BackgroundCompound dendrobium candidum (CDC) is formulated from Dendrobium candidum and fragrant peony. Preliminary studies have demonstrated that the combination of CDC with conventional antihypertensive medications exhibits significant synergistic effects in lowering blood pressure. The objective of this study was to evaluate the synergistic effect of combining CDC with antihypertensive medications on refractory hypertension in spontaneously hypertensive rats (SHRs) and to elucidate the underlying mechanisms involved.MethodsSHRs were treated with either CDC alone or CDC combined with two or three antihypertensive agents including irbesartan, amlodipine, or terazosin, for a duration of 6 weeks. The alterations in blood pressure, angiotensin II (Ang II), insulin, blood sugar, angiotensin II type I receptor (AT1R), angiotensin II type II receptor (AT2R), insulin receptor, insulin α receptor, and insulin β receptor levels were assessed. Glomerular endothelial cells from refractory SHR were then taken for overexpression and knockdown of AT2R gene and co‐cultured with CDC serum to measure the expression levels of Ang II receptor gene and protein.ResultsIn comparison to the findings observed in the irbesartan + amlodipine + terazosin (IAT) group, the addition of CDC significantly enhanced antihypertensive efficacy. The rate of achieving blood pressure targets (< 150 mmHg) in SHRs with refractory hypertension increased from 0% to 100%. Treatment with CDC significantly reduced the compensatory increase in AT1R and AT2R levels caused by IAT treatment and showed a significant antihypertensive and synergistic effect. Primary glomerular endothelial cells extracted from SHRs and Wistar rats and treated with 0.5% CDC‐containing serum showed significantly reduced AT2R levels in the AT2R‐overexpression condition. The combination of CDC and antihypertensive drugs was effective in reducing the messenger RNA (mRNA) and protein expression levels of AT1R and AT2R in glomerular endothelial cells.ConclusionsCDC in combination with antihypertensive drugs showed a synergistic effect in controlling refractory hypertension. The mechanism of action may be related to the attenuation of excessive expression of AT2R. This study offers a novel approach for the treatment of clinically resistant hypertension.

This review examines the bidirectional relationship between the gut microbiota and cardiovascular diseases (CVDs), aiming to understand how microbial dysbiosis contributes to CVDs, including atherosclerosis, hypertension, and heart failure. Recent research emphasizes the gut microbiota’s role in modulating immunity via SCFAs and tryptophan metabolites, maintaining intestinal barrier integrity, and producing metabolites such as SCFAs (acetate, propionate, butyrate) and pro‐atherogenic TMAO. Dietary patterns, particularly the Mediterranean versus Western diet, significantly influence gut microbiota composition and CVD risk. Polyphenols and exercise have shown positive effects on gut microbiota and cardiovascular outcomes. A significant interplay exists between gut microbiota and cardiovascular health. Dysbiosis and metabolites like TMAO and LPS are implicated in CVD, while SCFAs and a balanced microbiota offer protection. Future research should focus on precision medicine, next‐gen probiotics, optimized FMT, and multiomics approaches to identify personalized CVD therapies.

BackgroundAlthough previous studies have revealed the correlation between inflammatory markers and coronary heart disease (CHD), this study aims to explore the relationship between inflammatory markers and CHD in the male and female population, respectively.MethodsThis study includes participants from the National Health and Nutrition Examination Survey (NHANES) from 2003 to 2018. Inflammatory markers included the following: systemic immune‐inflammation index (SII), lymphocyte‐to‐monocyte ratio (LMR), neutrophil‐to‐lymphocyte ratio (NLR), and platelet‐to‐lymphocyte ratio (PLR). Multivariate logistic regression was performed to investigate the correlation between these inflammatory markers and CHD. The trend test was employed to examine potential linear trend associations, and the restricted cubic splines (RCSs) were utilized to depict nonlinear relationships.ResultsThe NHANES database including 40,177 participants was stratified into two cohorts: the CHD group (n = 1667) and the non‐CHD group (n = 38,510). With further gender stratification, we found that LMR, PLR, and SII all exhibited negatively significant correlation with CHD in the male group, while LMR and NLR were meaningful factors in the female group. We also detected that LMR, PLR, and SII all have nonlinear relationship with CHD in the male group (p for nonlinear < 0.05), while PLR had nonlinear relationship with CHD in the female group (p for nonlinear < 0.05).ConclusionsOur study revealed that LMR, PLR, and SII are significantly negative correlative markers of CHD in males, while LMR and NLR are more accurate predictors of CHD in females.

