Frontiers in Cardiovascular Medicine最新文献

Heart rate variability (HRV), the variation in intervals between consecutive heartbeats, reflects autonomic nervous system function and has been studied as a potential biomarker in cardiovascular disease (CVD). While reduced HRV has been linked to arrhythmias, heart failure, and ischaemic heart disease, findings across studies are mixed and its prognostic value remains debated. This review evaluates HRV's diagnostic, prognostic, and therapeutic roles in CVD. HRV can reveal autonomic dysfunction early, predict outcomes such as sudden cardiac death and recurrent myocardial infarction, and track recovery after cardiac events. It also shows promise in monitoring comorbid conditions like heart failure and depression that exacerbate cardiovascular risk. Advancements in wearable technology and machine learning are expanding HRV's potential. Wearable devices enable continuous, non-invasive HRV monitoring, while machine learning algorithms enhance the precision and predictive power of HRV analysis. These innovations may facilitate real-time data collection and tailored treatment plans, though their clinical utility requires validation in larger, prospective trials. Key challenges remain, including measurement variability, lack of standardisation, and limited incremental prognostic value over established risk factors. This review highlights HRV's emerging role in personalised cardiovascular care while acknowledging the substantial research needed before widespread clinical adoption.

Background: Atrial septal defects (ASDs) are associated with an increased risk of atrial arrhythmias due to right atrial dilation, electrical remodeling, and conduction abnormalities. In addition to arrhythmias, autonomic dysfunction may also occur. Although several studies have investigated the impact of transcatheter ASD closure on arrhythmia risk in pediatric patients, direct comparative analyses between surgical and transcatheter closure techniques remain limited in the current literature.

Methods: This study included patients who underwent ASD closure via surgical or transcatheter methods before age 18 and had at least 12 months of follow-up. A control group of healthy, age- and sex-matched children without cardiac disease was also included. All participants underwent 12-lead electrocardiography (ECG) and 24 h Holter monitoring. Patient data included arrhythmia symptoms, closure method, age at closure, defect size, and catheterization findings. Individuals with other cardiac anomalies, genetic syndromes, or medications affecting conduction were excluded.

Results: The study included 131 participants: 91 ASD patients (56 surgical, 35 transcatheter) and 40 controls. Supraventricular premature beats (SVPB) was significantly more frequent in both intervention groups compared to controls, with the highest frequency in the surgical group (p < 0.001). P-wave dispersion was also highest in the surgical group. In the surgical group, Lowns grade correlated positively with Qp/Qs, mean pulmonary artery pressure, and follow-up duration. Heart rate variability (HRV) parameters were significantly lower in the surgical group, indicating sympathetic dominance.

Conclusion: Atrial septal defect repair increases atrial arrhythmia risk, particularly following surgical intervention. While autonomic function remained comparable to controls after transcatheter closure, surgical closure was associated with reduced HRV and increased sympathetic activity.

Background: Myocardial infarction is the most common cause of pathological Q waves on electrocardiogram (ECG), but other conditions that cause myocardial injury or abnormal conduction (such as cardiomyopathy, myocarditis, cardiac tumors or amyloidosis, WPW, etc.) can also produce pathological Q waves. Whether myocardial calcification can lead to pathological Q waves remains uncertain.

Case summary: A 24-year-old man with a solitary kidney and multiple childhood abdominal surgeries had been on maintenance hemodialysis since 2017 (three times weekly), with a dialysis vintage of approximately 8 years. He was admitted for left upper-limb swelling of 2 months' duration. On admission his temperature was 36.6°C, blood pressure 93/75 mmHg, and heart rate 95 bpm. ECG showed complete left bundle branch block (cLBBB) and pathological Q waves in leads I, aVL, V5 and V6, without significant ST-T elevation. Transthoracic echocardiography(TTE) revealed global cardiac enlargement with marked systolic and diastolic dysfunction (LVEF ≈ 22%, LVEDD 80 mm), and an irregular hyperechoic mass at the cardiac apex measuring approximately 3.0 × 4.0 cm. Contrast chest CT confirmed focal calcifications in the high lateral wall and a hemispherical calcified lesion at the apex. Laboratory tests showed severe renal impairment (serum creatinine 827 µmol/L), markedly elevated NT-proBNP (32,961 pg/ml), mildly elevated troponin I (0.216 ng/ml) and myoglobin >1,000 ng/ml. Prior records documented severe disturbances of mineral metabolism: serum calcium 1.88 mmol/L, serum phosphorus 3.27 mmol/L, 25-OH vitamin D 13.05 ng/ml, and iPTH up to 2,000 pg/ml.

