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Introduction: Vascular surgery has been greatly evolved during the last decades and novel minimally invasive techniques have been introduced. Aim of this review is to briefly present all these advances and compare them with traditional repairs. Areas covered: The authors have extensively searched literature through the Pubmed and Embase databases. All articles published up to December 2021 referring to minimally invasive techniques used for treatment of peripheral artery disease, carotid disease, aortic aneurysms, and venous disease were evaluated. Minimally invasive techniques under investigation included endovascular and hybrid techniques, robot-assisted and laparoscopic approaches. Expert Opinion: Several minimally invasive techniques such as endovascular and hybrid approaches have been extensively used during the last two decades to treat vascular surgery patients offering them lower mortality and morbidity risks. Novel robot-assisted techniques have shown promising results in preclinical studies although further clinical evaluation is needed. © 2022 Informa UK Limited, trading as Taylor & Francis Group.

This report aims to present a rare case of a common carotid artery (CCA) pseudoaneurysm with a concomitant internal carotid artery (ICA) stenosis that were treated with a hybrid technique. This strategy included the retrograde placement of a CCA covered stent under ICA clamping followed by standardized carotid endarterectomy. The technique will be discussed and compared with other possible treatments. © The Author(s) 2021.

Despite increased public health awareness, atherosclerosis remains a leading cause of mortality worldwide. Significant variations in response to statin treatment have been noted among different populations suggesting that the efficacy of statins may be altered by both genetic and environmental factors. The existing literature suggests that certain long noncoding RNAs (lncRNAs) might be up-or downregulated among patients with atherosclerosis. LncRNA may act on multiple levels (cholesterol homeostasis, vascular inflammation, and plaque destabilization) and exert athero-protective or atherogenic effects. To date, only a few studies have investigated the interplay between statins and lncRNAs known to be implicated in atherosclerosis. The current review characterizes the role of lncRNAs in atherosclerosis and summarizes the available evidence related to the effect of statins in regulating lncRNAs. © 2021 by the authors. Licensee MDPI, Basel, Switzerland.

Objective: Transcarotid/transcervical revascularisation (TCAR) is an alternative to carotid endarterectomy (CEA) and transfemoral carotid stenting (tfCAS). This review aimed to evaluate pooled data on patients undergoing TCAR. Data sources: Medline, Embase, Scopus, and Cochrane Library databases were used. Review methods: This systematic review was conducted under Systematic Reviews and Meta-Analysis guidelines. Eligible studies (published online up to September 2020) reported 30 day mortality and stroke/transient ischaemic attack (TIA) rates in patients undergoing TCAR. Data were pooled in a random effects model and weight of effect for each study was also reported. Quality of studies was evaluated according to Newcastle – Ottawa scale. Results: Eighteen studies (three low, seven medium, and eight high quality) included 4 852 patients (4 867 TCAR procedures). The pooled 30 day mortality rate was 0.7% (n = 32) (95% confidence interval [CI] 0.5 – 1.0), 30 day stroke rate 1.4% (n = 62) (95% CI 1.0 – 1.7), and 30 day stroke/TIA rate 2.0% (n = 92) (95% CI 1.4 – 2.7). Pooled technical success was 97.6% (95% CI 95.9 – 98.8). The cranial nerve injury rate was 1.2% (95% CI 0.7 – 1.9) (n = 14; data from 10 studies) while the early myocardial infarction (MI) rate was 0.4% (95% CI 0.2 – 0.6) (n = 16; data from 17 studies). The haematoma/bleeding rate was 3.4% (95% CI 1.7 – 5.8) (n = 135; data from 10 studies), with one third of these cases needing drainage or intervention. Within a follow up of 3 – 40 months the restenosis rate was 4% (95% CI 0.1 – 13.1) (data from nine studies; n = 64/530 patients) and death/stroke rate 4.5% (95% CI 1.8 – 8.4) (data from five studies; n = 184/3 742 patients). Symptomatic patients had a higher risk of early stroke/TIA than asymptomatic patients (2.5% vs. 1.2%; odds ratio 1.99; 95% CI 1.01 – 3.92); p =.046; data from eight studies). Conclusion: TCAR is associated with promising early and late outcomes, with symptomatic patients having a higher risk of early cerebrovascular events. More prospective comparative studies are needed in order to verify TCAR as an established alternative treatment technique. © 2021 European Society for Vascular Surgery

