Current Cardiology Reviews最新文献

Ferroptosis, an instance of iron-dependent programmable cell death that results from oxidative stress & lipid peroxidation, has garnered interest due to its associations with cardiovascular diseases, such as atherosclerosis, myocardial infarction, as well as heart failure. Unlike necrosis or apoptosis, ferroptosis involves unique metabolic pathways that disrupt cellular redox balance and lipid homeostasis, leading to substantial cell damage in cardiovascular tissues. It is becoming recognized that phytoconstituents-bioactive compounds derived from plants-can modify ferroptosis pathways and provide cardioprotective advantages. Compounds including curcumin, resveratrol, quercetin, tanshinone IIA, and epigallocatechin gallate (EGCG) have shown potential in preclinical studies by concentrating on significant ferroptotic processes. Finally, by controlling iron homeostasis, boosting antioxidant responses (such as Nrf2 pathway activation), and reducing lipid peroxidation, these phytochemicals may mitigate ferroptosisinduced cardiac cell death. In animal studies, these natural compounds have shown promise in reducing oxidative damage and improving heart function after injury. This article summarises the mechanisms via which a variety of phytoconstituents influence ferroptosis and discusses their potential as an adjuvant treatment for CVD. While these findings are encouraging, further research is needed to use them in clinical settings, with a focus on long-term safety in human populations, optimal dose, and absorption. The cardioprotective properties of phytoconstituents, which focus on ferroptosis, may provide a unique, plant-based therapeutic strategy for the treatment of CVDs.

Vascular aging profoundly affects the onset of cardiovascular diseases in the elderly, mostly as a result of mitochondrial dysfunction. This review examines the protective roles of mitochondrial-derived peptides such as humanin, MOTS-c, and small humanin-like peptides in mitigating vascular aging. These peptides, encoded by mitochondrial DNA, are crucial for regulating apoptosis, inflammation, and oxidative stress, which have a major role in vascular health. MDPs have significant prospects as therapeutic and biomarker possibilities for the early diagnosis and intervention of vascular aging. MDPs influence the functions of endothelial and vascular smooth muscle cells by modulating critical signaling pathways, including AMPK, mTOR, and sirtuins. These pathways are essential for facilitating cellular metabolism, enhancing stress resilience, and prolonging longevity. Moreover, MDPs are essential in mitochondrial bioenergetics and dynamics, vital for mitigating endothelial dysfunction and enhancing vascular resilience. Furthermore, MDPs contribute to immunological modulation and the regulation of inflammatory responses, underscoring their potential therapeutic applications in the treatment of age-related vascular disorders. This review analyzes the various functions of MDPs in vascular health and their therapeutic importance, advocating for more studies to optimize their clinical benefits. By understanding the comprehensive roles and mechanisms of these multifunctional peptides, we can better appreciate their capacity to prevent and treat vascular aging and associated cardiovascular disorders. Future research should aim to further elucidate their therapeutic effects and optimize their clinical applications.

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Introduction: The PCSK9 enzyme is present mainly in the liver and is responsible for the degradation of LDL-C receptors. Currently, there are some drugs that inhibit this enzyme, such as alirocumab and evolocumab. Consequently, these drugs reduce serum LDL-C levels. Therefore, a systematic review and a meta-analysis were carried out in order to compare alirocumab against evolocumab in reducing cardiovascular outcomes.

Methods: This systematic review was carried out in accordance with PRISMA and was registered in PROSPERO (CRD42024573217). The following databases were searched on July, 9, 2024: Pubmed, Web of Science and Scopus. Randomized clinical trials with a control group were included and meta-analyses were performed to assess relative risk (RR). The random effects model was used in heterogeneous samples. The articles were distributed into 2 subgroups: use of alirocumab and evolocumab.

Results: Initially, 2,213 articles were found, of which 6 were included. In total, 62,119 patients participated. The RR values were significant for alirocumab in the following outcomes: myocardial infarction (MI) 0.85 (95% CI 0.77-0.93), stroke 0.75 (95% CI 0.60-0.94) and hospitalization for unstable angina 0.58 (95% CI 0.39-0.86), while for evolocumab they were significant for MI 0.75 (95% CI 0.68-0.83) and coronary revascularization 0.81 (95 CI % 0.75-0.88). There was a statistically significant difference between the drugs for hospitalization for unstable angina (p=0.02).

