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Purpose: The post–endovascular abdominal aortic aneurysm repair (EVAR) inflammatory response, which is very often associated with fever, has been ascribed to a wide range of proinflammatory mediators and operative events. The aim of this study was to evaluate the impact of such factors in the development of fever of noninfectious origin after elective EVAR. Materials and Methods: A retrospective analysis of prospectively collected data of patients treated with standard elective EVAR between February 2017 and December 2020 was undertaken. The database included patients’ demographics and comorbidities, as well as laboratory inflammatory markers (white blood cell count, neutrophils, and C-reactive protein [CRP]) and anatomical characteristics (sac diameter, inferior mesenteric artery [IMA] patency and diameter, number of patent lumbar arteries, internal iliac artery [IIA] patency or occlusion). Intraoperative details, such as type of stent graft material and IIA overstenting, were also analyzed. Patients with infectious postoperative complications or previously receiving systemic anti-inflammatory medication were excluded. Statistical analysis was performed by SPSS 22.0 for Windows software (IBM Corp, Armonk, New York). Results: From 332 patients treated with elective EVAR between 2017 and 2020, 268 patients (all men) were included in the analysis. The mean age was 72.1±7.5 years and the mean aneurysm diameter was 59.1±12.1 mm. Seventeen patients were excluded due to a known infection site. From the study cohort, 114 (42.5%) patients presented with fever. Multivariate regression analysis confirmed that the occlusion of IMA ≥5 mm (pConclusion: Occlusion of an existing wide (≥5 mm) and patent IMA prior to EVAR may contribute to the development of post-EVAR pyrexia. The CRP is a reliable marker for post-EVAR fever. Further prospective studies are needed to corroborate these findings.

Background: Ascending aorta and aortic arch diseases have an increasing interest among cardiovascular specialists regarding diagnosis and management. Innovations in endovascular surgery and evolution of open surgery have extended the indications for treatment in patients previously considered unfit for surgery. The aim of this systematic review of the literature was to present and analyze current cardiovascular guidelines for overlap and differences in their recommendations regarding ascending aorta and aortic arch diseases and the assessment of evidence. Methods: The English medical literature was searched using the MEDLINE, EMBASE, and Cochrane Central Register of Controlled Trials databases from January 2009 to December 2020. Recommendations on selected topics were analyzed, including issues from definitions and diagnosis (imaging and biomarkers) and indications for treatment to management, including surgical techniques, of the most important ascending aorta and aortic arch diseases. Results: The initial search identified 2414 articles. After exclusion of duplicate or inappropriate articles, the final analysis included 5 articles from multidisciplinary, cardiovascular societies published between 2010 and 2019. The definition of non-A-non-B aortic dissection is lacking from most of the guidelines. There is a disagreement regarding the class of recommendation and level of evidence for the diameter of ascending aorta as an indication. The indication for treatment of aortic disease may be individualized in specific cases while the growth rate may also affect the decision making. The role of endovascular techniques has not been established in current guidelines except by 1 society. Supportive evidence level in the management of aortic arch diseases remains limited. Conclusion: In current recommendations of cardiovascular societies, the ascending aorta and aortic arch remain a domain of open surgery despite the introduction of endovascular techniques. Recommendations of the included societies are mostly based on expert opinion, and the role of endovascular techniques has been highlighted only from 1 society. The chronological heterogeneity apparent among guidelines and the inconsistency in evidence level should be also acknowledged. More data are needed to develop more solid recommendations for the ascending aorta and aortic arch diseases.

Objectives The aim of our study was to evaluate the role of flavonoids in the improvement of post-operative symptoms after endovenous thermal ablation (EVTA). Methods A prospective comparative study of 120 consecutive patients undergoing EVTA of the greater saphenous vein associated with phlebectomies was undertaken. Patients were grouped in those receiving micronized purified flavonoid fraction (MPFF- 60 patients) agent 500 mg Bid 7 days pre- and 30 days post- operatively (MPFF group) and those in the control group (60 patients) who did not. Demographics, intra-operative details, Clinical –Etiology- Anatomy- Pathophysiology (CEAP) clinical class, 10-cm Visual Analog Scale (VAS) for pain, Venous Clinical Severity Score (VCSS) and Chronic Venous Insufficiency Quality-of-Life Questionnaire (CΙVIQ-20) were recorded. Primary outcome was the postoperative pain assessement using the VAS scale and CIVIQ pain score. Secondary outcomes included assessement of VCSS and CΙVIQ-20 scores. Results There were no significant differences between the groups regarding demographics, clinical and procedural characteristics. Patients in MPFF group reported significantly lower VAS pain levels than control group at 7- (−3.6 ± 1.2 vs −2.7 ± 1.9, p Conclusions Administration of flavonoids in patients undergoing EVTA associated with phlebectomies reduces pain by a small amount during early postoperative period.