Background: The objective of the current study was to summarize and evaluate all published evidence regarding viscoelastic testing in the field of liver surgery. Methods: A systematic search of the literature was performed using Medline/PubMed, Scopus, Cochrane Library Central, Google Scholar, and clinicaltrials.gov databases. The following keywords were used:“Thromboelastography”, “Thromboelastometry”, “Viscoelastic tests OR testing”, “Sonoclot Devices”, “Point-of-care tests OR testing”, “Coagulation OR Haemostasis OR Hemostasis”, “Liver OR Hepatic Surgery”, “Cirrhosis.” Results: A total of 12 studies analyzing 348 patients who underwent viscoelastic testing of coagulation during liver surgery for benign or malignant diseases were included; 7 (58.3%) studies reported on the use of thromboelastography (TEG), and 5 (41.7%) reported on rotational thromboelastometry (ROTEM). Viscoelastic testing (TEG and ROTEM) identified normo-, hyper- and hypo-coagulable status in 77% (n = 268/348), 18.4% (n = 64/348), and 4.6% (n = 16/348) of patients, respectively. In contrast, conventional coagulation tests indicated normo-coagulability in 111 patients (34.2% out of 325) and hypo-coagulability in 214 (65.8% out of 325) patients following liver resection. No patient (0% out of 291) experienced postoperative hemorrhage, whereas 5.8% (n = 17/291) experienced postoperative thromboembolic events. Conclusions: Global viscoelastic testing may be a reasonable adjunct to conventional coagulation testing to provide a more robust assessment of the coagulation status of patients undergoing liver surgery. © 2020 International Hepato-Pancreato-Biliary Association Inc.

Background: In vascular endothelial cells, cysteine metabolism by the cystathionine γ lyase (CSE), generates hydrogen sulfide-related sulfane sulfur compounds (H2Sn), that exert their biological actions via cysteine S-sulfhydration of target proteins. This study set out to map the "S-sulfhydrome" (ie, the spectrum of proteins targeted by H2Sn) in human endothelial cells. Methods: Liquid chromatography with tandem mass spectrometry was used to identify S-sulfhydrated cysteines in endothelial cell proteins and β3 integrin intraprotein disulfide bond rearrangement. Functional studies included endothelial cell adhesion, shear stress-induced cell alignment, blood pressure measurements, and flow-induced vasodilatation in endothelial cell-specific CSE knockout mice and in a small collective of patients with endothelial dysfunction. Results: Three paired sample sets were compared: (1) native human endothelial cells isolated from plaque-free mesenteric arteries (CSE activity high) and plaque-containing carotid arteries (CSE activity low); (2) cultured human endothelial cells kept under static conditions or exposed to fluid shear stress to decrease CSE expression; and (3) cultured endothelial cells exposed to shear stress to decrease CSE expression and treated with solvent or the slow-releasing H2Sndonor, SG1002. The endothelial cell "S-sulfhydrome" consisted of 3446 individual cysteine residues in 1591 proteins. The most altered family of proteins were the integrins and focusing on β3 integrin in detail we found that S-sulfhydration affected intraprotein disulfide bond formation and was required for the maintenance of an extended-open conformation of the β leg. β3 integrin S-sulfhydration was required for endothelial cell mechanotransduction in vitro as well as flow-induced dilatation in murine mesenteric arteries. In cultured cells, the loss of S-sulfhydration impaired interactions between β3 integrin and Gα13 (guanine nucleotide-binding protein subunit α 13), resulting in the constitutive activation of RhoA (ras homolog family member A) and impaired flow-induced endothelial cell realignment. In humans with atherosclerosis, endothelial function correlated with low H2Sngeneration, impaired flow-induced dilatation, and failure to detect β3 integrin S-sulfhydration, all of which were rescued after the administration of an H2Snsupplement. Conclusions: Vascular disease is associated with marked changes in the S-sulfhydration of endothelial cell proteins involved in mediating responses to flow. Short-term H2Snsupplementation improved vascular reactivity in humans highlighting the potential of interfering with this pathway to treat vascular disease. © 2021 Lippincott Williams and Wilkins. All rights reserved.

