Iliac Pseudoaneurysm, Only a Manifestation With More Causes: A Case Report.

Pseudoaneurysm is due to a disruption in arterial wall continuity. It forms a sac that communicates with the vessel lumen and is surrounded by the compressed, surrounding tissues and not by the wall of the artery from which the lesion arises. Many causes can predispose to the formation of a pseudoaneurysm such as trauma, surgical procedures, anticoagulation. In our patient another important risk factor for the formation of a pseudoaneurysm is ADPKD (autosomal dominant polycystic kidney disease) that can cause vascular complication. The mechanisms leading to the genesis of the pseudoaneurysms in our patient are unknown, but the clinicians should bear in mind when evaluating this type of patients that ADPKD may have a various range of systemic cardiovascular manifestation.

Late patency of reconstructed visceral arteries after open repair of thoracoabdominal aortic aneurysm.

BACKGROUND: In the era of rising endovascular treatment of thoracoabdominal aortic aneurysms (TAAAs), the analysis of visceral vessel (VV) patency after open surgical repair is crucial to provide a future benchmark between these different approaches. This study reports the late outcomes of a single-center experience with open TAAA repair, focusing on the results of different techniques adopted for renal and splanchnic revascularization. METHODS: Data were analyzed for 382 consecutive open TAAA repairs performed between January 2009 and July 2015 (284 men; mean age, 66 ± 10 years). Follow-up of surviving patients was carried out by computed tomography angiography and office checkups at 3 and 12 months and yearly afterward. Kaplan-Meier analysis was performed for overall survival, patency of reconstructed VVs (celiac trunk, superior mesenteric artery, right renal artery, left renal artery), and reinterventions on visceral arteries. Furthermore, VV long-term patency was analyzed in subgroups of patients according to the revascularization strategy (patch inclusion of all vessels, group 1; one-vessel separate reattachment and patch inclusion of the remaining vessels, group 2; separate reattachment of all VVs, group 3). RESULTS: In-hospital mortality and paraparesis/paraplegia occurred in 7.6% and 8.1% of patients, respectively. Among the 353 survivors, 338 complied with the follow-up protocol, and adequate computed tomography angiography images were available in 247 patients (952 VVs were analyzed). Overall follow-up survival was 94%, 91%, and 70% at 1 year, 2 years, and 5 years, respectively. At the same time points, VV patency was 99%, 98%, and 98% for celiac trunk; 100%, 100%, and 100% for superior mesenteric artery; 100%, 96%, and 96% for right renal artery; and 91%, 87%, and 82% for left renal artery (log-rank test, P < .0001). Estimates for reinterventions on VVs were 1.2%, 6.3%, and 17% at the same time points. Freedom from occlusion of any VV at 1 year and 3 years was 95% and 87% for group 1, 89% and 79% for group 2, and 92% and 92% for group 3, respectively (log-rank test, P = .13). CONCLUSIONS: Long-term patency of VVs after open TAAA repair performed in high-volume centers is high, regardless of the technique employed for revascularization. The left renal artery appears to be most prone to occlusion over time.

Results after elective open repair of pararenal abdominal aortic aneurysms.