Cardiovascular societies have developed recommendations regarding the management of thoracic aortic diseases. While improvements in treatment have been observed during the past decade in regard to patient selection, thoracic endovascular aortic repair (TEVAR) and associated techniques, and high-volume centralization, the broad expansion of TEVAR has raised considerations about its indications, appropriateness, limitations, and application. The aim of this systematic review was to assess the similarities and differences among current cardiovascular societies’ guidelines for the management of thoracic aortic diseases. The MEDLINE, EMBASE, and Cochrane Central Register of Controlled Trials were searched from January 2009 to May 2020. The initial search identified 990 articles. After exclusion of duplicate or inappropriate articles, the final analysis included 5 articles from cardiovascular societies published between 2010 and 2020. Selected controversial topics were analyzed, including diagnosis, imaging, spinal cord ischemia prevention, and management of the most important thoracic aortic pathologies. The analysis included data concerning the therapeutic approach in acute and chronic type B aortic dissection, penetrating aortic ulcer, intramural hematoma, thoracic aortic aneurysm, and traumatic aortic injury, as well a discussion of inflammatory aneurysms, aortitis, and genetic syndromes. The review presents consistent and controversial recommendations, as well as “gray zone” issues that need further investigation. There was significant overlap and agreement among the 5 societies regarding the management of thoracic aortic diseases. Especially in dissection and aneurysm management, TEVAR has established its role as the treatment of choice. However, robust evidence is still needed in many aspects of the management of thoracic aortic pathologies.

Background To assess the treatment of superficial vein thrombosis (SVT) with intermediate dose of tinzaparin in a setting of real world practice. Methods Prospective observational study of consecutive patients treated by vascular physicians in the private sector with tinzaparin (131 IU/Kg) once daily. Treatment duration was at the treating physician’s discretion. The outcomes of the study were symptomatic venous thromboembolism, extension of thrombus and bleeding complications. Results 660 patients were included and followed up for at least 3 months. Median duration of treatment was 30 days (14–120). History of prior deep vein thrombosis (HR 2.77; 95% CI= 1.18–6.49; p = 0.018) and current SVT above the knee (HR1.84; 95% CI = 1.33–3.53; p = 0.0002) were associated with prolonged treatment duration. Primary efficacy outcomes occurred in 20 (3%) patients. The median time to the event was 24 (6–92) days and was not related to treatment duration. Conclusions Tinzaparin at intermediate dose is an effective and safe treatment for SVT.

Objectives COVID-19 associated arterial thrombosis has been attributed to multiple inflammation and coagulation mechanisms. The aim of this study was to report the experience of a tertiary center on COVID-19 patients managed for acute peripheral arterial thrombosis. Methods A single-center case series was conducted, including retrospectively collected data from all COVID-19 patients presenting arterial thrombosis, from March 2020 to February 2022. Intensive care unit (ICU) and non-ICU cases were included. The primary outcomes were mortality, successful revascularization, and amputation at 30 days. Results Twenty patients presented peripheral arterial thrombosis (90% males, mean age 65 years (16–82 years)). Eighteen were diagnosed with the Delta variant and none was previously vaccinated. All cases presented acute lower limb ischemia; in 20% with bilateral involvement. Nine patients were hospitalized in the ward while 11 in the ICU. From the non-ICU cases, five presented Rutherford IIb and four cases, Rutherford’s IIa ischemia. Six cases underwent revascularization (67%). Two of them were finally amputated (33%) and two died during hospitalization (33%). Two revascularizations were considered successful (33%). The ICU group presented mainly with Rutherford’s III ischemia (54.5%). The mortality in the ICU cohort was 72.7%. Only one patient underwent successful revascularization and two were amputated in this subgroup. Early mortality was 50% for the total cohort while the type of management was not related to mortality. Conclusions Covid-19 related arterial thrombosis in non-vaccinated population is associated with 50% early mortality; increased up to 72% in the ICU patients. The amputation rate was 20% while only 40% of the revascularizations were considered successful.