The proper management of small abdominal aortic aneurysms (AAAs), namely those under the threshold of 5.5 cm in diameter, has been under investigation for years. Risk of rupture for this group of AAAs is higher than the general population, although it remains low enough not to require a repair. However, specific factors have been associated with increased expansion or rupture rate, and these factors could identify potential candidates for earlier intervention. This review aims to collect and present all available data on the development and progress of small AAAs. Moreover, recommendations on proper management are discussed as well. © 2019 Elsevier Inc.

Introduction: Asymptomatic carotid artery stenosis (ACAS) may cause future stroke and therefore patients with ACAS require best medical treatment. Patients at high risk for stroke may opt for additional revascularization (either surgery or stenting) but the future stroke risk should outweigh the risk for peri/post-operative stroke/death. Current risk stratification for patients with ACAS is largely based on outdated rand-omized-controlled trials that lack the integration of improved medical therapies and risk factor control. Furthermore, recent circulating and imaging biomarkers for stroke have never been included in a risk stratification model. The TAXINOMISIS Project aims to develop a new risk stratification model for cerebrovascular complications in patients with ACAS and this will be tested through a prospective observational multicentre clinical trial performed in six major European vascular surgery centres. Methods and analysis: The risk stratification model will compromise clinical, circulating, plaque and imaging biomarkers. The prospective multicentre observational study will include 300 patients with 50%-99% ACAS. The primary endpoint is the three-year incidence of cerebrovascular complications. Biomarkers will be re-trieved from plasma samples, brain MRI, carotid MRA and duplex ultrasound. The TAXINOMISIS Project will serve as a platform for the development of new computer tools that assess plaque progression based on radiology images and a lab-on-chip with genetic variants that could predict medication response in individual patients. Conclusion: Results from the TAXINOMISIS study could potentially improve future risk stratification in patients with ACAS to assist personalized evidence-based treatment decision-making. © 2020 The Authors.

Aims: Levosimendan (LEVO) a clinically-used inodilator, exerts multifaceted cardioprotective effects. Case-studies indicate protection against doxorubicin (DXR)-induced cardiotoxicity, but this effect remains obscure. We investigated the effect and mechanism of different regimens of levosimendan on sub-chronic and chronic doxorubicin cardiotoxicity. Methods and results: Based on preliminary in vivo experiments, rats serving as a sub-chronic model of doxorubicin-cardiotoxicity and were divided into: Control (N/S-0.9%), DXR (18 mg/kg-cumulative), DXR+LEVO (LEVO, 24 μg/kg-cumulative), and DXR+LEVO (acute) (LEVO, 24 μg/kg-bolus) for 14 days. Protein kinase-B (Akt), endothelial nitric oxide synthase (eNOS), and protein kinase-A and G (PKA/PKG) pathways emerged as contributors to the cardioprotection, converging onto phospholamban (PLN). To verify the contribution of PLN, phospholamban knockout (PLN-/-) mice were assigned to PLN-/-/Control (N/S-0.9%), PLN-/-/DXR (18 mg/kg), and PLN-/-/DXR+LEVO (ac) for 14 days. Furthermore, female breast cancer-bearing (BC) mice were divided into: Control (normal saline 0.9%, N/S 0.9%), DXR (18 mg/kg), LEVO, and DXR+LEVO (LEVO, 24 μg/kg-bolus) for 28 days. Echocardiography was performed in all protocols. To elucidate levosimendan's cardioprotective mechanism, primary cardiomyocytes were treated with doxorubicin or/and levosimendan and with N omega-nitro-L-arginine methyl ester (L-NAME), DT-2, and H-89 (eNOS, PKG, and PKA inhibitors, respectively); cardiomyocyte-toxicity was assessed. Single bolus administration of levosimendan abrogated DXR-induced cardiotoxicity and activated Akt/eNOS and cAMP-PKA/cGMP-PKG/PLN pathways but failed to exert cardioprotection in PLN-/- mice. Levosimendan's cardioprotection was also evident in the BC model. Finally, in vitro PKA inhibition abrogated levosimendan-mediated cardioprotection, indicating that its cardioprotection is cAMP-PKA dependent, while levosimendan preponderated over milrinone and dobutamine, by ameliorating calcium overload. Conclusion: Single dose levosimendan prevented doxorubicin cardiotoxicity through a cAMP-PKA-PLN pathway, highlighting the role of inotropy in doxorubicin cardiotoxicity. © 2019 Published on behalf of the European Society of Cardiology. All rights reserved.

