Rupture after endovascular abdominal aortic aneurysm repair: a multicenter study.

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.

Predictors affecting in-hospital mortality of ruptured abdominal aortic aneurysms: a Greek multicenter study.

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.

Macrophage infiltration and smooth muscle cells content associated with haptoglobin genotype in human atherosclerotic carotid plaques.

We assessed the association between the haptoglobin (Hp) genotype and 2 common indicators of atherosclerotic plaque instability: macrophage infiltration and the smooth muscle cell (SMC) content. A total of 70 consecutive patients who underwent carotid endarterectomy were included in the study. For immunohistochemical study the anti-CD68 and anti-a-actin antibodies were used on adjacent serial sections; 36 plaques from patients with the Hp 1-1 or 2-1 genotype and 34 plaques from patients with the Hp 2-2 genotype were analyzed. The macrophage content (CD68+) was significantly higher in the Hp 2-2 group compared with that in the Hp 1-1 or 2-1 group (P < .001). In plaques from patients with diabetes, the SMC content was significantly lower in the Hp 2-2 group (P = .034). Carotid plaques from diabetic patients with Hp 2-2 genotype had higher macrophage infiltration and lower SMC content. Both parameters are indicators of atherosclerotic plaque instability.

Association of haptoglobin genotype and common cardiovascular risk factors with the amount of iron in atherosclerotic carotid plaques.

INTRODUCTION: The aim of this study was to evaluate the iron burden of carotid atherosclerotic plaques removed from patients treated for carotid disease and find any relation with haptoglobin genotype and other common cardiovascular risk factors. METHODS: Consecutive patients undergoing carotid endarterectomy were included in the study. All patients had high-grade carotid stenosis (>70%). The clinical characteristics and serum parameters of the study population were recorded and the haptoglobin genotype was determined. The presence of hemosiderin deposits in the plaques was identified using Perl's stain on adjacent serial sections. RESULTS: 70 specimens were processed for histologic examination: 27 plaques from diabetic patients (16 with the Hp 1-1 or 2-1 genotype and 11 with the Hp 2-2 genotype) and 43 plaques from non diabetic patients (20 with the Hp 1-1 or 2-1 genotype and 23 with the Hp 2-2 genotype). In plaques from diabetic patients the density of Perl's iron stain was significantly higher in the Hp 2-2 group compared with that in the Hp 1-1 or 2-1 group (p = 0.008). The correlation and regression analysis of all possible clinical and laboratory predictors of intraplaque iron deposition showed that four factors were independently associated with intraplaque iron deposition: male gender, serum homocysteine, Hp 2-2 genotype and diabetes mellitus treatment. CONCLUSIONS: Male diabetic patients with increased plasma levels of homocysteine and the Hp 2-2 genotype had higher carotid plaque iron deposition. Current evidence and pathophysiological considerations suggest that the increased intraplaque iron deposition may be associated with increased oxidative stress, affecting the stability of the carotid plaque.

Hyperperfusion syndrome after carotid revascularization.

Cerebral hyperperfusion syndrome is a rare, serious complication of carotid revascularization either after carotid endarterectomy or carotid stent placement. Impaired cerebral autoregulation and post-revascularization changes in cerebral hemodynamics are the main mechanisms involved in the development of the syndrome. Hyperperfusion syndrome may be fatal once an intracranial hemorrhage occurs. This article reviews the literature, intending to make a synthesis of all new data concerning the clinical manifestations of hyperperfusion syndrome, the pathophysiologic pathways involved in its development, the prediction, and the appropriate management. Also, a review of the most recent series of hyperperfusion syndrome following carotid revascularization, both with classic open endarterectomy and carotid artery stenting has been performed.

The effect of negative pressure therapy on the femoral vein blood flow and wall structure.

Negative pressure therapy has been recently used for managing lymphatic or infective groin complications. The aim of this study was to investigate any possible association between application of negative pressure therapy in the groin area and deep-vein thrombosis. Acute surgical wounds were created at the inguinal areas in 7 pigs. Different negative pressures ranging from -50 to -200 mmHg were applied directly over the femoral vessels, and blood flow alterations were studied using a Doppler ultrasound. Femoral vein specimens were also removed for histological examination after 12 hours of therapy. It has been demonstrated that negative pressure therapy does not significantly alter the baseline lower limb venous return. Histology demonstrated several changes, which are associated with vein thrombogenesis. The hemodynamic and pathological findings still leave a potential for thrombogenic effects of negative pressure therapy and warrant care to protect the femoral veins, with the use of thrombosis prophylaxis measures.

Cardiac troponin I in patients with acute lower limb ischemia.