Management and outcome: The patient underwent diagnostic evaluation, vascular access revision, and continued dialysis; his symptoms improved and he was discharged. He continues regular outpatient hemodialysis and is under follow-up.

Conclusion: We report a rare case of focal myocardial calcification with pathological Q waves in a maintenance dialysis patient. Chronic kidney disease (CKD)-related disturbances of calcium-phosphate metabolism can cause metastatic myocardial calcification. Severe focal calcification may produce mechanical compression and cell necrosis, disrupt electrical coupling, create electrically silent zones, and result in pathological Q waves. In CKD patients with abnormal ECG findings, myocardial calcification should be included in the differential diagnosis and evaluated using imaging and metabolic data.

Background: Acute myocardial infarction (AMI) is a leading cause of morbidity and mortality worldwide. Beyond ischemic injury, sterile inflammation and immune activation critically shape infarct expansion, healing, and adverse remodeling. However, immune-related genes (IRGs) that distinguish AMI from stable coronary artery disease (sCAD) and reflect patient heterogeneity remain incompletely characterized.

Methods: Two microarray datasets (GSE59867 and GSE62646) were retrieved from database and integrated after batch correction. Differential expression analysis and weighted gene co-expression network analysis (WGCNA) were combined with CIBERSORT to identify differentially expressed immune-related genes (DEIRGs) and hub genes associated with immune infiltration. Consensus clustering was then applied to explore molecular subtypes of AMI. Finally, hub genes were preliminarily validated by RT-qPCR in a clinical cohort and in an independent public dataset (GSE60993).

Results: A total of 155 differentially expressed genes (DEGs) and 27 DEIRGs were identified. WGCNA highlighted the MEblue module as most strongly associated with AMI, and intersection analysis yielded 13 overlapping DEIRGs. Protein-protein interaction analysis prioritized six hub genes (CSF3R, CD14, AQP9, S100A9, SLC11A1, and IL1RN), which were mainly correlated with neutrophil and monocyte fractions. Consensus clustering indicated three molecular subtypes with distinct hub-gene expression patterns. RT-qPCR confirmed significantly increased expression of AQP9, S100A9, and SLC11A1 in AMI compared with sCAD. External validation in GSE60993 supported the diagnostic potential of the identified genes.

Conclusions: AQP9, S100A9, and SLC11A1 are promising immune-related biomarkers and may reflect heterogeneity in inflammatory responses among AMI patients. These findings provide mechanistic clues and candidate targets for future experimental and translational studies.

Background: Coronary heart disease is a leading cause of mortality and disability worldwide, posing significant challenges to public health and necessitating effective strategies for improving patient outcomes and quality of life.This study aims to analyze the health status of Coronary heart disease patients using a patient-reported outcomes scale, exploring differences across five dimensions: physical health, mental health, social health, spiritual health, and specific symptoms. The goal is to provide a foundation for personalized medical interventions and health management.

Methods: This is a Cross-sectional study, 240 patients were selected for latent profile analysis to categorize their health statuses. Key influencing factors were identified through univariate analysis and multivariate logistic regression analysis.

Results: The health status of patients was categorized into three groups, stable and healthy model (n = 146), social psychological fluctuation model (n = 78), and symptom prominent instability model (n = 16). Significant differences were observed among these concerning glycated hemoglobin, high-density lipoprotein, low-density lipoprotein, age, monthly income, education level, and comorbid chronic obstructive pulmonary disease. The health status of social psychological fluctuation model and symptom prominent instability model was independently influenced by glycated hemoglobin, age, education level, and COPD (P < 0.05).

Conclusion: The health status of CHD patients can be classified into distinct categories influenced by multiple factors and comorbidities. As a crucial assessment tool, PRO facilitates the categorization of patient health statuses and provides a reference for precision medicine and personalized interventions. Future efforts should focus on developing targeted interventions tailored to the specific characteristics.

