Current Vascular Pharmacology - Volume 23, Issue 2, 2025
Volume 23, Issue 2, 2025
- Medicine, Cardiology, Pharmacology, Peripheral Vascular Disease
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Cognitive Behavioral Therapy in Cardiovascular Disease
Authors: Theodora A. Manolis, Antonis A. Manolis and Antonis S. ManolisIntroduction/ObjectiveThe 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).
MethodsA 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.
ResultsAmong 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.
ConclusionThere 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.
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Neutrophil Migration is a Crucial Factor in Wound Healing and the Pathogenesis of Diabetic Foot Ulcers: Insights into Pharmacological Interventions
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.
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Atrial Fibrillation-Related Bradycardia and/or Bradycardia-Related Atrial Fibrillation: When and How to Intervene
Authors: Antonis A. Manolis, Theodora A. Manolis and Antonis S. ManolisIntroduction/ObjectiveAtrial 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.
MethodsAn 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.
ResultsAF 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.
ConclusionBalancing 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.
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The Systemic Immune Inflammation Index as a Novel Predictive Biomarker for Contrast-Induced Acute Kidney Injury Risk Following Percutaneous Coronary Intervention: A Meta-Analysis of Cohort Studies
Authors: Yongqiang Zhang, Yong Xie, Chunyu Zhang, Jianglin Wang, Bin Liao and Jian FengBackgroundContrast-induced Acute Kidney Injury (CI-AKI) frequently occurs as a complication following percutaneous coronary intervention (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.
MethodsWe 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.
ResultsThis 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).
ConclusionThe 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.
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Volumes & issues
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Volume 23 (2025)
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Volume 22 (2024)
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Volume 21 (2023)
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Volume 20 (2022)
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Volume 19 (2021)
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Volume 18 (2020)
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Volume 17 (2019)
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Volume 16 (2018)
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Volume 15 (2017)
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Volume 14 (2016)
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Volume 13 (2015)
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Volume 12 (2014)
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Volume 11 (2013)
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Volume 10 (2012)
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Volume 9 (2011)
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Volume 8 (2010)
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Volume 7 (2009)
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Volume 6 (2008)
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Volume 5 (2007)
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Volume 4 (2006)
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Volume 3 (2005)
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Volume 2 (2004)
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Volume 1 (2003)
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