Current vascular pharmacology最新文献

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.

Diabetic foot ulcers (DFUs) pose a significant clinical challenge, characterized by impaired wound healing, chronic inflammation, and increased risk of infection. Neutrophils, as critical components of the innate immune response, play a pivotal role in the initial stages of wound healing, particularly during the inflammatory phase. This review explores the intricate relationship between neutrophil migration, inflammation, and the pathogenesis of DFU and drugs that can impact neutrophil production and migration. Neutrophils contribute to infection control through phagocytosis and release pro-inflammatory cytokines and reactive oxygen species, which, when dysregulated, can impede the wound healing process. Furthermore, the chronic hyperglycemic state characteristic of diabetes mellitus has been implicated in impairing neutrophil functions, including chemotaxis and oxidative burst. This compromised neutrophil response prolongs the inflammatory phase and disrupts the delicate balance required for efficient wound healing. Neutrophil extracellular traps (NETs), a unique form of neutrophil defence, have also been implicated in DFU pathogenesis, potentially exacerbating inflammation and tissue damage. Understanding the intricate interplay between neutrophil migration, dysregulated inflammatory responses, and hyperglycemia-driven impairments is essential for developing targeted therapeutic strategies for DFUs. This review sheds light on the critical role of neutrophils in DFU pathogenesis, and innovative and advanced treatment strategies for DFU, highlighting the potential for novel interventions to restore the balance between pro-inflammatory and wound healing processes, ultimately improving clinical outcomes for individuals with DFU.

Aims: To assess the efficacy and safety of sarpogrelate (300 mg) for symptom improvement in patients having peripheral arterial disease (PAD) and/or being at risk of PAD in clinical practice using the Peripheral Artery Questionnaire (PAQ).

Background: Symptomatic changes with antiplatelets in patients with PAD are limited.

Objective: To determine the effect and safety of sarpogrelate on the PAQ at 24 weeks from baseline.

Method: A total of 1003 patients having PAD and/or being at risk of PAD from 17 tertiary hospitals in South Korea who were treated with sarpogrelate, were enrolled in this study. PAQs were collected at baseline and at 12 and 24 weeks, together with physical examination and vital signs measurements. Lifestyle pattern was also investigated.

Results: The average PAQ Summary Score in the efficacy evaluation analysis group significantly improved from 62.9 ± 23.7 at baseline to 68.9 ± 21.7 at 24 weeks (P<0.0001). Physical limitation items significantly improved from 69.5 ± 30.0 at baseline to 72.9 ± 28.3 after 24 weeks (P=0.0011). Symptom stability also significantly improved from 52.1 ± 21.6 at baseline to 63.6 ± 22.9 after 24 weeks (P<0.0001). Symptoms, treatment satisfaction, quality of life, and social limitation domains all improved after treatment. A total of 201 patients reported adverse events (20.0%), not directly associated with treatment.

Conclusion: Treatment with 300 mg (orally) of sarpogrelate demonstrated statistically significant improvements in all domains and for the summary score of the PAQ at 24 weeks, it gave good results in terms of safety. Sarpogrelate may be helpful in reducing symptoms related to PAD.

Introduction/objective: The influence of cognitive behavioral therapy (CBT) and its modalities on various neuropsychiatric conditions is herein explored together with their impact on specific cardiovascular (CV) diseases (CVD).

Methods: A comprehensive review of the literature was undertaken via the PubMed, Scopus and Google Scholar on the above relevant topics. The focus was on large randomized controlled trials and meta-analyses.

Results: Among the various neuropsychiatric disorders, depression and anxiety commonly occur in CVD patients, frequently eluding clinician's attention. This reciprocal liaison may incur higher rates of morbidity/mortality, through physiological and behavioral mechanisms. Multimodal psychiatric interventions, using medications and psychotherapies, such as CBT, seem promising. Such mindfulness-based interventions have the potential to be an efficacious complementary strategy to address psychological stress in CVD patients. As the cost of CBT is relatively low, such a supportive approach for stress management provides high patient acceptability, with a positive impact on improving quality of life, by promoting CV health and mitigating CV complications.

Conclusion: There is ample evidence of a reciprocal liaison between heart and mind. Several CV risk factors are strongly affected by diseases of the mind, and the clinical course of various CVDs is influenced by affective or other psychiatric disorders. CBT and relevant mindfulness-based interventions have a significant supportive role in patients with various CVDs by targeting CV risk factor(s) or the underlying specific CVD and by identifying and addressing psychosocial issues. In this direction, various CBT interventions can provide the means to favorably influence both CV risk factors and CVDs.