Background: The role of right ventricular (RV) incision during tetralogy of Fallot (TOF) repair remains controversial. Although RV incisions facilitate the closure of ventricular septal defects (VSDs) and relieve right ventricular outflow tract (RVOT) obstruction, concerns remain regarding late ventricular dysfunction. Alternative approaches that limit or avoid RV incision have been advocated; however, most evidence derives from single-center retrospective reports, leaving the clinical impact uncertain.

Method: We retrospectively analyzed 237 patients who underwent repair of TOF at two tertiary centers between 2015 and 2019. Patients were stratified into three groups: Group 1 (no RV incision), Group 2 (incision confined to the infundibulum), and Group 3 (incision extending beyond the infundibulum). The primary endpoint was major adverse events (MAEs, defined as in-hospital mortality, need for extracorporeal membrane oxygenation, malignant arrhythmias, delayed sternal closure, reoperation requiring cardiopulmonary bypass, and reintubation). Secondary endpoints included length of intensive care unit (ICU) stay, total hospital stay, ventilation duration, 24-h drainage output, and other postoperative complications. Both crude and propensity score-matched (PSM) analyses were performed.

Results: In crude analyses, delayed sternal closure was more frequent in Group 2 but did not reach statistical significance (P = 0.052), while rates of infection and transfusion were higher in Group 3 compared with Group 1. After PSM, differences between Groups 2 and 3 persisted, whereas Group 1 continued to demonstrate more favorable outcomes, likely reflecting more favorable baseline anatomy. Hemodynamic parameters and residual RVOT gradients were comparable across groups after matching.

Conclusion: The extent of RV incision during repair of TOF was associated with distinct perioperative risk profiles; however, rates of major adverse events did not differ significantly after adjustment for baseline imbalances. The more favorable outcomes observed in patients without an RV incision primarily reflected anatomical advantages rather than an intrinsic superiority of the surgical approach. These findings suggest that RV incision should be minimized when technically feasible while ensuring adequate relief of RVOT to ensure procedural safety. Prospective multicenter studies with long-term, imaging-based follow-up are required to determine the impact of incision strategy on RV function, pulmonary regurgitation, and late outcomes.

Objectives: To evaluate the improvement in the quality of life of surgical cardiac valve disease patients based on their perceptions at three distinct points: preoperative, immediate postoperative, and late postoperative.

Background: Quality of life has been increasingly recognized as a central outcome in cardiovascular care, especially in valvular diseases. Despite the extensive international literature on postoperative recovery and favorable clinical outcomes, few studies have examined quality of life from the patient's perspective within a structured care pathway model, particularly in developing countries such as Brazil. This study contributes by assessing quality of life longitudinally and from the patient's perspective, within an interdisciplinary Care Line Model implemented at a high-complexity cardiovascular center.

Methods: This retrospective, observational longitudinal study included patients with significant valvular disease undergoing surgery. These patients were assessed at three time points by the psychology team: preoperative, immediate postoperative (after discharge from the Intensive Care Unit and before hospital discharge), and late postoperative (6 months after hospital discharge). Quality of life was measured from the patients' perspective using two instruments: SF-36 and EQ-5D, as part of the surgical valve disease care model implemented at the institution.

Results: Patients reported significant improvements in quality of life after surgery. The EQ-5D and EQ-VAS scores increased substantially in the late postoperative period compared to preoperative values. SF-36 domains, particularly functional capacity, vitality, pain, general health, and mental health, showed robust improvement. All analyses were based strictly on comparisons between assessment points; no assumptions of linear postoperative improvement were made.

Conclusion: Valve surgery is associated with meaningful improvements in patients' perceived quality of life, especially regarding mobility, pain/discomfort, self-care, and emotional and social functioning. These findings reinforce the relevance of multidisciplinary and longitudinal follow-up and demonstrate the potential contribution of structured care pathways, such as the Surgical Valve Disease Care Line, to enhance recovery and patient-centered outcomes.

Objective: Currently, there is a lack of clinical studies on how to stratify endothelial dysfunction based on the severity of co-existing hypertension and OSAHS. This evidence gap hinders clinicians' ability to accurately assess disease burden and determine the best timing and intensity of intervention for these high-risk patients. This study aimed to investigate the impact of hypertension combined with OSAHS on vascular endothelial function.