Sodium-glucose cotransporter-2 (SGLT-2) inhibitors have been established to decrease hospitalizations and cardiac death within all heart failure groups. The exact mechanisms by which the oral antidiabetic medication dapagliflozin achieves this advantage are still unknown. The potential beneficial effects of dapagliflozin on inflammation and the immune system may contribute to these mechanisms. The laboratory and echocardiographic data of 191 consecutive patients who were started on dapagliflozin due to heart failure were compared before and 6 months after the treatment began. The systemic immune-inflammation index (SII) and the systemic inflammation response index (SIRI) were calculated using the following formulae: (platelet × neutrophil)/lymphocyte and (neutrophil × monocyte)/lymphocyte, respectively. The mean age of the patients included in the study was 66.17 ± 10.7 years. A total of 156 patients (81.7%) had diabetes mellitus. Seventy patients (36.6%) had heart failure with reduced ejection fraction (HFrEF), 31 (16.2%) had heart failure with mildly reduced ejection fraction (HFmrEF), and 90 (47.1%) had heart failure with preserved ejection fraction (HFpEF). While no significant change was observed in echocardiographic parameters with dapagliflozin treatment (p > 0.05), a significant decrease was detected in the SII and SIRI (1357.4 ± 1404.3 vs. 805.8 ± 586.7, p < 0.001 and 3.68 ± 3.6 vs. 2.19 ± 1.7, p < 0.001). In these indices, a consistently significant decrease was observed in all groups, irrespective of the type of heart failure and the presence of diabetes mellitus (p < 0.005). With dapagliflozin treatment, the most recent inflammation parameters, SII and SIRI, have significantly decreased. This effect may be one reason for the cardiovascular benefits of dapagliflozin treatment.

ObjectiveThis study investigates the effect of peak glycemia on the no‐reflow phenomenon in patients with ST‐elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI) to examine the relationship between elevated blood glucose (BG) levels and no‐reflow.MethodA total of 252 STEMI patients (81.7% male) who underwent PPCI were enrolled. BG was measured by a glucometer every 6 h for 24 h, starting at the time of patient admission. The maximum measured BG was considered the peak glycemic level. A corrected TIMI frame count (CTFC) of less than 27 was used to define the no‐reflow phenomenon in this study.Results42.4% of participants experienced no flow, with a significant association between this condition and diabetes mellitus, peak glycemia, smoking history, and elevated LDL cholesterol levels. Specifically, peak glycemia levels above 180 mg/dL independently increased the odds of no‐reflow occurrence (OR = 8.16, 95% CI = 4.1–16.2, p < 0.001).ConclusionThe importance of monitoring BG levels in STEMI patients, as well as the critical role of a multidisciplinary approach, regardless of diabetic status, in mitigating the risk of no‐reflow and improving clinical outcomes, should be highlighted.