Discussion: This study highlights the benefits of PCSK9 inhibitors, especially alirocumab, in reducing major cardiovascular events. Alirocumab significantly lowered hospitalizations for unstable angina, with a 42% reduction, and showed favorable outcomes in reducing myocardial infarction, coronary revascularization, and stroke. These reductions are clinically meaningful, as they lower morbidity, improve patient quality of life, and reduce healthcare costs. Both alirocumab and evolocumab are effective and safe, offering important therapeutic options for high-risk cardiovascular patients.

Conclusion: The use of alirocumab is preferable if the focus is to avoid hospitalizations for unstable angina or stroke, while evolocumab may be an option if one wants to avoid coronary revascularization. Both drugs are effective in reducing cardiovascular outcomes, but alirocumab was superior to evolocumab.

Objective: The objective of this study was to compare the quality of life and hemodynamic changes before and after transcatheter atrial septal shunt implantation.

Methods: A systematic search was conducted in the Cochrane Library, PubMed, and Embase from inception to September 2023 for studies reporting on hemodynamics or quality of life in patients with chronic heart failure after atrial septal shunt implantation. A meta-analysis was performed, in which a total of 1026 participants from 13 articles were included.

Results: Following the implantation, pulmonary capillary wedge pressure (PCWP) decreased by 2.60 mmHg. Right atrial pressure (RAP) increased by 1.30 mmHg and left ventricular ejection fraction (LVEF) increased by 2.13%. However, there were no significant differences in cardiac output and mean pulmonary artery pressure (mPAP) after operation. Minnesota Living with Heart Failure (MLWHF) Score decreased by -19.28, while the Kansas City Cardiomyopathy Questionnaire (KCCQ) score increased by 25.41. Moreover, 6-minute walking distance (6MWD) increased by 32.22 m. The results of subgroup analysis showed that for patients with heart failure with preserved ejection fraction (HFpEF) and heart failure with mildly reduced ejection fraction (HFmrEF), LVEF increased by 3.09% while CO increased by 1.01 L/min after operation. Meanwhile, PCWP significantly decreased by 2.67 mmHg and MLWHF scores decreased by 19.28. Additionally, 6MWD significantly increased by 27.5 m. However, there were no significant changes in RAP and mPAP after operation. For patients with heart failure with reduced ejection fraction (HFrEF), interatrial shunt device implantation did not achieve a significant increase in LVEF.

Conclusion: These findings suggest that while atrial septal shunt implantation might not yield LVEF elevation among patients with HFrEF, it improves hemodynamic parameters, exercise endurance, and QoL among individuals with HFpEF/HFmrEF.

Enhancer RNAs (eRNAs), a class of non-coding RNAs transcribed from enhancer regions, have emerged as critical regulators of gene expression in cardiovascular diseases (CVDs), which are among the leading causes of morbidity and mortality in China. The pathogenesis of CVD is complex, involving precise regulation of diverse biological processes. Recent advances in epigenetics have highlighted the pivotal role of eRNAs in gene regulation. This review summarizes the fundamental characteristics of eRNAs and their mechanisms of action in CVD, focusing on how they regulate gene expression through enhancer-promoter looping, chromatin remodeling, and transcriptional control. Key eRNAs, including IRENES, CARMEN, LINC00607, HERNA1, PSMB8-AS1, and WISPER, are discussed in detail, emphasizing their roles in pathological processes, such as cardiac development, vascular remodeling, atherosclerosis, and fibrosis. These eRNAs interact with transcription factors and others to influence cardiovascular gene regulatory networks. Advances in high-throughput sequencing have identified eRNAs as potential biomarkers and therapeutic targets in CVDs, offering implications for diagnosis, treatment, and precision medicine. For instance, targeting CARMEN may attenuate atherosclerosis, while LEENE could address endothelial dysfunction. Despite their therapeutic potential, further studies are needed to elucidate the mechanisms underlying eRNAs function and their roles in CVD pathogenesis. A deeper understanding of eRNAs may pave the way for novel therapeutic strategies in cardiovascular medicine.

