 11.8 [10.6-13.2], p < 0.001). Log-transformed BNP level (logBNP) decreased in the HIF-PHI-treated patients but not in those treated with oral iron despite the similar improvement in hemoglobin levels (HIF-PHIs 2.74 [2.28-2.99] vs. 2.47 [2.16-2.66], p = 0.005; oral iron 2.38 [1.89-2.66] vs. 2.37 [1.90-2.50], p = 0.711). The levels of iron metabolism-related parameters after treatment were comparable between the two groups. ΔlogBNP/ΔHb slope was significantly steeper in the HIF-PHI group than the oral iron supplementation group (-0.100 vs. -0.047, p = 0.039), meaning that HIF-PHIs further reduced BNP levels than anticipated by the increase of hemoglobin with conventional treatment. Conclusion:HIF-PHIs reduce BNP levels more than anticipated by the elevation of hemoglobin levels compared to oral iron supplementation. HIF-PHIs may have therapeutic benefits against heart failure beyond the correction of anemia in the heart failure patients.
Background:Heart failure (HF) is a major global public health problem, and identifying modifiable environmental risk factors is important for prevention. We evaluated the association between blood cadmium levels and the risk of HF in US adults. Methods:We analyzed data from the National Health and Nutrition Examination Survey (NHANES) 2009-2014. A total of 10,542 adults with complete information on blood cadmium and HF status were included. Weighted multivariable logistic regression models were used to assess the relationship between blood cadmium and self-reported HF. Restricted cubic spline (RCS) regression and two-piecewise linear models were applied to explore potential dose-response relationships. Results:A cohort of 10,542 US adults from the NHANES 2009-2014 dataset was analyzed, including 321 individuals diagnosed with HF. In fully adjusted, weighted logistic regression models, elevated blood cadmium levels were significantly correlated with an increased prevalence of HF. Specifically, each 1 μg/L increment in blood cadmium was associated with a 42% higher likelihood of HF (odds ratio [OR] = 1.42; 95% confidence interval [CI]: 1.18-1.72; p < 0.001). Participants in the highest quartile of blood cadmium levels exhibited more than a threefold increase in the odds of HF compared to those in the lowest quartile (OR = 3.15; 95% CI: 1.81-5.50; p < 0.001), with a significant linear trend observed across quartiles (p < 0.001). RCS analysis demonstrated a monotonic positive relationship, with an apparent inflection point at approximately 0.13 μg/L, beyond which the risk continued to escalate. This association was generally consistent across various subgroups but was notably stronger among smokers (p for interaction < 0.05). Conclusions:Elevated blood cadmium is an independent risk factor for HF in the United States. These findings suggest that reducing cadmium exposure may be a novel strategy for HF prevention. Prospective studies are warranted to clarify causal relationships and underlying mechanisms.
Background:Carvedilol, commonly used to treat hypertension and known for its vasodilatory and pleiotropic effects, has been studied in various patient populations. However, its specific impact on diastolic dysfunction and heart failure with preserved ejection fraction (HFpEF) remains unclear. Aim:The aim of the study is to evaluate carvedilol's efficacy in preventing concentric cardiac remodelling in at-risk individuals and modulating it in patients with HFpEF. Methods:In adherence to PRISMA guidelines, we searched PubMed and ScienceDirect up to March 2024 using terms related to carvedilol and HFpEF. We included randomised controlled trials and prospective cohort studies published in English. Outcomes include changes in natriuretic peptides and echocardiography parameters of diastolic function. Exclusion criteria encompassed non-English studies, nonhuman studies and studies not using carvedilol or exclusively involving HFrEF patients. Risk of bias was assessed using the revised Cochrane tool and Newcastle-Ottawa Scale. Data synthesis was performed using a random-effects meta-analysis with sensitivity analyses and a leave-one-out procedure to explore heterogeneity. Results:Eighteen studies involving 2233 participants were included. Various populations were included: those with HFpEF or undergoing cardiotoxic chemotherapy. Meta-analysis did not reveal significant effects of carvedilol on echocardiography parameters such as E/A ratio (mean difference 0.04, 95% CI -0.01 to 0.08), E/e' ratio (mean difference -0.50, 95% CI -1.39 to 0.39) and LVMI (mean difference 0.21, 95% CI -3.13 to 3.55), with substantial heterogeneity observed in LVEF, LVMI and BNP. Conclusion:Carvedilol does not significantly impact diastolic dysfunction across various populations. However, the diversity of study populations and outcomes contributes to the heterogeneity of results.