Herein we report nine cases of carotid endarterectomy in which we used a cold atmospheric helium plasma device (J-Plasma; Apyx Medical Corporation, Clearwater, Fla). Although clinical reports are limited, experimental data indicate that this technology could be used for dissection and coagulation during surgery, yielding limited adjacent tissue damage. As a result, it could be extremely useful in procedures like carotid endarterectomy that necessitate careful dissection and coagulation with limited damage of adjacent neurovascular structures. © 2020 The Author(s)

Suprarenal aortic clamping during abdominal aortic aneurysm (AAA) repair results in ischemia-reperfusion injury (IRI) in local (i.e. kidney) and distant (i.e. heart) tissue. To investigate perioperative approaches that mitigate IRI-induced tissue damage, Wistar rats underwent suprarenal aortic clamping either alone or in combination with short cycles of ischemic conditioning before and/or after clamping. Serum analysis revealed significant reduction in key biochemical parameters reflecting decreased tissue damage at systemic level and improved renal function in conditioned groups compared to controls (p < 0.05), which was corroborated by histolopathological evaluation. Importantly, the levels of DNA damage, as reflected by the biomarkers 8-oxo-G, γH2AX and pATM were reduced in conditioned versus non-conditioned cases. In this setting, NADPH oxidase, a source of free radicals, decreased in the myocardium of conditioned cases. Of note, administration of 5-HD and 8-SPT blocking key protective signaling routes abrogated the salutary effect of conditioning. To further understand the non-targeted effect of IRI on the heart, it was noted that serum TGF-β1 levels decreased in conditioned groups, whereas this difference was eliminated after 5-HD and 8-SPT administration. Collectively, conditioning strategies reduced both renal and myocardial injury. Additionally, the present study highlights TGF-β1 as an attractive target for manipulation in this context. © 2020, The Author(s).

Cystathionine γ lyase (CSE) is the major source of hydrogen sulfide-derived species (H2Sn) in endothelial cells and plays an important role in protecting against atherosclerosis. Here we investigated the molecular mechanisms underlying the regulation of CSE expression in endothelial cells by fluid shear stress/flow. Fluid shear stress decreased CSE expression in human and murine endothelial cells and was negatively correlated with the transcription factor Krüppel-like factor (KLF) 2. CSE was identified as a direct target of the KLF2-regulated microRNA, miR-27b and high expression of CSE in native human plaque-derived endothelial cells, was also inversely correlated with KLF2 and miR-27b levels. One consequence of decreased CSE expression was the loss of Prx6 sulfhydration (on Cys47), which resulted in Prx6 hyperoxidation, decamerization and inhibition, as well as a concomitant increase in endothelial cell reactive oxygen species and lipid membrane peroxidation. H2Sn supplementation in vitro was able to reverse the redox state of Prx6. Statin therapy, which is known to activate KLF2, also decreased CSE expression but increased CSE activity by preventing its phosphorylation on Ser377. As a result, the sulfhydration of Prx6 was partially restored in samples from plaque containing arteries from statin-treated donors. Taken together, the regulation of CSE expression by shear stress/disturbed flow is dependent on KLF2 and miR-27b. Moreover, in murine and human arteries CSE acts to maintain endothelial redox balance at least partly by targeting Prx6 to prevent its decamerization and inhibition of its peroxidase activity. © 2019 The Authors