Methods: Patients aged 35-60 years with hypertension and OSAHS were consecutively recruited from the outpatient department of the Department of Cardiology at the Chengdu Pidu District People's Hospital, from July 1, 2023, to December 31, 2023. AHI, RHI and endothelial damage-related markers [Von Willebrand Factor (VWF), Vascular Endothelial Growth Factor (VEGF), and Endothelial Microparticles (EMPs)] were measured. Routine examination data were collected.

Results: The correlation analysis between AHI, RHI, and hypertension grade and hypertension stage showed correlation coefficients less than 0.2, indicating almost no linear relationship. The correlation coefficient between AHI and RHI was -0.58 (P < 0.001). The correlation coefficients between AHI and VWF, VEGF, and EMPS were 0.56 (P < 0.001), 0.49 (P < 0.001), and 0.66 (P < 0.001). The correlation coefficients between RHI and VWF, VEGF, and EMPS were -0.62 (P < 0.001), -0.63 (P < 0.001), and -0.67 (P < 0.001). The RHI showed significant inverse associations with the studied variables.A 1-SD increase in AHI, vWF, VEGF, and EMPs was associated with a decrease in RHI of 0.02, 0.62, 0.63, and 0.67 units, respectively. (β = -0.02, adjusted β = -0.60, P < 0.01; β = -0.62, adjusted β = -0.64, P < 0.01; β = -0.63, adjusted β = -0.64, P < 0.01; β = -0.67, adjusted β = -0.71, P < 0.01).

Conclusion: In patients with hypertension combined with OSAHS, RHI can be used as an important indicator in routine tests of vascular endothelial function to predict the degree of vascular endothelial injury.

Postoperative atrial fibrillation (POAF) affects 38%-63% of patients undergoing surgical replacement for calcific aortic valve stenosis (CAVS), increasing morbidity, stroke risk, and hospital stay. POAF results from an interplay between pre-existing arrhythmogenic substrates, acute surgical triggers, unresolved inflammation, and autonomic nervous system (ANS) imbalance. Specialized pro-resolving mediators (SPMs) orchestrate inflammation resolution and tissue homeostasis; their deficiency may sustain valvular inflammation and promote arrhythmogenesis. Transcutaneous vagus nerve stimulation (tVNS) is a non-invasive approach that enhances parasympathetic tone, restores sympathovagal balance, and modulates inflammatory pathways. While tVNS has been applied postoperatively, its preoperative, preventive use in POAF has not been explored, representing a novel therapeutic strategy. In patients with CAVS, preoperative tVNS could reduce POAF by regulating ANS activity and limiting perioperative inflammation. Mechanistic insights may be gained through perioperative sampling, analysis of excised valvular and atrial tissue, and biomechanical assessments comparing stimulated and control groups. Preoperative tVNS thus offers a promising strategy to prevent POAF while addressing valvular inflammation, bridging translational physiology with clinical cardiology and potentially opening new avenues for the management of CAVS.

Objective: To develop and validate a nomogram for the individualized prediction of persistent coronary artery aneurysms (CAAs) in children with Kawasaki disease (KD) who have developed CAAs in the acute phase.

Methods: This retrospective cohort study enrolled children diagnosed with KD and complicated by CAA between September 2015 and December 2023. The primary outcome was defined as the persistence of CAA 90 days after disease onset. Predictor selection was performed using 1,000 bootstrap resamples combined with LASSO regression for stability. A predictive model was constructed using multivariate logistic regression. The model's discrimination, calibration, and clinical utility were assessed by the area under the receiver operating characteristic curve (AUC), calibration curves, and decision curve analysis (DCA).

Results: A total of 135 children were included, of whom 80 (59.3%) had persistent CAAs. Stability selection identified the maximum coronary artery Z-score (ZM), age < 12 months (Age1), and total bile acid (TBA) as key predictors. The parsimonious model (Model B) built on these predictors demonstrated excellent performance, with an optimism-corrected AUC of 0.933 (95% CI: 0.905-0.960). It was well-calibrated, and DCA showed a positive net benefit across a wide threshold probability range of 5%-100%.

Conclusion: This study successfully developed a nomogram based on ZM, Age1, and TBA. This tool can effectively identify KD children at risk of persistent CAAs, providing an intuitive and quantitative decision-making aid for precise risk stratification and optimized long-term management in this high-risk population.