The presence, cause, and clinical significance of elevated cardiac troponin I in patients with acute lower limb ischemia is yet unknown. Forty-six patients (20 men [43%]; mean age 72 +/- 10 years, range 42 to 92) with acute lower limb ischemia were enrolled in this study. Serial creatine kinase (CK), CK isoenzyme MB (CK-MB), and troponin I measurements were obtained in all consecutive patients. Peak levels were evaluated for each patient. Twenty-four patients (52%) had elevated peak troponin I levels (>0.2 ng/ml) during their hospitalization. Patients were divided into 3 groups according to their peak troponin I levels: 11 patients (24%) had peak troponin I levels >1 ng/ml (the high troponin I group), 13 (28%) had levels of 0.2 to 1 ng/ml (the intermediate troponin I group), and the remaining 22 (48%) had peak troponin I levels <0.2 ng/ml (the low troponin I group). The peak CK levels were 10,263 +/- 16,513, 1,294 +/- 1,512, and 934 +/- 1,045 IU/ml (p = 0.04) in the 3 different troponin I subgroups, respectively, and the peak CK-MB levels were 143 +/- 170, 38 +/- 31, and 38 +/- 43, respectively (p = 0.04). Troponin I was positively correlated with CK (R = 0.35, p = 0.017) and CK-MB (R = 0.38, p = 0.009). The mean length of hospitalization was 8.3 +/- 6.2 days for the whole study group and did not vary among the 3 troponin I groups (10.5 +/- 10.9 vs 8.6 +/- 4.9 vs 7.2 +/- 4.0 days, p = 0.762). There were no differences in mortality during hospitalization among the 3 groups (4 of 11 vs 1 of 13 vs 4 of 22 patients, p = 0.22). In conclusion, patients with acute lower limb ischemia often have elevated cardiac troponin I levels. Elevated troponin I levels were not associated with the duration of hospitalization or with in-hospital mortality in this group of patients.

Statin treated patients have reduced intraplaque angiogenesis in carotid endarterectomy specimens.

BACKGROUND: Treatment with statins is considered a first line therapy in atherosclerotic disease. Intraplaque angiogenesis is involved in plaque progression and instability. It remains unclear whether the beneficial effect of statin treatment in humans is achieved through reduced intraplaque angiogenesis. The aim of this study was to evaluate the capillaries density in carotid plaques removed from patients treated with statin versus untreated patients. METHODS AND RESULTS: We studied 102 patients who underwent carotid endarterectomy: 98 of them met the inclusion criteria and entered the study; 75 men and 23 women; mean age 66+/-8 years (range 42-83 years). Forty-three patients (44%) were on statin treatment at least 3 months before endarterectomy and 55 (56%) had never received statin treatment. The intensity of intraplaque angiogenesis was evaluated with immunohistochemistry using the antibody CD34. The number of capillaries per mm(2) was measured with a custom designed image tool analysis. With the exception of serum total cholesterol levels and serum low-density cholesterol levels, the two groups of patients did not vary significantly in cardiovascular risk factors and in parameters pertaining to the procedure profile. Patients on statin treatment had less capillaries per mm(2) than patients not receiving this kind of drugs (0.97+/-0.61 per mm(2) versus 1.39+/-0.98 per mm(2), p=0.031). Univariate associations between possible explanatory variables and number of capillaries per mm(2) were tested using Spearman rank R. Variables associated with a p-value <0.20 (age, serum creatinine, serum total cholesterol, serum low-density lipoprotein, serum homocysteine, presence of diabetes mellitus and statin treatment) were entered in a multivariable model. Multivariate analysis showed that statin treatment was the only independent predictor (t=-5.39, p<0.001) of intraplaque angiogenesis. CONCLUSIONS: Statin therapy is associated with reduced intraplaque angiogenesis in the carotid arteries. This could provide an explanation for the beneficial effects of this kind of drug on patients with atherosclerotic disease.

Covered stent-graft treatment of traumatic internal carotid artery pseudoaneurysms: a review.

OBJECTIVE: To review the literature concerning the management with placement of covered stent-grafts of traumatic pseudoaneurysms of the extracranial internal carotid artery (ICA) resulting from penetrating craniocervical injuries or skull base fractures. METHOD: We have reviewed, from the Medline database, all the published cases in the English literature since 1990 and we have added a new case. RESULTS: We identified 20 patients with traumatic extracranial ICA pseudoaneurysms due to penetrating craniocervical injuries or skull base fractures who had been treated with covered stent-graft implantation. Many discrepancies have been ascertained regarding the anticoagulation therapy. In 3 patients the ICA was totally occluded in the follow-up period, giving an overall occlusion rate 15%. No serious complication was reported as a result of the endovascular procedure. CONCLUSION: Preliminary results suggest that placement of stent-grafts is a safe and effective method of treating ICA traumatic pseudoaneurysms resulting from penetrating craniocervical injuries or skull base fractures. The immediate results are satisfactory when the procedure takes place with appropriate anticoagulation therapy. The periprocedural morbidity and mortality and the early patency are also acceptable. A surveillance program with appropriate interventions to manage restenosis may improve the long-term patency.