OBJECTIVE: This study presents a retrospective analysis of long-term outcomes and factors influencing early and late results of a 20-year experience with open repair of atherosclerotic pararenal abdominal aortic aneurysms (PAAAs). METHODS: Records of consecutive patients who underwent open repair of PAAA between 1990 and 2010 at a tertiary referral care center were analyzed for demographics, comorbidities, operative variables, complications, and 30-day mortality. Long-term results were also assessed through a local electronic medical database and direct follow-up. Variables influencing early and late results were evaluated by univariate and multivariate logistic regression analyses, stepwise backward elimination, and Cox proportional hazard regression. RESULTS: The study included 200 patients (94% men; mean age, 69.5 years) who were monitored for a mean of 107.3 months. The aneurysm was juxtarenal in 78% of patients, suprarenal in 19.5%, and type IV thoracoabdominal in 2.5%. Mortality at 30 days was 2.5%. At least one major complication occurred in 51.5%. Postoperative acute renal failure (pARF) occurred in 11% of the patients, 3% had temporary hemodialysis, but only 0.5% required chronic hemodialysis. pARF was significantly related to preoperative renal function (P = .009), visceral ischemia >30 minutes (P = .05), and supraceliac or supramesenteric clamp site (P = .005). Respiratory complications (13.8%) were associated with an increasing stage of chronic obstructive pulmonary disease (P = .020), proximal clamp site (P = .047), and intraoperatively infused crystalloids (P = .014). Cardiac complications (12.8%) were related to previous myocardial infarction (P = .031) and proximal clamp site (P = .003). Late deaths were observed in 21.5%. Mean survival was 50 months, with Kaplan-Meier survival estimates of 78% at 5 years and 60.5% at 10 years. Variables influencing long-term survival included age (hazard ratio [HR], 2.67; P = .01), chronic obstructive pulmonary disease stage 2 (HR, 5.14; P = .01) and stage 3 (HR, 4.54; P = .03), postoperative cardiac complication (HR, 3.93; P ≤ .00), previous myocardial infarction (HR, 1.47; P = .02), peripheral artery disease (HR, 1.97; P = .03), and smoking (HR, 1.17; P = .02). Survival and late-onset renal insufficiency were unaffected by preoperative renal function. Late renal failure was observed in 6.2% of the patients but did not predict mortality. CONCLUSIONS: Conventional surgical repair of PAAAs can be performed with acceptable short-term and long-term mortality. Although pARF is frequent, chronic hemodialysis at discharge is rare. Cardiac and respiratory complications are also common and associated with worse survival. Our data represent a potentially useful benchmark for complex endovascular repairs of this type of aneurysm.

Development and validation of an improved classification and risk stratification system for carotid body tumors: Multinational collaborative cohort study.

BACKGROUND: This study aims to develop and validate a new classification system that better predicts combined risk of neurological and neurovascular complications following CBT surgery, crucial for treatment decision-making. METHODS: Multinational retrospective cohort study with 199 consecutive cases. A cohort of 132 CBT cases was used to develop the new classification. To undertake external validation, assessment was made between the actual complication rate and predicted risk by the model on an independent cohort (n = 67). RESULTS: Univariate analyses showed statistically significant associations between developing a complication and the following factors: craniocaudal dimension, volume, Shamblin classification, and Mehanna types. In the multivariate prognostic model, only Mehanna type remained as a significant risk predictor. The risk of developing complications increases with increasing Mehanna type. CONCLUSIONS: We have developed and then validated a new classification and risk stratification system for CBTs, which demonstrated better prognostic power for the risk of developing neurovascular complications after surgery.

Controversial results of the Revised Cardiac Risk Index in elective open repair of abdominal aortic aneurysms: Retrospective analysis on a continuous series of 899 cases.

BACKGROUND: Low reliability of Revised Cardiac Risk Index (RCRI) in predicting major cardiac events (MACE) among Vascular Surgery patients emerged in recent literature, suggesting procedure-specific risk evaluation - particularly in major surgery. METHODS-RESULTS: Comorbidities, perioperative variables, RCRI and MACE were retrospectively analyzed in a consecutive series of 899 elective open abdominal aortic aneurysm (AAA) repairs performed at our Institution. Possible MACE predictors were studied through univariate/multivariable analysis (logistic regression, MVRE) and stepwise-backward elimination/odds ratio (MVR-SBE/OR). Patients were divided by clampsite in 2 subgroups: 1. infrarenal (690 cases); 2. pararenal (209 cases). RCRI resulted predictive for MACE in the whole dataset but its performance resulted lower for pararenal aneurysms (p = 0.11) than for infrarenal ones (p ≤ 0.00). Among RCRI covariates of the whole cohort, dilated cardiomyopathy (p ≤ 0.001), ischemic cardiopathy (p ≤ 0.01) and cerebrovascular disease (p ≤ 0.02) resulted predictive. Peripheral arteriopathy also related to MACE (p ≤ 0.03). At MVR-SBE/OR analysis, the following resulted to be MACE predictors: dilated cardiomyopathy (p ≤ 0.001), cerebrovascular disease (p ≤ 0.02), and surgical access (p = 0.04) in subgroup 1; previous myocardial infarction (p ≤ 0.01), congestive failure (p ≤ 0.03) and chronic pneumopathy (p = 0.04) in subgroup 2. CONCLUSIONS: Predictability of RCRI in elective AAA surgery is influenced by clampsite and resulted to be lower in aneurysms requiring suprarenal clamping. Variables included in the RCRI show to have different weights when patients are stratified by clampsite. Some variables not included in the RCRI model significantly affect the onset of MACE. RCRI should be revised to elaborate a specific score for AAAs including further MACE predictors, to improve risk assessment and to support proper surgical strategy.