Introduction: This study aimed to assess the association of renal impairment (RI) severity on short and mid-term outcomes in patients undergoing cardiac surgery for infective endocarditis (IE).

Methods: Patients undergoing cardiac surgery for IE between January 2010 and October 2022 were included. They were stratified based on preoperative renal function into four groups: Normal (N: Creatinine clearance (CrCl) >85mL/min), moderate RI (M: CrCl 51-85mL/min), severe RI (S: CrCl ≤50mL/min), and haemodialysis-dependent (H). Each group was compared with group N. Survival analysis was performed using Kaplan-Meier curves.

Results: A total of 487 patients (N: 198; M: 154; S: 96; H: 39) were included. Mean age 55.92 ± 14.60 years, 375 (77%) males. Groups M, S, and H vs N demonstrated more atrial fibrillation [17 (11.0%), 20 (20.8%), 6 (15.4%) vs 8 (4.0%); p<0.05]. Groups S and H vs. N had increased incidence of left ventricular ejection fraction <50% [43 (44.8%), 22 (56.4%) vs 43 (21.7%); p<0.001] and preoperative cardiogenic shock [16 (16.7%), 13 (33.3%) vs 9 (4.5%); p<0.001]. The need for postoperative haemodialysis was 21 (13.6%) in M and 23 (23.0%) in S vs. 13 (6.6%) in N (p<0.05). In-hospital mortality was 13 (8.4%), 21 (21.9%), and 11 (28.2%) vs. 12 (6.1%) (p=0.388, <0.001, <0.001), and mortality at a mean of 69.1months was 49 (31.8%), 46 (46.9%), 30 (76.9%) vs. 49 (24.7%) (p=0.142, <0.001, <0.001) in groups M, S, H vs. N, respectively.

Conclusions: The incidence of renal impairment in patients with IE undergoing surgery remains high. Early and mid-term outcomes of those with severe RI and haemodialysis dependence are significantly worse.

Heart failure (HF) is a complex clinical syndrome that arises from structural or functional impairment of ventricular filling or ejection of blood, resulting in previous characteristic symptoms of fatigue, dyspnea, and fluid retention. Among the complications of heart failure is the development of spontaneous echo contrast (SEC), characterized by a smoke-resembling appearance on echocardiograms, which indicates blood stasis in heart chambers. Despite being identified as an echocardiographic marker in the left atrium that correlates with thrombus formation and causes thromboembolic events, the clinical importance of left ventricular spontaneous echo contrast (LV-SEC) and the appropriate management for patients with this condition remain uncertain due to insufficient data. Anticoagulant therapy is generally recommended for patients with established left ventricular thrombus (LVT). However, for patients with heart failure with reduced ejection fraction (HFrEF) and sinus rhythm (SR), as a result of a decrease in thromboembolic events over time, it is typically not recommended. The main challenge lies in assessing the thromboembolic risk and determining appropriate management in patients with HFrEF, sinus rhythm (SR), and left ventricular spontaneous echo contrast (LV-SEC), compared to those with left ventricular thrombus (LVT) and those with HFrEF and SR without LV-SEC. The aim of this paper is to review the guidelines and trials on clinical characteristics, outcomes, and management of patients with LV-SEC and compare the suggested management with the established management for LVT and HF patients with sinus rhythm without LV-SEC.