Objective: Growing evidence indicates that depressive disorders (DDs) are an important risk factor for atherosclerosis. The aim of this study was to evaluate the presence of common carotid artery (CCA) intima-media thickness (IMT) and circulation inflammation markers in patients with DD. Methods: A cross-sectional prospective study was undertaken comparing 40 patients with DD to 40 individuals free of depression, matched for age and gender. The Beck Depression Inventory questionnaire, serum total cholesterol, triglycerides, high-sensitivity C-reactive protein, interleukin-6, tumor necrosis factor α, P-selectin, and E-selectin levels were measured. The CCA-IMT was assessed with duplex sonography. Results: Patients with DD were more likely to smoke (65% vs 40%; P = .03) and have higher levels of serum total cholesterol (211 mg/dL vs 181 mg/dL; P = .010), triglycerides (138 mg/dL vs 97 mg/dL; P = .005), and P-selectin (0.87 ng/mL vs 0.61 ng/mL; P = .05) and lower levels of interleukin 6 (4.4 ± 2.1 pg/mL vs 10.3 ± 1.1 pg/mL; P = .002). The CCA-IMT was similar in both groups (0.07 ± 0.02 cm vs 0.06 ± 0.01 cm; P = .31). Among those with CCA-IMT in the upper quartile, subjects in the DD group had lower levels of interleukin 6 ( P = .05) and triglycerides ( P = .01) and higher levels of soluble P-selectin ( P = .03). Conclusion: Patients with DD do not present with higher CCA-IMT than a control group, although smoking and a higher level of serum lipids are present. Inflammatory biomarkers seem to be higher in patients with DD.

Environmental and genetic risk factors contribute to the etiology of abdominal aortic aneurysms (AAAs). Matrix metalloproteinases (MMPs) have been associated with the pathophysiology of AAAs. A prospective, nonrandomized case–control study was undertaken to investigate the risk factors for large AAAs (≥5.5 cm) among 175 male Greek AAA patients and to compare the results with a cohort of 166 male controls free from any aortic dilatation, as confirmed by ultrasonography from an existing AAA screening program in the same region. We also assessed the potential association between 2 functional single nucleotide polymorphisms in the genes MMP9 (−1561C/T; rs3918242) and MMP13 (−77A/G; rs2252070), and the presence of large AAAs. Multiple logistic regression analysis revealed AAA family history ( P = .028), hypercholesterolemia ( P < .001), and current smoking ( P < .001) as AAA risk factors. Statistical difference was reached in genotype ( P = .047) and allele ( P = .037) frequencies for rs2252070, but the results did not remain significant after correction for multiple testing. No significant differences in genotype or allele frequencies for rs3918242 were detected. In summary, AAA family history, hypercholesterolemia, and current smoking were found to be risk factors for large AAAs.

Hemodynamic changes occurring at the initial segments of the arterial bifurcations appear to play an important role in the development of atherosclerotic plaque. Therefore, arterial geometry might be a potential marker for atherosclerosis. Considerable evidence suggests that geometry can influence local hemodynamics at the carotid bifurcation contributing to the development of atheroma. Bifurcation angle, differences in the area ratios including the flare, proximal curvature, sinus bulb width, and tortuosity of the internal or external carotid artery have been listed as potential contributory elements. These morphometric details have been studied not only in postmortem examination but also with the help of imaging modalities such as ultrasound, digital subtraction angiography, computed tomography angiography, and the assistance of computational models and magnetic resonance angiography. The establishment of certain anatomical and geometrical details in addition to traditional risk factors may help in the identification of patients at high risk of developing carotid artery disease. We reviewed the literature to highlight the evidence on the importance of various geometrical details in the development of carotid atheroma and to suggest areas of future research.

A prospective nonrandomized cohort study on consecutive diabetic patients with foot ulcer was undertaken to assess the factors associated with the healing process or limb salvage and evaluate the impact of their treatment on their quality of life. Quality of life was evaluated using Diabetic Foot Ulcer Scale–Short Form (DFS-SF) questionnaire before and after treatment. A total of 103 diabetic patients with ulcer (mean age 69.7 ± 9.6 years, 77% male) were treated and followed up for 12 months. Ulcer healing, minor amputation, and major amputation rates were 41%, 41%, and 18%, respectively, while the mortality rate was 18%. Ulcer healing was associated with University of Texas wound grade 1 and the Study of Infections in Diabetic feet comparing Efficacy, Safety and Tolerability of Ertapenem versus Piperacillin/Tazobactam trial’s diabetic foot infection wound score. Limb loss was associated with nonpalpable popliteal artery, longer in-hospital stay, and delay until referral. Quality of life was improved in all domains of DFS-SF ( P < .0001) throughout the cohort of our patients regardless of their outcome, and no outcome (healing, minor amputation, or major amputation) was superior to other. Significant improvement was observed in all domains of hygiene self-management after consultation during the follow-up period.

