Cranial Nerve Injury After Carotid Endarterectomy: Incidence, Risk Factors, and Time Trends.

OBJECTIVE/BACKGROUND: To review the incidence of post-carotid endarterectomy (CEA) cranial nerve injury (CNI), and to evaluate the risk factors associated with increased CNI risk. METHODS: The study was a meta-analysis. Pooled rates with 95% confidence intervals (CIs) were calculated for CNIs after primary CEA. Odds ratios (ORs) were calculated for potential risk factors. A fixed-effects model or a random effects model (Mantel-Haenszel method) was used for non-heterogeneous and heterogeneous data, respectively. Meta-regression analysis was performed to examine the influence of publication year upon CNI rate. RESULTS: Twenty-six articles, published between 1970 and 2015, were included in the meta-analysis, corresponding to 20,860 CEAs. Meta-analysis revealed that the vagus nerve was the most frequently injured cranial nerve (pooled injury rate 3.99%, 95% CI 2.56-5.70), followed by the hypoglossal nerve (3.79%, 95% CI 2.73-4.99). Fewer than one seventh of these injuries are permanent (vagus nerve: 0.57% [95% CI 0.19-1.10]; hypoglossal nerve: 0.15% [95% CI 0.01-0.39]). A statistically significant influence of publication year on the vagus and hypoglossal nerve injury rate was found, with the injury rate having decreased from about 8% to 2% and 1%, respectively, over the last 35 years. Urgent procedures (OR 1.59, 95% CI 1.21-2.10; p = .001), as well as return to the operating room for a neurological event or bleeding (OR 2.21, 95% CI 1.35-3.61; p = .002) were associated with an increased risk of CNI, whereas no statistically significant association was found between CNIs and the type of anaesthesia, the use of a patch, redo operation, and the use of a shunt. CONCLUSION: The vagus nerve appears to be the most frequently injured cranial nerve after CEA, followed by the hypoglossal nerve, with only a small proportion of these injuries being permanent. The CNI rate has significantly decreased over the past 35 years to a point indicating that CNIs should not be considered a major influencing factor in the decision making process between CEA and stenting.

A Review of Open and Endovascular Treatment of Superior Vena Cava Syndrome of Benign Aetiology.

BACKGROUND: The widespread use of central venous catheters, ports, pacemakers, and defibrillators has increased the incidence of benign superior vena cava syndrome (SVCS). This study aimed at reviewing the results of open and endovascular treatment of SVCS. METHOD: Medical literature databases were searched for relevant studies. Studies with more than five adult patients, reporting separate results for the SVC were included. Nine studies reported the results of endovascular treatment of SVCS including 136 patients followed up for a mean of 11-48 months. Causes of SVCS were central venous catheters and pacemakers (80.6%), mediastinal fibrosis (13.7%), and other (5.6%). Percutaneous transluminal angioplasty (PTA) and stenting was performed in 73.6%, PTA only in 17.3%, and thrombolysis, PTA, and stenting in 9%. Four studies reported the results of open repair of SVCS including 87 patients followed up between 30 months and 10.9 years. The causes were mediastinal fibrosis (58.4%), catheters and pacemakers (28.5%), and other (13%). Operations performed included a spiral saphenous interposition graft, other vein graft, PTFE graft, and human allograft. Thirteen patients required re-operations (15%) before discharge mainly for graft thrombosis. RESULTS: In the endovascular group technical success was 95.6%. Thirty day mortality was 0%. Regression of symptoms was reported in 97.3%. Thirty-two patients (26.9%) underwent 58 secondary procedures. In the open group the 30 day mortality was 0%. Symptom regression was reported in 93.5%. Twenty-four patients (28.4%) underwent a total of 33 secondary procedures. CONCLUSIONS: Endovascular is the first line treatment for SVCS caused by intravenous devices, whereas surgery is most often performed for mediastinal fibrosis. Both treatments show good results regarding regression of the symptoms and mid-term primary patency, with a significant incidence of secondary interventions.

Galectin-3, Carotid Plaque Vulnerability, and Potential Effects of Statin Therapy.

