Current vascular pharmacology最新文献

The adventitia, the artery's most intricate layer, has received little attention.. During atherosclerosis, adventitia components undergo significant changes, such as angiogenesis, lymphangiogenesis, Artery Tertiary Lymphoid Organ (ATLO) formation, axon density increase, fibroblast activation, and stem cell differentiation. The reasons behind these changes and their contribution to atherosclerosis are beginning to be understood. In this review, we summarize the adventitia components and their role in normal arteries and then discuss the changes, pathogenesis, and potential clinical application of the adventitia in atherosclerosis.

Neutrophil elastase (NE), a major protease in neutrophils, is important in promoting inflammation and multiple pathological processes. While NE is released abundantly in ischemiareperfusion (I/R) injury, the intricate relationship between NE and I/R injury remains unclear. We examine several aspects of how NE is involved in I/R injury. We also discuss the possibility of NE inhibitors used for abbreviating various types of I/R injury, such as myocardial infarction, based on preclinical research and clinical trials. Furthermore, we highlight the key question, the balance of NE and NE inhibitors, and propose new research directions. This review is useful for understanding the intrinsic interplay between NE and I/R injury-related diseases and expects to facilitate the development of effective NE inhibitors applied for I/R injury.

Background: Cardioimmunology is an emerging branch of medicine whose development has been facilitated by more sophisticated diagnostic procedures. Recent studies have mainly focused on the immune response during myocardial infarction (MI), and there is evidence that both resident and external immune cells participate in acute inflammatory disease, as well as tissue remodeling. Cardiac Innate Immune Cells: Following MI, macrophages, dendritic cells (DCs) and mast cells (MCs) are the main players in the heart. Under steady-state conditions, cardiac resident macrophages (CRMs) protect the heart against stress and infectious events, being involved in cell and matrix turnover, as well as phagocytosis of apoptotic cells. Moreover, CRMs contribute to the resolution of inflammation via release of interleukin (IL)-10, and efferocytosis of dying cells. Conversely, CCR2+ monocyte-derived macrophages promote inflammation in the acute phase of myocardial damage, with the release of pro-inflammatory cytokines. Conventional (c) DCs possess enhanced capacity to present antigens to T lymphocytes. In MI patient autopsies, massive infiltration of T helper (Th) cells and CDs has been detected in the myocardium. Cardiac MCs play a dual role during MI, with the production of cytokines for early inflammatory response, and the release of anti-inflammatory cytokines, IL10 and IL-13 during the resolution phase. Adaptive Immune Response: In experimental coronary artery ligation, the myocardium is infiltrated with Th1, Th2, Th17, and T regulatory (TREG) cells, which participate in the acute inflammation. In cardiac repair, T cell reparative response is mediated by TREG cells, with improved ventricular remodeling and function post-ischemia.

Specific aims: In this review, emphasis will be placed on the innate and adaptive immune response during and post-MI. At the same time, immunotherapy-based cardiac failure following chimeric antigen receptor T-cell and immune checkpoint inhibitory therapy will be pointed out.

Background: Gut microbiota-derived metabolite Trimethylamine-N-oxide (TMAO) is increasingly recognized as a potential novel prognostic biomarker for cardiovascular disease. Our research work aimed to investigate the potential utility of TMAO measurement in patients with STelevation Myocardial Infarction (STEMI).

Methods: We performed a systematic literature search in PubMed from inception to the 1st of February 2024 to identify all studies examining the association between plasma TMAO levels and disease complexity or clinical outcomes in STEMI patients.

Results: A total of eight prospective cohort studies were included, encompassing a total of 2,378 STEMI patients. Three of the studies provided only in-hospital evidence (i.e., increased odds for more severe coronary artery disease, plaque rupture, and plaque healing in patients with increased TMAO levels). Four studies examined the long-term prognostic value of TMAO after 10-12 months of follow-up post-STEMI (i.e., increased risk of adverse cardiovascular events in patients with increased TMAO levels), while one study provided data for both in-hospital and mid-term prognosis, indicating that 4-months after STEMI patients with greater TMAO elevation had larger infarct size.

Conclusion: Higher TMAO levels were associated with a greater prevalence of high-risk coronary plaque characteristics and worse in-hospital and follow-up outcomes in STEMI patients. Further study is needed on whether modulating the diet-dependent TMAO levels could improve clinical outcomes in these patients.

Registration number: [(OSF): https://doi.org/10.17605/OSF.IO/WNG8V].

Introduction: Sodium Glucose cotransporter-2 inhibitors (SGLT2is) possess pleiotropic effects, such as antioxidant, antifibrotic, anti-inflammatory, and vascular remodeling activities. Considering the lack of literature, a network meta-analysis was conducted to explore the impact of SGLT2is on endothelial dysfunction and arterial stiffness in the diabetic population.

Methods: Electronic databases were searched to identify randomized clinical trials evaluating the effects of SGLT2is on outcomes, such as Flow-mediated Vasodilation (FMV), Pulse Wave Velocity (PWV), and Augmentation Index (AIx). Direct, indirect, and mixed treatment comparisons generated pooled estimates using random-effects modeling. Effect sizes were reported as Hedges' g with 95% Confidence Interval (95% CI). Bootstrap and permutation meta-analyses were performed using ranking plots. The certainty of evidence was graded.