Mendelian Randomization (MR) studies have emerged as a powerful tool for investigating causal relationships between modifiable risk factors and clinical outcomes, using genetic variants as instrumental variables. In the context of vitamin D research, MR is a promising approach to elucidate the effects of vitamin D on various health outcomes, including adverse cardiovascular events. However, the validity of MR analyses relies heavily on the strength of the genetic associations found. "Weak instrument bias", arising from instruments with low explanatory power for the exposure of interest, can lead to biased estimates and compromise causal inference. We have, herein, briefly reviewed the challenges posed by weak instrument bias in a large MR study on vitamin D [25(OH)D] and stroke, exploring implications for the study's validity and reliability of findings. We have then added an original meta-analysis stratified by 25(OH)D levels. By using aggregated data from a recent MR study, an original meta-analysis stratified by population mean levels of 25(OH)D has indicated that interventions based on vitamin D supplementations in population mean levels ranging from 50 to 70 nmol/L are likely to translate into a 13% reduction of stroke risk (pooled odds ratio=0.873, 95% CI: 0.764-0.997, p-value=0.04). MR studies are a valuable approach for discerning causal relationships between exposures, such as vitamin D, and health outcomes. However, the effectiveness of MR analyses depends on the robustness of the genetic instruments employed. By recognizing and addressing weak instrument bias in MR studies of vitamin D, researchers can enhance the credibility and utility of causal inference in understanding the health effects of this essential nutrient. A metaanalysis stratified by population mean levels of 25(OH)D has revealed the potential benefits of targeted interventions with vitamin D supplementations for stroke.

Cardiovascular disorders (CVDs) are reported to occur with very high rates of incidence and exhibit high morbidity and mortality rates across the globe. Therefore, research is focused on searching for novel therapeutic targets involving multiple pathophysiological mechanisms. Oxidative stress plays a critical role in the development and progression of various CVDs, such as hypertension, pulmonary hypertension, heart failure, arrhythmia, atherosclerosis, ischemia-reperfusion injury, and myocardial infarction. Among multiple pathways generating reactive oxygen species (ROS), NADPH defines all abbreviations oxidases of the NOX family as the major source of ROS generation and plays an intricate role in the development and progression of CVDs. Therefore, exploring the role of different NADPH oxidase isoforms in various cardiovascular pathologies has attracted attention to current cardiovascular research. Focusing on NADPH oxidases to reduce oxidative stress in managing diverse CVDs may offer unique therapeutic approaches to prevent and treat various heart conditions. The current review article highlights the role of different NADPH oxidase isoforms in the pathophysiology of various CVDs. Moreover, the focus is also to emphasize different experimental studies that utilized various NADPH oxidase isoform modulators to manage other disorders. The present review article considers new avenues for researchers/scientists working in the field of cardiovascular pharmacology utilizing NADPH oxidase isoform modulators.

Atrial fibrillation (AF) is the commonest cardiac arrhythmia, constituting a major cause of morbidity and mortality, with an age-dependent incidence and prevalence ranging from 1-2% in the general population to ~10% in persons aged >60 years. The global prevalence of AF is rapidly increasing, mostly due to the aging population. If not properly and timely managed, this arrhythmia adversely affects left ventricular function, increases the risk of stroke five-fold, impairs quality of life, and shortens longevity. There is a genetic, hence non-modifiable, predisposition to the arrhythmia, while several life-style and cardiometabolic inciting factors, such as hypertension, heart failure, coronary disease, metabolic syndrome, alcohol use, and thyroid disorders, can be addressed, attesting to the importance of a holistic approach to its management. Thromboembolism is a serious consequence of AF, which could lead to a disabling stroke or have a lethal outcome. The risk of a thromboembolic complication can be estimated as based on a scoring system that takes into consideration the patient's age, previous thromboembolic events, and clinical comorbidities. In addition, rapid AF could affect cardiac performance, leading to an elusive type of arrhythmia-induced cardiomyopathy and heart failure with grave consequences if undetected and untreated. Furthermore, AF may cause silent brain infarcts and/or its hemodynamic perturbations can account for a type of dementia that needs to be taken into account, emphasizing the need for AF screening and prevention strategies. All these issues are herein detailed, the causes of the arrhythmia are tabulated, and an algorithm illustrates our current approach to its management.