Background: There has been a dramatic increase in worldwide health care spending over the last several decades. Operative procedures and perioperative care in the USA represent some of the most expensive episodes per patient. In view of both the rising cost of health care in general and the rising cost of surgical care specifically, policymakers and stakeholders have sought to identify ways to increase the value—improving quality of care while controlling (or diminishing) costs. In this context, we reviewed data relative to achieving the “value proposition” in the delivery of gastrointestinal surgical care. Methods: The National Library of Medicine online repository (PubMed) was text searched for human studies including “cost,” “quality,” “outcomes,” “health care,” “surgery,” and “value.” Results from this literature framed by the Donabedian conceptual model (identifying structures, processes, and outcomes), and the resulting impact of efforts to improve quality on costs. Results: The relationship between quality and costs was nuanced. Better quality care, though associated with better outcomes, was not always reported as concomitant with low costs. Moreover, some centers reported higher costs of surgical care commensurate with higher quality. Conversely, higher costs in health care delivery were not always linked to improved outcomes. While higher quality surgical care can lead to lower costs, higher costs of care were not necessarily associated with better outcomes. Strategies to improve quality, reduce cost, or achieve both simultaneously included regionalization of complex operations to high-volume centers of excellence, overall reduction in complications, introducing evidence-based improvements in perioperative care pathways including as enhanced recovery after surgery (ERAS), and elimination of inefficient or low-value care. Conclusions: The relationship between quality and cost following gastrointestinal surgical procedure is complex. Data from the current study should serve to highlight the various means available to improve the value proposition related to surgery, as well as encourage surgeons to become more engaged in the national conversation around the Triple Aim of better health care quality, lower costs, and improved health care outcomes. © 2020, The Society for Surgery of the Alimentary Tract.

Introduction: This study compares the incidence of vascular complications and other major outcomes between patients undergoing transcatheter aortic valve implantation, with and without a standardized preoperative vascular surgeon consultation. Methods: This retrospective study evaluated all patients scheduled for transcatheter aortic valve implantation during a five-year period at a Hellenic University Hospital. Two main periods were evaluated: Group A (early period (2014–2015), without a standardized preoperative vascular surgeon consultation) and Group B (late period (2016–2018), with a standardized preoperative vascular surgeon consultation). All vascular complications as well as other major outcomes (early death, stroke, myocardial infarction, and treatment) were recorded. Univariate and multivariate analyses were also conducted. Results: Overall, 382 transcatheter aortic valve implantation procedures were conducted (Group A: n = 115; duration = 19 months; Group B: n = 267; duration = 41 months). Overall, 58 vascular complications were recorded (21 patients in Group A and 37 patients in Group B (18.3% versus 13.9%; P = 0.279)). However, vascular complications that necessitated a vascular surgeon’s interference were more frequent during the first period (13% versus 4.9%; P = 0.009). Among patients with a vascular complication, early mortality was higher during the first period (14.3% versus 0%; P = 0.034) although stroke and myocardial infarction rates were similar. Age >80 years (OR = 1.856 [1.134–3.452]; P = 0.03) and preoperative vascular surgeon consultation (OR = 0.345 [0.132–0.756]; P = 0.015) were the only independent predictors for vascular complications. Conclusions: A standardized preoperative evaluation by a vascular surgeon may decrease the risk for vascular complications that necessitate a repair as well as early mortality among patients undergoing transcatheter aortic valve implantation procedures. © The Author(s) 2020.