Introduction This study aimed to investigate the correlation between the differences in pulse wave harmonic indices between the left and right hands and the SYNTAX score and to explore the potential of pulse wave harmonics in predicting the degree of coronary artery lesions. Methods The arterial pressure wave signals from both hands of the patients scheduled for coronary angiography were recorded using photoplethysmography. According to the "visceral resonance theory," taking integer multiples of the heartbeat from 0 to 11 as the resonance frequencies, the collected arterial pressure waves were decomposed into the 0th to 11th harmonics via the Fourier transform method. The harmonic characteristics were quantified by amplitude (Cn), phase (Pn), and energy (Dn) (n is the harmonic serial number), and the coefficient of variation of the indices was calculated and suffixed as CV. The difference between the measured values of the left- and right-hand parameters of the same patient was calculated (ΔCn,ΔPn,ΔDn,ΔCnCV,ΔPnCV), and the absolute value of the difference was obtained (|ΔCn|, |ΔPn|, |ΔDn|, |ΔCnCV|, |ΔPnCV|). Based on the coronary angiography imaging data, SYNTAX scores were computed for all participants, who were stratified by gender into male and female cohorts. For each group, logistic regression models were established with SYNTAX score≥22 as the dependent variable, and harmonic index differences as the independent variables. To determine the best prediction model, the Akaike Information Criterion (AIC) was used and model with the lowest score was selected. Finally, the discriminant ability of the prediction model was evaluated using the ROC curve analysis and the Bootstrap internal validation method. Results: A total of 348 patients were included, with 249 males and 99 females. In the male group, the discriminant model was based on |ΔC10|,ΔD6, |ΔD9|, |ΔD10|, |ΔP8|, |ΔP10|, ΔP1CV, and ΔC9CV, with the minimum AIC value of 105.47, the area under the ROC curve (AUC) of 0.89, and the average AUC of 0.85 in the Bootstrap internal validation. In the female group, the discriminant model was based on |ΔD2|, |ΔD3|, |ΔD5|, |ΔD6|, |ΔD9|, |ΔC2CV|, |ΔC4CV|, |ΔC5CV|, | ΔC6CV|, and |ΔC9CV|, with the minimum AIC value of 59.34. The AUC of the ROC curve of this prediction model was 0.92, and the average AUC in the Bootstrap internal validation was 0.84. Discussion In this study, the degree of coronary artery occlusion was evaluated through a noninvasive method combined with the SYNTAX score, providing a valuable noninvasive tool for clinical evaluation of CAD. This detection method is easy to operate, has high repeatability, and the equipment is small in size, making it suitable for various environments, it can be operated independently by the patients. Yet, the current study, being cross-sectional, only found an association rather than a causal relationship, calling for future prospective studies to clarify the causal link. Conclusion: The different ch

Background: The estimated prevalence of ventricular extra systole (VES) in the general population is about 1-4% on ECG, but 24-hour Holter monitoring has shown a prevalence of 40-75%. While it may be asymptomatic in many patients, frequent VES persisting for a long time can negatively affect left ventricular (LV) systolic function in patients without structural heart disease. The etiology of VES is not completely known. In this study, we investigated the role of neuropeptide Y (NPY) in the occurrence of VES.

Material and methods: In this study, we included 150 patients with VES and 86 cases without VES as the control group. 24-hour Holter monitoring was performed on all subjects. Patients with VES were divided into two subgroups according to the frequency of VES as those >15,000 (Group 1, n= 48) and <15,000 (Group 2, n= 102). Venous blood was collected from all cases for biochemistry parameters and NPY level measurement.

Results: There were statistically significant differences between the two groups in terms of gender, smoking, LVEF, NPY, total cholesterol, LVEDD, SDNN, SDNNINDEX, RMSD, PNN50, LF, HF, VLF, and LF/HF (p<0.05, for all). Correlation analysis showed a significant positive correlation between serum NPY level and number of VES (r=0.577, p=0.001), LF (r=0140, p=0.032), LVEDD (r=0.162, p=0.013), and LVESD (r=0.290, p=0.001). Conversely, a negative correlation was observed between NPY and RMSSD (r=-0.162, p=0.012), SDNNINDEX (r=-0.136, p=0.037). Multivariate logistic regression analysis showed that NPY (odds ratio [OR]: 1.204; 95% confidence interval [CI]: 1.103-1.315; p=0.001) was an independent predictor of VES development. ROC curve analysis showed that NPY ≥ 47.9 ng/L predicted the occurrence of VES with a sensitivity of 82.0% and specificity of 81.4%. In addition, NPY ≥ 79.8 predicted the frequency of VES with a sensitivity of 85.5% and specificity of 87.3 %.

Conclusion: Our study showed that serum NPY levels may play an important role in the development of VES. Also, it was found that the frequency of VES increased as the NPY level increased.