Objective To investigate which factors other than history of superficial vein thrombosis (SVT) are associated with recurrent spontaneous SVT episodes in patients with varicose veins (VVs). Materials and methods Patients with a history of spontaneous SVT and VVs were followed up for a mean period of 55 months. Demographics, comorbidities, and thrombophilia screening test were analyzed. Patients were grouped according to the clinical–etiology–anatomy–pathophysiology classification. A multiple logistic regression analysis with the forward likelihood ratio method was undertaken. Results Thirteen patients out of 97 had a recurrence SVT episode during the follow-up period. All those patients were identified to have a thrombophilia defect. Protein C and S, antithrombin, and plasminogen deficiencies were more frequently present in patients without recurrence. Gene mutations were present in 38% in the nonrecurrence group and 77% in the recurrence group. After logistic regression analysis, patients with dislipidemia and mutation in prothrombin G20210A (FII) had an increased risk for recurrence by 5.4-fold and 4.6-fold, respectively. No deep vein thrombosis or pulmonary embolism occurred. Conclusions Dislipidemia and gene mutations of F II are associated with SVT recurrence in patients with VVs. A selection of patients may benefit from anticoagulation in the short term and from VVs intervention in the long term.

Aim To identify patients who are under higher threat for migration because of an old generation stent graft application. Methods A systematic review and meta-analysis of the literature was undertaken to identify all studies which included older generation endografts and data reporting on graft migration after EVAR. Outcome data were pooled and combined, and were calculated using fixed or random effects models. Results From 2000 to 2014, 22 retrospective studies were identified reporting on stent- graft migration after EVAR (8.6%). From those patients, 39% received re-intervention with the mean time of identification ranging from 12 to 36 months. Six of these retrospective nonrandomized studies were eligible for meta-analysis. AAA diameter (AAA diameter: 0.719 mm; 95% confidence interval [CI]: 0.00065–1.4384 mm; p = 0.00497) and neck length (neck length: 4.36 mm; 95% CI: 1.3277–7.394; p = 0.0048) were the only significant factors associated with stent- graft migration. Neck diameter and neck angulation did not have any important influence on stent-graft migration. Conclusions Patients with large AAA and short necks who were treated with older generation stent grafts such as AneurX and Talent are in higher risk for endograft migration than others. Stent- graft migration consists of an insidious and underestimated threat.

Type II endoleak after endovascular aortic aneurysm repair still remains the Achilles’ heel of the treatment, the source of which regularly is difficult to identify and treat. We present a patient with a persistent type II endoleak associated with a continuous aneurysm sac expansion after endovascular aortic aneurysm repair for which many diagnostic modalities were used during his follow-up such as duplex scan, computed tomography angiography and magnetic resonance angiography. Attempts were undertaken to treat the source of endoleak including coil micro-embolisation of lumbar arteries and subsequent open ligation of the inferior mesenteric artery, but they failed to eliminate the endoleak. Finally, a middle sacral artery was identified as the source of the endoleak. At that time, the patient was subjected to surgery for sigmoid carcinoma, and simultaneously, a ligation of the sacral artery was undertaken which eventually eliminated the endoleak completely. This case highlights that type II endoleak may be evoked by various sources and there can be a great difficulty to identify these feeding vessels; thus, careful planning for its management is mandatory.

A total of 22 patients with ruptured abdominal aortic aneurysms (rAAAs) after previous endovascular aortic repair (EVAR; rAAAevar) were presented to 7 referral hospitals in Greece, between January 2006 and April 2012. Type Ia endoleak and endograft migration were identified in 72.7% and 50%, respectively. Compliance to follow-up protocol prior to rupture was 31.8%. In-hospital mortality was 36.4% (9.1% for those treated with secondary EVAR and 63.6% for those treated with open surgical repair, P = .02). An increase in the proportion of patients with rAAAevar among the total number of patients with rAAAs from 1.3% in 2007 to 18.2% in 2012 ( P for trend = .04) was recorded, corresponding to an annual increase of 2.8% (b = 2.84, P = .04). Rupture after EVAR seemed to be a clinical entity encountered with increasing frequency over the past years. Type I endoleak and endograft migration were most frequently observed, whereas compliance to follow-up was low.