Background: The aim of this study is to present the experience of a Vascular Division at a Hellenic University hospital concerning the management of iatrogenic vascular injuries (IVIs) of the abdomen or pelvis. Patients and Methods: This is a retrospective study evaluating all IVIs reported during a 10-year period in our institution. Only injuries warranting a vascular surgeon consultation were included in the study. Non-iatrogenic injuries were not included. Mortality and major complications within 30 days were evaluated. Results: Overall, 70 cases were recorded, with 41% being venous and 59% being arterial injuries. Iliac arteries (51%) were the most common location and rupture/lacerations (73%) were the most common type of injury. General surgery (61.5%) and cardiology (30%) procedures were the most frequently involved procedures. A 30-day mortality was 5.7%, with 30% of cases treated conservatively. Synthetic bypass grafting (odds ratio [OR] = 65.0; 95% confidence interval [CI], 4.022-1050.358; P =.003) and male gender (OR = 83.77; 95% CI, 4.040-1736.738; P =.004) were associated with death. Conclusions: Iatrogenic vascular injuries of the abdomen or pelvis are usually associated with general surgery and endovascular procedures. When vascular consultation is requested early, mortality could remain low. However, a selected number of stable patients with retroperitoneal or pelvic hematomas could be treated conservatively, yielding satisfying results. © The Author(s) 2019.

Background: Hydrogen sulfide (H2S), generated by cystathionine γ lyase (CSE), is an important endogenous regulator of vascular function. The aim of the present study was to investigate the control and consequences of CSE activity in endothelial cells under physiological and proatherogenic conditions. Methods: Endothelial cell CSE knockout mice were generated, and lung endothelial cells were studied in vitro (gene expression, protein sulfhydration, and monocyte adhesion). Mice were crossed onto the apolipoprotein E-deficient background, and atherogenesis (partial carotid artery ligation) was monitored over 21 days. CSE expression, H2S bioavailability, and amino acid profiling were also performed with human material. Results: The endothelial cell-specific deletion of CSE selectively increased the expression of CD62E and elevated monocyte adherence in the absence of an inflammatory stimulus. Mechanistically, CD62E mRNA was more stable in endothelial cells from CSE-deficient mice, an effect attributed to the attenuated sulfhydration and dimerization of the RNA-binding protein human antigen R. CSE expression was upregulated in mice after partial carotid artery ligation and in atheromas from human subjects. Despite the increase in CSE protein, circulating and intraplaque H2S levels were reduced, a phenomenon that could be attributed to the serine phosphorylation (on Ser377) and inhibition of the enzyme, most likely resulting from increased interleukin-1β. Consistent with the loss of H2S, human antigen R sulfhydration was attenuated in atherosclerosis and resulted in the stabilization of human antigen R-target mRNAs, for example, CD62E and cathepsin S, both of which are linked to endothelial cell activation and atherosclerosis. The deletion of CSE from endothelial cells was associated with the accelerated development of endothelial dysfunction and atherosclerosis, effects that were reversed on treatment with a polysulfide donor. Finally, in mice and humans, plasma levels of the CSE substrate l-cystathionine negatively correlated with vascular reactivity and H2S levels, indicating its potential use as a biomarker for vascular disease. Conclusions: The constitutive S-sulfhydration of human antigen R (on Cys13) by CSE-derived H2S prevents its homodimerization and activity, which attenuates the expression of target proteins such as CD62E and cathepsin S. However, as a consequence of vascular inflammation, the beneficial actions of CSE-derived H2S are lost owing to the phosphorylation and inhibition of the enzyme. © 2019 American Heart Association, Inc.

Purpose: The use of platelet-rich plasma (PRP) for the treatment of nonhealing ulcers is a relatively new technique. Although it seems to result in a satisfying level of healing and low complication rates, data regarding its effectiveness remain sparse. This study aims to evaluate the potential therapeutic effects of PRP on chronic nonhealing ulcers. Materials and Methods: This was a prospectively designed study comparing outcomes between patients treated with PRP (Group A, n=15) and patients treated conventionally (Group B, n=12) for different types of nonhealing ulcers. In Group A, PRP was produced from the patients’ own peripheral blood samples and was applied on the ulcer once every week. In Group B, patients were treated conventionally, without applying PRP. The total treatment period was 5 weeks. Results: Both groups were similar regarding age, sex, comorbidities, and time of treatment. In Group A, patients showed a nonsignificant reduction of 4.5 mm2 in ulcer area (P=0.190) and a reduction of more than 1 mm in depth (P=0.0006), while Group B showed an increase of 108±80.5 mm2 in ulcer area after 5 weeks (P=0.016). The healing rate (HR) in Group A was stable and positive throughout the treatment period, while HR in Group B was initially negative but became positive after the 3rd week. Conclusion: PRP application once a week promotes the healing of chronic ulcers. It improves the ulcer’s depth and HR, although its effect on ulcer area seems to be nonsignificant. However, larger comparative series are still needed to confirm these findings. Copyright © 2019, The Korean Society for Vascular Surgery.

