2025年 · 第05卷第02期

Pulmonary hypertension (PH) is a condition marked by elevated blood pressure in the pulmonary arteries. Advancements have recently been made in understanding PH pathophysiology, methods of diagnosis, risk assessment, and treatment options. Sympathetic nerve activity plays a significant role in the occurrence and development of PH. Percutaneous pulmonary artery denervation (PADN) is a therapeutic approach for PH that targets sympathetic denervation at 3 crucial points in the main pulmonary artery and the orifice of the left pulmonary artery. The Cardiovascular Clinical Research Group and Pulmonary Vascular Disease Group of the Chinese Society of Cardiology have developed an expert advisory aimed at creating standardized treatment protocols for PH using PADN. The advisory covers experimental foundations, evidence from evidence-based medicine, indications for treatment, and detailed procedural steps for PADN.

Objective: This study aimed to elucidate the effect of the lipopolysaccharides/toll-like receptor 4 (LPS/TLR4) pathway on early atherosclerosis (AS) development and its associated changes in fecal metabolites, thereby providing an experimental foundation for strategies to prevent and treat early AS. Methods: Twelve Tibetan miniature pigs aged 4-5 months were divided into normal control (NC) group and AS group (6 pigs in each). The group assignment was primarily based on body weight; Secondary criteria, including glucose, lipid profiles, and inflammatory indices, were considered to ensure balanced baseline characteristics between the 2 groups (all P > 0.05). AS group received a high-fat diet for 16 weeks to establish an AS model, while the NC group received a normal diet. Subsequently, serum levels of lipids and various inflammation and oxidative stress markers were measured. Pathological changes in the aorta and colon tissue, LPS/TLR4 pathway-associated protein expressions in the aorta, as well as occludin and zonula occludens-1 in the colon were also assessed. Proton nuclear magnetic resonance spectra technology was employed for the metabolomic analysis of fecal extracts. Results: The lipid metabolism was disrupted in AS group, with significantly higher total cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol levels ((12.24 ± 5.24) mmol/L vs. (1.86 ± 0.27) mmol/L, P = 0.004,6; (2.39 ± 0.50) mmol/L vs. (0.83 ± 0.07) mmol/L, P = 0.000,5; (6.94 ± 2.87) mmol/L vs. (0.77 ± 0.18) mmol/L, P = 0.003,3), as compared to that in NC group. Serum factors, including LPS, tumor necrosis factor-α, and malondialdehyde levels of AS group were significantly higher than that of NC group ((1,230.00 ± 192.70) EU/L vs. (695.70 ± 213.70) EU/L), P = 0.001,1; (424.20 ± 176.90) ng/L vs. (51.20 ± 26.61) ng/L, P = 0.023,5; (3.60 ± 0.77) nmol/mL vs. (2.62 ± 0.21) nmol/mL, P = 0.025,4). Pathological evaluations revealed prominent lipid deposition area in the aortic arch, thoracic aorta, and abdominal aorta of the AS group compared with that of the NC group (4.17% ± 2.30% vs. 0, P = 0.006,7; 6.23% ± 2.95% vs. 0, P = 0.003,6; 3.78% ± 2.18% vs. 0, P = 0.008,1). TLR4, nuclear factor kappa-B p65, and tumor necrosis factor-α expression in the aorta tissue of the AS group were upregulated, whereas occludin and zonula occludens-1 expression in colon tissues was downregulated. Additionally, metabolomics identified significant differences in 21 metabolites in the feces of the AS group compared to the NC group, with further analysis linking these differences to amino acid metabolism. Conclusions: The Tibetan miniature pig model of early AS induced by high-fat intake displayed pronounced chronic inflammation. Preliminary findings suggest that the underlying mechanisms may be associated with the LPS/TLR4 pathway and intestinal metabolic disorders.

Objective: This study aimed to evaluate the immune cell populations in patients with acute myocardial infarction (AMI). Methods: The keyword "myocardial infarction" was searched in the Gene Expression Omnibus database, and only transcriptomes from peripheral blood studies of patients with AMI within 12 h of symptom onset were included. Patients without myocardial infarction from the same database were included in the control group. The differential analysis of expressed genes, the enrichment of metabolic pathways associated with the significant genes, and the proportions and absolute values of immune cells between 2 groups (AMI and control) were analyzed. To validate the findings, neutrophil and lymphocyte counts were obtained from blood counts and correlated with creatine kinase-MB levels in 22 patients with AMI from Hospital Geral Roberto Santos. Results: Two microarray datasets from the Gene Expression Omnibus database were analyzed, containing a total of 31 eligible blood transcriptome samples. These samples included 14 patients with AMI and 17 non-infarcted patients (control group). Patients with AMI showed significant gene expression differences compared to the control group (P < 0.05). The enrichment analysis of the significant genes revealed an association with immune cells. The proportions of cell populations in patients with AMI from both datasets revealed an increase in neutrophils and a decrease in T and B lymphocytes, which were statistically significant (P = 0.018, P = 0.047, respectively). The analysis of absolute cell numbers demonstrated higher neutrophil values and lower T cell values in patients with AMI compared to the control group (all P < 0.05 in GSE61144 and GSE60993 datasets). The data from Hospital Geral Roberto Santos showed that the percentage of neutrophils showed a positive correlation (r = 0.5, P = 0.018), while the percentage of lymphocytes showed a negative correlation (r = -0.45, P = 0.034) with creatine kinase-MB levels in patients with AMI. Conclusion: This study suggests that data derived from differential cell counts could serve as an additional parameter to diagnose AMI. Neutrophilia and lymphopenia in AMI should not be used as isolated parameters, but they indicate the need for further investigation, particularly in patients with uncertain diagnoses.