Results: Twelve low risk of bias articles (706 participants) were included. SGLT2is were associated with significant improvements in FMV (g: 0.48; 95% CI: 0.08, 0.88), confirmed by bootstrap metaanalysis (g: 0.48; 95% CI: 0.1, 0.85) and permutation meta-analysis of FMD (g: 0.48; 95% CI: 0.05, 0.9). Within SGLT2is, dapagliflozin (g: 0.39; 95% CI: 0.14, 0.65) and empagliflozin (g: 0.66; 95% CI: -0.65, 1.97) significantly improved FMV, and dapagliflozin (g: -0.61, 95% CI: -0.98, -0.24) and tofogliflozin (g: -3.51; 95% CI: -4.05, -2.98) significantly improved PWV. A low risk of publication bias was observed, and the ranking plots revealed dapagliflozin to have the best probability (0.99) of being the most effective for improving FMV. Low certainty of evidence was observed for all outcomes.

Conclusion: SGLT2 inhibitors improve endothelial function and arterial stiffness in the diabetic population. Clinical studies evaluating the association between improvements in endothelial function with SGLT2is and reduced adverse cardiovascular and cardiorenal events and mortality are urgently needed.

Introduction/objective: Atrial fibrillation (AF) could present with slow ventricular-response; bradycardia could facilitate the emergence of AF. The conviction that one "does not succumb" from bradycardia as an escape rhythm will emerge unless one sustains a fatal injury following syncope is in stark difference with ventricular tachyarrhythmia (VA), which may promptly cause cardiac arrest. However, this is not always the case, as a life-threatening situation may emerge during the bradycardic episode, i.e., the development of bradycardia-induced VAs, which could be fatal if there is no prompt intervention.

Methods: An extensive review of the literature was undertaken with key words including but not limited to AF, bradycardia, bradyarrhythmia, AF and bradycardia, slow ventricular response, sinus node dysfunction, sick sinus syndrome, tachycardia-bradycardia syndrome.

Results: AF is the commonest cardia arrhythmia worldwide and may be part of sick sinus syndrome, commonly presenting as bradycardia-tachycardia syndrome. Importantly, bradycardia-related cardiomyopathy and heart failure, as well as an adverse influence on brain function, may all be eluding consequences of this type of syndrome. Bradycardia could be the inciting mechanism for the occurrence of AF, and when the bradycardia is eliminated, AF may not recur. The bradycardia-related long-short-long sequence triggering VAs can be averted by pacing at rates ~80-110 bpm either via temporary or permanent pacing as needed.

Conclusion: Balancing the benefits and risks of bradycardia together with other risks of antiarrhythmic drug and/or pacing management of AF versus those of catheter ablation is indeed a vexing problem; all these issues are herein discussed, tabulated, and pictorially illustrated.

Introduction/objective: Emotional, mental, or psychological distress, defined as increased symptoms of depression, anxiety, and/or stress, is common in patients with chronic diseases, such as cardiovascular (CV) disease (CVD).

Methods: Literature was reviewed regarding data from studies and meta-analyses examining the impact of emotional stress on the occurrence and outcome of several CVDs (coronary disease, heart failure, hypertension, arrhythmias, stroke). These influences' pathophysiology and clinical spectrum are detailed, tabulated, and pictorially illustrated.

Results: This type of stress is a newly recognized risk and prognosticator for CVD including coronary artery disease, heart failure, hypertension, cardiac arrhythmias, and stroke, independently of conventional risk factors. It can impact CV outcomes, and also affect health care utilization, with more patient visits to health care facilities. The biological systems activated by mental stress comprise the sympathetic nervous system (SNS), the renin-angiotensin system (RAS), and the hypothalamic- pituitary-adrenal (HPA) axis, while several other biological processes are disrupted, such as endothelial function, inflammatory responses, oxidative stress, mitochondrial function and the function of the amygdala which is the central nervous system processing center of emotions and emotional reactions.

Conclusion: Emotional stress that aggravates symptoms of depression, anxiety, and/or perceived mental stress is common in patients with chronic diseases, such as CVD. It is a newly recognized risk and prognosticator for several CVDs. It can influence CV outcomes, and also affect health care utilization. The biological systems activated by mental stress comprise the SNS, the RAS, and the HPA axis, while several other biological processes are disrupted.

Background: Contrast-induced Acute Kidney Injury (CI-AKI) frequently occurs as a complication following PCI, making the identification of high-risk patients challenging. While the systemic immune inflammation index (SII) might aid in predicting CI-AKI, the current evidence remains insufficient.

Methods: We conducted a systematic literature search using PubMed, Web of Science, Embase, and the Cochrane Library, with a cut-off date of 3/20/2024. We included observational studies that examined the predictive value of SII for the risk of CI-AKI.

Results: This meta-analysis encompassed 8 studies with a combined total of 6301 participants. Results showed pooled sensitivity and specificity of 0.73 (95% CI 0.69-0.76) and 0.68 (95% CI 0.57- 0.77), respectively. The sROC curve analysis indicated an AUC of 0.74 (95% CI 0.70-0.78). The risk of publication bias was low (p = 0.18).

Conclusion: The results of this study suggest that SII has a relatively high sensitivity and could function as a biomarker for the prediction of CI-AKI risk in people receiving PCI treatment.