Peripheral artery disease (PAD) is the third most common manifestation of atherosclerosis after coronary artery (CAD) and cerebrovascular disease (CVD). People with PAD have plaque findings in other vascular territories as well and, thus, are at increased risk of major adverse cardiovascular or cerebrovascular events (MACCE), including myocardial infarction, and stroke. In that context, the COMPASS multicenter, randomized controlled trial showed that the risk of MACCE was significantly reduced by 24% in the rivaroxaban plus aspirin arm compared with aspirin alone (4.1% vs 5.4% respectively; HR: 0.76, 95% CI: 0.66 to 0.86). Interestingly, the rivaroxaban/aspirin arm also showed a reduction in cardiovascular death (HR: 0.78; 95% CI: 0.64-0.96]) and all-cause mortality (HR: 0.82; 95% CI: 0.71-0.96) by 22% and 18%, respectively. Recently, the FDA approved the use of the dual pathway approach, rivaroxaban 2.5 mg twice daily plus aspirin 75-100mg once daily, to reduce the risk of major cardiovascular (CV) events, such as CV death, myocardial infarction and stroke, in people with CAD as well as PAD. In comparing rivaroxaban plus aspirin versus aspirin alone, a preliminary economic analysis showed that saving per patient was USD 462 for events and USD 220 for procedures with a total reduction of USD 682 per participant in the US with the combination group (rivaroxaban plus aspirin). The data from COMPASS trial suggest that low dose rivaroxaban plus aspirin may be a preferred treatment strategy in PAD patients in whom the bleeding risk is deemed to be favourable. © 2018 Bentham Science Publishers.

Antithrombotic treatment including anticoagulants and antiplatelets has evolved during the last decades, and several recommendations have been included in the latest guidelines regarding the proper management of patients undergoing vascular surgery. However, there are significant differences compared to older recommendations, and indications vary among patients with peripheral artery disease, carotid disease, and abdominal aortic aneurysm. In this mini review, we critically evaluate all these data to produce useful conclusions for everyday clinical practice. © 2018 Hellenic Society of Cardiology

The repair of an abdominal aortic aneurysm (AAA) is a high-risk surgical procedure related to hormonal and metabolic stress-related response with an ensuing activation of the inflammatory cascade. In contrast to open repair (OR), endovascular aortic aneurysm repair (EVAR) seems to decrease the postoperative stress by offering less extensive incisions, dissection, and tissue manipulation. However, these beneficial effects may be offset by the release of cytokines and arachidonic acid metabolites during intra-luminal manipulation of the thrombus using catheters in endovascular repair, resulting in systemic inflammatory response (SIR), which is clinically called post-implantation syndrome. In this systematic review we compared OR with EVAR in terms of the post-interventional inflammatory response resulting from alterations in the circulating cytokine levels. We sought to summarize all the latest evidence regarding post-implantation syndrome after EVAR. We searched Medline (PubMed), ClinicalTrials.gov and the Cochrane library for clinical studies reporting on the release of cytokines as part of the inflammatory response after both open/conventional and endovascular repair of the AAA. We identified 17 studies examining the cytokine levels after OR versus EVAR. OR seemed to be associated with a greater SIR than EVAR, as evidenced by the increased cytokine levels, particularly IL-6 and IL-8, whereas IL-1β, IL-10 and TNF-α showed conflicting results or no difference between the two groups. Polyester endografts appear to be positively correlated with the incidence of post-implantation syndrome after EVAR. Future large prospective studies are warranted to delineate the underlying mechanisms of the cytokine interaction in the post-surgical inflammatory response setting. © 2018 CPS and SIMM.