Objective: Oral anticoagulation is recommended for stroke prophylaxis in patients with non-valvular atrial fibrillation. Novel oral anticoagulants (NOACs) elicit better renal outcomes than warfarin. However, the differences among individual NOACs remain unclear. In this study, 3 commercially available NOACs—dabigatran, rivaroxaban, and apixaban were compared in terms of renal outcomes. Methods: By December 31, 2017, a search of a database of the New Territories West Cluster of the Hospital Authority of Hong Kong, China identified patients with non-valvular atrial fibrillation taking 1 of the 3 NOACs. Three cohorts (rivaroxaban vs. dabigatran, apixaban vs. dabigatran, and apixaban vs. rivaroxaban) were set up for comparison, and inverse probability of treatment weighting was used to balance the baseline characteristics. Patients were tracked until drug discontinuation or June 30, 2019 (study end date), whichever came first. The primary endpoint included a combination of a greater than 30% decline in the estimated glomerular filtration rate, acute kidney injury, doubling of serum creatinine, and renal failure. The Cox proportional hazards regression model was used for survival analysis. Results: A total of 1,153 patients were included in the analyses. Rivaroxaban was associated with a higher incidence of the primary endpoint compared to dabigatran (hazard ratio: 1.43, 95% confidence interval: 1.20-1.70, P < 0.001). Apixaban was associated with a lower risk compared to rivaroxaban in the analysis of the subgroup of patients with an estimated glomerular filtration rate ≥ 60 mL/(min·1.73 m2) (hazard ratio: 0.62, 95% confidence interval: 0.31-0.94, P = 0.010). No significant differences were observed between dabigatran and apixaban. Conclusions: Rivaroxaban was associated with worse renal outcomes compared to dabigatran in the main cohort and compared to apixaban in the subgroup analysis. Variations in renal outcomes exist among the NOACs.

Atrial fibrillation (AF) is the most common sustained arrhythmia worldwide and is associated with poor clinical outcomes and a huge economic burden on healthcare systems. Optimized anticoagulation, better symptom control via rhythm or rate control, and comprehensive comorbidity/risk factor management are 3 essential pillars of current AF management, where much progress has been made during the past decades. However, numerous challenges in AF management remain at the disease, patient, and population levels, including an incomplete understanding of basic mechanisms that can be clinically targeted; heterogenous progressive natural history; poor correlation between rhythm and symptoms/outcomes; as well as suboptimal detection methods and treatment options. Recent advances in disease perception in combination with modern monitoring devices, state-of-the art computational models, and novel antiarrhythmic drugs and ablation strategies can contribute to addressing these issues, ultimately leading to a paradigm shift in AF diagnosis, classification, and treatment. This narrative review summarizes these key challenges and future opportunities in the field of AF management.

The heart-brain axis involves complex interactions between the cardiovascular and nervous systems via a network of cortical and subcortical structures working with the autonomic nervous system and intracardiac nervous system. Heart-brain interactions may be divided into 2 broad categories: cardiac effects of neurological disease and neurological effects of cardiac disease. The pathogenesis of neurogenic cardiac effects is thought to involve a neurogenic cascade where sudden shifts in autonomic balance lead to an exaggerated catecholamine release. This can occur in acute neurological conditions such as ischemic stroke, intracranial hemorrhage, and epilepsy. Cardiovascular complications include the stroke-heart syndrome, neurogenic pulmonary edema and cardiomyopathy, Takotsubo syndrome, arrhythmias, and even sudden cardiac death. Certain areas of the brain, such as the insular cortex, play key roles in cardiac autonomic regulation, and disorders affecting these areas have greater effects on the heart. On the other hand, cardiac conditions can also adversely impact the neurological system. Atrial fibrillation and left ventricular thrombus can cause cardioembolic strokes, whereas heart failure and severe aortic stenosis have been linked to the development of cognitive impairment. This review aims to provide a broad overview of key topics in neurocardiology as well as delve into the evidence and pathophysiology behind these conditions.

Congenital long QT syndrome (LQTS) is a life-threatening ion channelopathy caused by mutations in genes encoding specific ion channels, which can result in malignant arrhythmia of the torsades de pointes type. LQTS type 4 represents less than 1% of inherited LQTS cases, in contrast to the 90% attributable to types 1-3, it is specifically caused by loss-of-function mutations in the membrane-binding domain of ANK2. Here, a novel ANK2 variant (ANK2c 2245 A>C, resulting in p.Lys749Gln) associated with LQTS type 4 and Wolff-Parkinson-White syndrome was identified in a previously healthy 61-year-old male patient who suffered paroxysmal palpitations and pre-syncope due to recurrent torsades de pointes.