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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. [ABSTRACT FROM PUBLISHER]

Background: Endovascular aortic repair (EVAR) is being used with increasing frequency for the treatment of ruptured abdominal aortic aneurysms (rAAAs), although conflicting results have been reported concerning perioperative mortality. The aim of our study was to evaluate potential difference in mortality rates between EVAR and open surgical repair (OSR) and identify independent risk factors for in-hospital mortality in rAAAs. This study also aimed to evaluate the Glasgow Aneurysm Score (GAS) in predicting in-hospital mortality. A time-trend analysis of EVAR for ruptured AAAs was also performed., Methods: Prospectively collected data from 7 public hospitals in Greece concerning rAAA repairs between January 2006 and April 2012 were analyzed. Primary outcome was in-hospital mortality. Multivariate logistic regression analysis was used to identify independent risk factors. The receiver-operator characteristic curve was used to determine the value of the GAS in predicting in-hospital death. Time-trend analysis, depicting annual changes (%), concerning EVAR for ruptured AAAs was also conducted., Results: A total of 418 patients (92.3% men, mean age = 74.3 ± 8.8) with rAAAs were recorded during the study period. Among them, 113 patients (27%) underwent EVAR. Overall in-hospital mortality was 45.2%, whereas in-hospital mortality after EVAR and OSR was 20.4% and 54.3%, respectively (P < 0.001). Multivariate analysis evidenced that hemodynamic instability (P < 0.001), OSR (P < 0.001), age ≥80 years (P < 0.001), coronary artery disease (P < 0.001), and renal insufficiency (P = 0.02) independently increased in-hospital mortality. Area under the curve of GAS was 0.80 (95% confidence interval [CI] = 0.75-0.85, P < 0.001) for OSR and 0.64 (95% CI = 0.51-0.77, P = 0.04) for EVAR. Annual increase of proportion (%) of EVAR for rupture was 5% (P = 0.004)., Conclusions: EVAR is being used with increasing frequency for the treatment of rAAAs and it appears to be associated with lower in-hospital mortality compared with OSR, after adjustment for hemodynamic instability and known atherosclerotic risk factors. Preoperative predictors of in-hospital mortality such as GAS should be probably modified in these patients., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Objective: Osteopontin (OPN) and osteoprotegerin (OPG) are well-known vascular calcification inhibitors, which have been recently demonstrated to correlate with inflammation and cardiovascular events incidence. The aim of this cross-sectional study is to survey whether OPN and OPG are involved in carotid plaque vulnerability. For this reason, we assessed serum OPN and OPG levels in patients with carotid stenosis, and we explored their relationship with carotid plaque echogenicity and subsequent cerebrovascular ischemic events., Methods: A total of 164 Whites were selected from a large cohort of 297 subjects to participate. In particular, 114 patients (61 men, 53 women), aged 55 to 80, had recently-diagnosed ICA stenosis higher than 50%. A group of 50 age-, sex-, and body mass index (BMI)-matched healthy individuals served as healthy controls. Patients with renal failure, hypothyroidism, osteoporosis, and lipid-lowering therapy were excluded. Images of both carotids were obtained from all participants using a high-resolution color duplex ultrasound and the gray-scale median (GSM) score was calculated. Brain computed tomography (CT), and magnetic resonance imaging (MRI) scans when CT was questionable, were performed on all patients with carotid stenosis. Clinical parameters, lipid and glycemic indexes, hsCRP, fibrinogen, white blood cells (WBC) count, OPN, and OPG were measured. Independent t test, one-way ANOVA, Pearson correlation, and multiple regression analysis were used for statistical analysis., Results: Among patients with carotid stenosis, 60 had history of ipsilateral stroke or TIA and positive CT or MRI findings (group A), while 54 had no neurological symptoms and negative CT and MRI scan (group B). Overall, patients with carotid stenosis showed worse lipid profile and increased waist circumference, blood pressure, hsCRP, fibrinogen, WBC count, OPN, and OPG levels compared with healthy subjects (group C) (P <.05). Statistical analysis revealed that group A had significantly lower levels of GSM than group B (57.41 +/- 38.19 vs 76.32 +/- 36.72; P = .008) and higher levels of hsCRP, OPN, and OPG than groups B and C (P < .05). Concerning the latter, biochemical markers group B showed only elevated OPG levels compared with group C (P = .038). Notably, GSM was considerably associated with serum OPN and OPG and waist circumference in patients with carotid atherosclerosis in univariate (r = -0.333; P = .032, r = -0.575; P < .001, r = -0.590; P =.006, respectively) and multiple regression analysis (R(2) = 0.445; P =.006)., Conclusions: The present study demonstrated elevated serum OPN and OPG levels in patients with carotid stenosis and documented an independent association between these biochemical markers, GSM and carotid-induced symptomatology. Therefore bone-matrix proteins combined with GSM could be potential markers for vulnerable carotid plaques.