Cardiology Research and Practice最新文献

Background: 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.

Method: 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.

Results: 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).

Conclusion: 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.

Background: Although 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.

Methods: This 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.

Results: The 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).

Conclusions: Our 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.

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.

Objective: Based on the NLR, we aim to investigate the prognostic factors of CHF and establish a nomogram model to predict the OS of CHF patients.

Methods: We 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.

Results: Multivariate 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).

Conclusion: This 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.

Objectives: This 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.

Methods: We 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.

Results: The 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%.

Conclusions: MDCT 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.

Background: Mild alanine transaminase (ALT) elevation is common in older patients with acute myocardial infarction (AMI), but its prognostic value and implications for statin therapy remain unclear.

Methods: This retrospective cohort study included 321 AMI patients aged ≥ 75 years admitted from 2014 to 2019 at Guangdong Provincial People's Hospital. Mild ALT elevation was defined as ALT between the upper limit of normal (ULN) and 3 × ULN, and significant elevation as ALT > 3 × ULN. Patients were grouped by admission ALT into normal (N, n = 201), mildly elevated (ME, n = 104), and significantly elevated (SE, n = 16). Logistic regression analyses in SPSS 26.0 and R 3.4.3 assessed the association between ALT levels and in-hospital mortality, adjusting for cardiac function, infarct size, renal function, and treatment factors.

Results: Among survivors with elevated ALT, 87.4% achieved normalization before discharge. Statin intolerance was identified in 58 patients (18.9%) at admission and persisted in 6.7% at discharge. The ALT-ME group had significantly higher statin intolerance (36.5% vs. 2.0%, p < 0.001) and higher in-hospital mortality (18.3% vs. 6.0%, p = 0.001) compared with the ALT-N group. Logistic regression analysis demonstrated that ALT elevation was independently associated with higher in-hospital mortality (per 10 U/L ALT elevation, odds ratio 1.164, p = 0.010).

Conclusion: In older patients with AMI, mild elevation in ALT levels upon admission is associated with worse in-hospital outcomes, and statin intolerance is common and mostly reversible. Short-term substitutes for statins should be considered in these patients.

Introduction: Transducin beta-like 1 X-linked receptor 1 (TBL1XR1) is significantly upregulated in the peripheral blood of patients with coronary artery disease (CAD). This study aimed to validate the differential expression of TBL1XR1 in CAD and investigate its role in CAD progression using RNA interference.

Methods: The expression of TBL1XR1 at the mRNA and protein levels was detected in patients with CAD and controls using reverse transcription-polymerase chain reaction (RT-PCR) and western blotting. Additionally, the effects of TBL1XR1 gene silencing in human liver cells through RNA interference on PPARα expression and intracellular triglyceride (TG) levels were determined.

Results: TBL1XR1 expression was significantly higher in the peripheral blood of CAD patients compared to controls at both mRNA (1.71 ± 0.96 vs. 1.00 ± 0.34, p < 0.01) and protein levels (0.41 ± 0.19 vs. 0.13 ± 0.07, p = 0.038). Logistic regression analysis revealed that high TBL1XR1 expression is an independent risk factor for CAD. Relative TBL1XR1 expression positively correlated with serum TG levels (rs = 0.56, p < 0.01) and Gensini score (rs = 0.53, p < 0.01), indicating an association with CAD severity. In human liver cells, TBL1XR1 silencing significantly increased peroxisome proliferator-activated receptor alpha (PPARα) expression at both mRNA (p < 0.05) and protein levels (p < 0.01) while reducing intracellular TG levels (0.24 ± 0.16 vs. 0.51 ± 0.09, p < 0.01).

Conclusion: TBL1XR1 is a key factor for risk assessment, diagnosis, and evaluating coronary lesion severity in patients with CAD. Its role in promoting atherosclerosis initiation and development may be associated with regulation of TG metabolism via the PPARα pathway.

Objective: To explore the feasibility of continuous low-dose isoproterenol (ISP) in identifying atrial fibrillation (AF) triggers under conscious sedation and to investigate the association between unmappable triggers and postablation recurrence.