Carotid and coronary artery disease are two major atherosclerotic conditions that have shown an increased prevalence in the last three decades that is associated with high morbidity and mortality. Recent data have revealed that the development of the atherosclerotic plaque — the basic entity in both diseases — may share similar characteristics and mechanisms irrespective of the location site. Even though the biology of atherosclerotic process is similar, there are differences in plaque morphology and characteristics. Indeed, plaque erosion, calcified nodules, fibrous cap thickness and macrophage accumulation may be different in the setting of coronary and carotid artery disease. The perivascular adipose tissue surrounding the coronary arteries (but not carotids) could also affect plaque biology. In this review we focus on comparative the characteristics of both types of atherosclerotic plaques and summarize existing knowledge to provide useful conclusions about current and future treatment strategies. © 2017 Elsevier Ltd

The molecular and cellular mechanisms underlying plaque destabilization remain obscure. We sought to elucidate the correlation between NO, H2S and CO-generating enzymes, nitro-oxidative stress and plaque stability in carotid arteries. Carotid atherosclerotic plaques were collected from 62 patients who had undergone endarterectomy due to internal artery stenosis. Following histological evaluation the plaques were divided into stable and unstable ones. To investigate the impact of simvastatin we divided patients with stable plaques, into those receiving and to those not receiving simvastatin. Expression and/or levels of p-eNOS/eNOS, pAkt/t-Akt, iNOS, cystathionine beta synthase (CBS), cystathionine gamma lyase (CSE), heme oxygenase-1(HO-1), soluble guanyl cyclase sGCα1, sGCβ1, NOX-4 and HIF-1α were evaluated. Oxidative stress biomarkers malondialdehyde (MDA) and nitrotyrosine (NT) were measured. NT levels were decreased in stable plaques with a concomitant increase of eNOS phosphorylation and expression and Akt activation compared to unstable lesions. An increase in HIF-1α, NOX-4, HO-1, iNOS, CBS and CSE expression was observed only in unstable plaques. 78% of patients under simvastatin were diagnosed with stable plaques whereas 23% of those not receiving simvastatin exhibited unstable plaques. Simvastatin decreased iNOS, HO-1, HIF-1α and CSE whilst it increased eNOS phosphorylation. In conclusion, enhanced eNOS and reduced iNOS and NOX-4 were observed in stable plaques; CBS and CSE positively correlated with plaque vulnerability. Simvastatin, besides its known effect on eNOS upregulation, reduced the HIF-1α and its downstream targets. The observed changes might be useful in developing biomarkers of plaque stability or could be targets for pharmacothepary against plaque vulnerability. © 2017

Adenosine-to-inosine (A-to-I) RNA editing, which is catalyzed by a family of adenosine deaminase acting on RNA (ADAR) enzymes, is important in the epitranscriptomic regulation of RNA metabolism. However, the role of A-to-I RNA editing in vascular disease is unknown. Here we show that cathepsin S mRNA (CTSS), which encodes a cysteine protease associated with angiogenesis and atherosclerosis, is highly edited in human endothelial cells. The 3′ untranslated region (3′ UTR) of the CTSS transcript contains two inverted repeats, the AluJo and AluSx + regions, which form a long stem-loop structure that is recognized by ADAR1 as a substrate for editing. RNA editing enables the recruitment of the stabilizing RNA-binding protein human antigen R (HuR; encoded by ELAVL1) to the 3′ UTR of the CTSS transcript, thereby controlling CTSS mRNA stability and expression. In endothelial cells, ADAR1 overexpression or treatment of cells with hypoxia or with the inflammatory-γ 3 and tumor-necrosis-factor-α induces CTSS RNA editing and consequently increases cathepsin S expression. ADAR1 levels and the extent of CTSS RNA editing are associated with changes in cathepsin S levels in patients with atherosclerotic vascular diseases, including subclinical atherosclerosis, coronary artery disease, aortic aneurysms and advanced carotid atherosclerotic disease. These results reveal a previously unrecognized role of RNA editing in gene expression in human atherosclerotic vascular diseases. © 2016 Nature America, Inc. All rights reserved.