ObjectivesThis study aimed to evaluate the prevalence and anatomical characteristics of myocardial bridge (MB) using multidetector computed tomography (MDCT) and to investigate its relationship with coronary artery calcification and atherosclerotic burden.MethodsWe retrospectively analyzed 7024 patients who underwent MDCT for cardiac complaints between November 2010 and December 2020. The length and thickness of MBs were measured, and coronary calcification was quantified using the Agatston score. Patients were categorized according to the degree of coronary stenosis (< 50% or ≥ 50%) to assess the association between MB and calcification severity.ResultsThe prevalence of MB was 7.7% (542 patients). The most common complaints in patients with MB were atypical chest pain (76%) and stable angina (24%). MB was most commonly detected in the middle segment of the LAD artery (65.68%). Mild atherosclerotic plaque (31%), moderate atherosclerotic plaque (13%), and severe atherosclerotic plaque and stenosis (5%) were present in 51% of patients with MB. Significant calcification was found in 23% of MB patients, who had higher calcification scores, particularly those with coronary artery stenosis greater than 50%.ConclusionsMDCT serves as an effective noninvasive method not only for detecting MB but also for evaluating concomitant coronary calcification and early atherosclerotic changes. Early identification of calcification in MB patients may guide individualized cardiovascular assessment, focusing on noninvasive imaging, risk factor control, and preventive therapy similar to standard protocols for atherosclerosis management.

ObjectiveBased on the NLR, we aim to investigate the prognostic factors of CHF and establish a nomogram model to predict the OS of CHF patients.MethodsWe selected 566 CHF patients from the NHANES database surveyed between 1999 and 2018 as the study population and randomly divided the data into training and validation sets in a 7:3 ratio. We used multivariate Cox regression analysis to determine the factors affecting the prognosis of CHF patients. Additionally, we evaluated the stratification of the NLR and the nomogram total risk score using the Kaplan–Meier survival curves and log‐rank tests. To evaluate the predictive accuracy of the nomogram, we used the area under the ROC and the calibration curve method. Finally, we used decision curve analysis to explore the value of the nomogram in clinical applications.ResultsMultivariate Cox regression analysis revealed that the NLR, age, and gender were risk factors affecting the OS of CHF patients, whereas hemoglobin and platelets were protective factors. We established a nomogram based on NLR, age, gender, hemoglobin, and platelets and calculated the area under the survival rate curve for 3, 5, and 10 years in both the training and validation sets, indicating good predictive capacity of the model (training set AUCs were 0.822, 0.82, and 0.803, respectively; validation set AUCs were 0.726, 0.769, and 0.775, respectively). Calibration curves and decision curve analysis indicated the model’s accuracy and clinical applicability. The risk stratification was performed using NLR and the nomogram total score, and the Kaplan–Meier survival curves and log‐rank tests showed that CHF patients with higher NLR had worse prognosis and those with lower nomogram total score had better prognosis than those in high‐risk groups. There was a significant difference in OS between the high‐ and low‐risk groups (P < 0.001).ConclusionThis study found that NLR, age, gender, hemoglobin, and platelets are closely related to the prognosis of CHF patients. We successfully constructed a nomogram model based on these factors, which can accurately predict the prognosis of CHF patients

Arrhythmia is an important cause of cardiovascular disease deaths and a serious threat to human health, but the current means of identification are limited. Biomarkers, with the advantages of easy access and rapid detection, have shown significant value in arrhythmia risk prediction, precision diagnosis, and prognosis assessment. In recent years, with the development of molecular biology and multiomics technology, some novel biomarkers have made great breakthroughs in revealing the pathological mechanisms of arrhythmia. However, clinical translation still faces challenges such as a lack of standardization of assays and insufficient clinical prospective validation. This review comprehensively searched studies published between 2010 and 2025 in PubMed, Web of Science, Embase, and CENTRAL databases, focusing on the mechanisms underlying the role of arrhythmia biomarkers in inflammation, fibrosis, autoimmunity, and electrical remodeling and clinical translation potential. Future research should focus on the combined application of multiple biomarkers and the discovery of subtype-specific markers. Conducting large-scale, multicenter studies to validate these biomarkers and ultimately integrate them into clinical practice is crucial for advancing biomarker-guided individualized antiarrhythmic therapy.

[This corrects the article DOI: 10.1155/crp/9970541.].

[This corrects the article DOI: 10.1155/crp/2729462.].