Methods: In 50 PAF patients (Group 1), standardized ISP infusion (2-4 μg/min) was administered to provoke triggers, followed by adenosine triphosphate (ATP) challenge (30-40 mg) if no arrhythmia was induced. A matched control cohort (n = 96, Group 2) was selected based on baseline characteristics. Pulmonary vein isolation (PVI) was performed in all patients. Those with mappable triggers underwent additional ablation based on triggers. Additional ablation for other patient was guided by operators' discretion.

Results: In Group 1, provocative testing identified mappable triggers in 35 patients (Group 1A: 34 PV triggers and 10 non-PV triggers) and unmappable triggers in 5 (Group 1B), with 10 patients showing no inducible arrhythmia (Group 1C). After 12-month follow-up, Group 1B showed significantly higher recurrence than all other groups (60.0% vs. Group 1A: 5.7%, Group 1C: 0%, and Group 2: 14.6%; p < 0.05).

Conclusions: Continuous low-dose ISP challenge provides a pragmatic approach for intraprocedural AF trigger identification, particularly under conscious sedation. The high recurrence rate in patients with unmappable triggers underscores the imperative for advanced mapping modalities to precisely localize arrhythmogenic foci origins.

Introduction: Angiogenesis is a critical adaptation to regular physical exercise, primarily driven by hypoxia-inducible factor-1 alpha (HIF-1α). However, prolonged exercise has been associated with the downregulation of HIF-1α, potentially mediated by increased expression of its negative regulators, prolyl hydroxylase domain (PHD) and factor-inhibiting HIF-1 (FIH).

Objectives: This study aimed to investigate the effects of short-term (acute) and long-term (chronic) moderate-intensity exercise on HIF-1α, PHD, and FIH mRNA expression in Wistar rat hearts.

Methods: Twenty Wistar rats (age: 8 weeks, body weight: 200-250 g) were divided into four groups: acute control (AC) (15 days) (n = 5), acute exercise (AE) (15 days) (n = 5), chronic control (CC) (8 weeks) (n = 5), and chronic exercise (CE) (8 weeks) (n = 5). The exercise groups underwent moderate-intensity treadmill exercise with 20 m/min for 30 min each day for 5 times a week. At the end of the experiment, rats were sacrificed 1 h (acute group) and 24 h (chronic group) after exercise using isoflurane anesthesia, followed by cervical dislocation. Left ventricular heart muscle samples were collected for mRNA expression analysis of HIF-1α, PHD, and FIH using real-time PCR.

Results: Exercise significantly altered the expression of HIF-1α, PHD, and FIH. HIF-1α mRNA was significantly higher in the AE group versus AC (AC vs AE, p=0.006) and in the CE group versus CC (CC vs CE, p=0.004). PHD expression likewise increased with exercise (AE vs AC, p=0.001; CE vs CC, p ≤ 0.001). In contrast, FIH showed no significant differences (acute p=0.472; chronic p=0.095). Exploratory one-way analyses confirmed overall group effects for HIF-1α (p ≤ 0.001) and PHD (p=0.016), but not for FIH (p=0.105).

Conclusion: Chronic moderate-intensity exercise upregulates the expression of HIF-1α negative regulators (PHD and FIH) in the myocardium, suggesting a shift from acute hypoxia-driven responses to oxygen-dependent regulation. These findings offer insight into the molecular adaptations of cardiac tissue to prolonged exercise and their potential role in angiogenesis regulation.

Background: Andersen-Tawil syndrome (ATS) is a rare inheritable potassium channelopathy, accompanied by ventricular arrhythmias due to long QT intervals, muscle weakness, and dysmorphic features. Next-generation sequencing can identify the genetic causes of the phenotype.

Methods: Whole-exome sequencing (WES) was performed on a 12-year-old girl with long QT syndrome and dysmorphic features. Sanger sequencing was subsequently used to confirm the variant and perform segregation analysis in the proband and all available family members.

Results: WES identified a novel homozygous likely pathogenic missense variant (chr17, c.G598A, p.V200M; hg19; NM_017755.5) in KCNJ2 in the proband. Some of her family members were heterozygous for the variant but remained asymptomatic with no cardiac manifestation.

Conclusions: We propose that patients with dysmorphic skeletal findings and cardiac arrhythmias be evaluated via NGS for possible genetic variants.