C-Reactive Protein Binds to Cholesterol Crystals and Co-Localizes with the Terminal Complement Complex in Human Atherosclerotic Plaques.

Inflammation is a part of the initial process leading to atherosclerosis and cholesterol crystals (CC), found in atherosclerotic plaques, which are known to induce complement activation. The pentraxins C-reactive protein (CRP), long pentraxin 3 (PTX3), and serum amyloid P component (SAP) are serum proteins associated with increased risk of cardiovascular events and these proteins have been shown to interact with the complement system. Whether the pentraxins binds to CC and mediate downstream complement-dependent inflammatory processes remains unknown. Binding of CRP, PTX3, and SAP to CC was investigated in vitro by flow cytometry and fluorescence microscopy. CRP, PTX3, and SAP bound to CC in a concentration-dependent manner. CRP and PTX3 interacted with the complement pattern recognition molecule C1q on CC by increasing the binding of both purified C1q and C1q in plasma. However, CRP was the strongest mediator of C1q binding and also the pentraxin that most potently elevated C1q-mediated complement activation. In a phagocytic assay using whole blood, we confirmed that phagocytosis of CC is complement dependent and initiated by C1q-mediated activation. The pathophysiological relevance of the in vitro observations was examined in vivo in human atherosclerotic plaques. CRP, PTX3, and SAP were all found in atherosclerotic plaques and were located mainly in the cholesterol-rich necrotic core, but co-localization with the terminal C5b-9 complement complex was only found for CRP. In conclusion, this study identifies CRP as a strong C1q recruiter and complement facilitator on CC, which may be highly relevant for the development of atherosclerosis.

Lectin Pathway of Complement Activation Is Associated with Vulnerability of Atherosclerotic Plaques.

Inflammatory mechanisms may be involved in atherosclerotic plaque rupture. By using a novel histology-based method to quantify plaque instability here, we assess whether lectin pathway (LP) of complement activation, a major inflammation arm, could represent an index of plaque instability. Plaques from 42 consecutive patients undergoing carotid endarterectomy were stained with hematoxylin-eosin and the lipid core, cholesterol clefts, hemorrhagic content, thickness of tunica media, and intima, including or not infiltration of cellular debris and cholesterol, were determined. The presence of ficolin-1, -2, and -3 and mannose-binding lectin (MBL), LP initiators, was assessed in the plaques by immunofluorescence and in plasma by ELISA. LP activation was assessed in plasma by functional in vitro assays. Patients presenting low stenosis (≤75%) had higher hemorrhagic content than those with high stenosis (>75%), indicating increased erosion. Increased hemorrhagic content and tunica media thickness, as well as decreased lipid core and infiltrated content were associated with vulnerable plaques and therefore used to establish a plaque vulnerability score that allowed to classify patients according to plaque vulnerability. Ficolins and MBL were found both in plaques' necrotic core and tunica media. Patients with vulnerable plaques showed decreased plasma levels and intraplaque deposition of ficolin-2. Symptomatic patients experiencing a transient ischemic attack had lower plasma levels of ficolin-1. We show that the LP initiators are present within the plaques and their circulating levels change in atherosclerotic patients. In particular, we show that decreased ficolin-2 levels are associated with rupture-prone vulnerable plaques, indicating its potential use as marker for cardiovascular risk assessment in atherosclerotic patients.