OBJECTIVES: Galectin-3, a member of galectines, a family of b-galactoside-specific lectins, has been reported to propagate vascular inflammation. The role of galectin-3 in carotid atherosclerosis is controversial. The aim of this study was to investigate the relationship of galectin-3 with plaque vulnerability in patients with high grade carotid stenosis. METHODS: This was a cross sectional study of patients undergoing carotid endarterectomy (CEA). Carotid plaques obtained from 78 consecutive patients (40 symptomatic [SG], 38 asymptomatic [AG]) undergoing CEA were histologically analyzed for galectin-3, macrophages (CD68) and laminin. Pre-operatively the biochemical profile and plaque echogenicity (gray-scale median, GSM) score were determined. RESULTS: There were no significant differences in clinical and demographic parameters between SG and AG(p > .05). The SG had a lower GSM score (44.21 ± 18.24 vs. 68.79 ± 28.79, p < .001) and a smaller positive stained area for galectin-3 (4.89 ± 1.60% vs. 12.01 ± 5.91%, p < .001) and laminin (0.88 ± 0.71% vs. 3.46 ± 2.12%, p < .001) than the AG. On the other hand, intra-plaque macrophage content was increased in SG (p < .001). For the whole cohort, symptomatic status was independently associated with intra-plaque contents of both galectin-3 (OR=0.634, p < .001), and GSM score (OR=0.750, p < .001). Notably, patients on long term statin treatment had elevated galectin-3 and lowered macrophage intra-plaque concentrations compared with those on short term treatment (p < .05). CONCLUSIONS: A low galectin-3 intra-plaque concentration seems to correlate with clinically and ultrasonically defined unstable human carotid plaques. Long term statin treatment may induce increase of intra-plaque galectin-3 concentration mediating plaque stabilization.

Factors Predisposing to Endograft Limb Occlusion after Endovascular Aortic Repair.

OBJECTIVES: The aim of this study was to investigate risk factors for endograft limb occlusion after endovascular abdominal aneurysm repair (EVAR), using a case control design. METHODS: All patients presenting with endograft limb occlusion after elective EVAR between January 2010 and June 2013, along with age, sex, and type of endograft matched controls were included in the study. The impact of atherosclerotic risk factors, anatomic characteristics of the aneurysm, procedural details, and antiplatelet therapy was investigated. Multivariate logistic regression analysis and conditional logistic regression analysis for 1:3 matched pairs deriving adjusted odds ratios (ORs) with 95% confidence intervals (CIs) in order to detect significant risk factors for endograft limb occlusion among cases and controls were modeled. RESULTS: Of the 439 patients treated by EVAR, 18 patients (4.1%) presented with endograft limb occlusion. These patients were compared to 54 matched controls. Limb occlusion was associated with iliac artery angulation ≥ 60° (OR = 5.76, 95% CI =1.24-26.74; p = .03) or perimeter calcification ≥ 50% (OR =5.87, 95% CI = 1.10-31.32; p = .04). Limb occlusion was also associated with ≥ 15% endograft oversizing in the common iliac artery (OR = 5.54, 95% CI = 1.11-27.60; p = .04). No other risk factors for limb occlusion were recognized. CONCLUSIONS: The presence of significant angulation and calcification of the iliac arteries as well as excessive limb oversizing appear to be independent predictors of endograft limb occlusion after EVAR.

A new framework architecture for next generation e-Health services.

The challenge for fast and low-cost deployment of ubiquitous personalized e-Health services has prompted us to propose a new framework architecture for such services. We have studied the operational features and the environment of e-Health services and we led to a framework structure that extends the ETSI/Parlay architecture, which is used for the deployment of standardized services over the next generation IP networks. We expanded the ETSI/Parlay architecture with new service capability features as well as sensor, profiling and security mechanisms. The proposed framework assists the seamless integration, within the e-Health service structure, of diverse facilities provided by both the underlying communication and computing infrastructure as well as the patient's bio and context sensor networks. Finally, we demonstrate the deployment of a tele-monitoring service in smart home environment based on the proposed framework architecture.