Objectives: To determine the prevalence, distribution and extent of phlebosclerosis in an outpatient population referred to vascular clinic. Design: Prospective cohort study. Patients and Methods: Seven hundred and forty consecutive patients, 302 (41%) men with a cohort median age of 49 (range, 18–84), were referred to the vascular clinic for detection of lower extremity acute or chronic venous disease. A total of 1000 limbs were assessed using duplex ultrasonography. Deep veins were not assessed. Characteristics of venous wall and lumen were studied. Phlebosclerosis was diagnosed based on the increased echogenicity and thickness or calcification of the venous wall. Patients with known trauma or any surgery in the lower extremities were excluded. Two control groups were used for comparison, one of consecutive patients undergoing vein mapping ( n = 100) and the other of younger volunteers free of any vein disease ( n = 25). Results: Of the 1000 limbs (right: 458, left: 542) studied by duplex ultrasound, 21 limbs had intense brightness of the venous wall. Fifteen of them had also calcifications and 61 wall thickening. The prevalence of phlebosclerosis was significantly higher in the patient group when compared with control groups 1 (P = 0.019) and 2 (P = 0.011). The mean age of patients with phlebosclerosis was higher compared with the whole patient group (57 versus 49 years, P < 0.0001). Phlebosclerosis affected all superficial veins with greater prevalence in the small saphenous vein (SSV). The mean length of the phlebosclerotic lesion was 2 cm (range 1–7 cm). Conclusion: The prevalence of phlebosclerosis in the lower extremities appears to be low with no significant sex differences. Age and chronic venous disease are important factors for its development. It may be present in the absence of thrombosis or reflux. A greater prevalence of phlebosclerotic lesions was found in the SSV.

We investigated the prevalence of peripheral arterial disease (PAD). Primary Care Health Centers (n = 14) in Thessaly (central Greece) recruited 436 participants, mean age 71 (50-79) years. Peripheral arterial disease was considered present if the ankle–brachial index (ABI) was 1.4 in at least 1 leg. Asymptomatic PAD was defined as an abnormal ABI and no symptoms or history of limb revascularization. The prevalence of PAD was 13% (mostly asymptomatic, 11.7%). Only 5 (8.77%) of 57 patients with PAD were aware of their disease and only in these patients were the physicians aware of the presence of PAD. The risk factors associated with PAD were age, smoking, and the combination of diabetes mellitus and coronary artery disease. All symptomatic patients were on antiplatelet therapy but 33% did not take statins. For asymptomatic patients, 74.5% were not on antiplatelet therapy and 57% did not receive statins. In the primary health care setting, PAD is underdiagnosed and undertreated.

Lymphedema is an underrecognized and undertreated condition that requires a multidisciplinary approach in an individualized program that will address the special needs of each patient. In an ideal setting of an outpatient management program the team should be composed of a vascular surgeon, a dermatologist, a physiotherapist, a dietician, a psychologist, a social worker, and an office employee, working together in the assessment and management of all aspects of lymphedema. All treatment strategies and actions taken should ultimately focus on the improvement of the quality of life of patients suffering from lymphedema and on the prevention of lymphedema in high-risk patients.

The aim of the paper is to determine whether the angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism is associated with abdominal aortic aneurysm (AAA) and inguinal hernia. A case-control study was conducted in 264 subjects: 65 patients with AAA, 91 patients with inguinal hernia, 19 patients with both AAA and hernia, and 89 controls were investigated for the ACE I/D polymorphism. Genotype analysis was performed using a polymerase chain reaction technique. Significant differences in the genotype between the patient groups and controls were identified (aneurysm versus control, P = 0.011; aneurysm plus hernia versus control, P = 0.022; hernia versus control, P = 0.001), whereas no differences were found within patient groups. Patients with AAA and/ or hernia had an increased prevalence of I/D heterozygosity, which persisted even after adjusting for differences in confounding clinical variables (aneurysm versus control, OR 0.3, 95% CI 0.2–0.8, P = 0.005; aneurysm plus hernia versus control, OR 0.3, 95% CI 0.1-0.9, P = 0.040; hernia versus control, OR 0.4, 95% CI 0.2–0.7, P = 0.004). In conclusion, an association between the heterozygote ACE I/D state and the presence of AAA and/or hernia was identified. The role of the ACE I/D polymorphism in aneurysm and hernia needs further investigation.