Open Repair of Two Ipsilateral Extracranial Internal Carotid Artery Aneurysms.

INTRODUCTION: A patient with two ipsilateral extracranial internal carotid artery (ICA) aneurysms treated by open repair is reported, with an emphasis on pre-operative planning and decision making, and a review of literature. REPORT: A 44 year old man was diagnosed with a right thyroid lobe nodule and two asymptomatic ipsilateral aneurysms of the right ICA. Diagnostic workup using three dimensional reconstruction and centre lumen line measurements on computed tomography revealed two aneurysms of the right ICA, both > 20 mm. Surgery was planned with intra-operative mandibular subluxation to maximise distal exposure. Neuromonitoring consisted of transcranial Doppler ultrasound and electroencephalography. After mandibular subluxation and complete dissection of the aneurysms and digastric muscle division, adequate exposure of the distal ICA was obtained, followed by resection of both aneurysms, and reconstruction with a reversed greater saphenous vein graft. No complications occurred and one year follow up showed a patent graft without signs of stenosis or anastomotic aneurysm. DISCUSSION: Open repair of two ipsilateral extracranial ICA aneurysms can be performed safely after careful pre-operative planning using visualisation of the vascular anatomy and distance measurements, and maximising exposure with digastric muscle division, styloidectomy, if necessary, and mandibular subluxation.

Outcomes of open repair of postdissection abdominal aortic aneurysms.

BACKGROUND: Evidence to guide management of postdissection abdominal aortic aneurysms (PDAAA) is lacking. This study describes the outcomes of open repair of PDAAA. METHODS: A retrospective cohort study was conducted of all consecutive patients treated with open repair for PDAAA after a Stanford type A or type B thoracic aortic dissection between January 2006 and December 2017 in two vascular referral centers. Preceding type B dissection treatment could include conservative or surgical management. Primary outcomes were 30-day mortality, complication rates, survival, and reintervention-free survival. Survival and reintervention-free survival were analyzed using the Kaplan-Meier method. Reintervention was defined as any endovascular or surgical intervention after the index procedure. RESULTS: Included were 36 patients (27 men [75%]) with a median age of 64 years (range, 35-81 years). The 30-day mortality was 2.7%. The median follow-up was 16 months (range, 0-88 months). The postoperative course was uneventful in 21 patients (58%). The most frequent complications were postoperative bleeding requiring repeat laparotomy (n = 4), pneumonia (n = 3), congestive heart failure (n = 2), new-onset atrial fibrillation (n = 2), mesenteric ischemia requiring left hemicolectomy (n=1), and ischemic cerebrovascular accident (n = 1). Renal failure requiring hemodialysis developed in one patient. The overall survival at 1 year was 88.8%. Reintervention-free survival was 95.5% after 1 year and 88.6% after 2 years. CONCLUSIONS: Open repair of PDAAA can be performed with a low mortality rate and an acceptable complication rate, comparable with elective open repair of abdominal aortic aneurysms without dissection.

Long-term outcome and quality of life after ruptured abdominal aortic aneurysm repair.

Objectives To evaluate long-term outcome and quality of life after open and endovascular repair of ruptured abdominal aortic aneurysms. Methods All consecutive ruptured abdominal aortic aneurysm patients at the St. Antonius Hospital treated for ruptured abdominal aortic aneurysm between January 2005 and January 2015 were included. Mortality, morbidity, and re-interventions within 30 days and during follow-up were registered. Quality of life was measured with Short Form-36 questionnaire among survivors. Additional subgroup analysis between open repair and endovascular repair was performed. Results A total of 192 patients with ruptured abdominal aortic aneurysm were included: 76.6% (147/192) underwent open repair and 23.4% (45/192) endovascular repair. All-cause 30-day mortality rate was 31.3% (60/192), and 30-day morbidity rate was 70.3% (135/192). Median stay at the intensive care unit was two days for endovascular repair and four days for open repair ( p = 0.002). No other statistically significant differences between endovascular repair and open repair were observed. After a mean follow-up period of 62 months (range 9-126), 72.4% (76/105) of the responders had equivalent Short Form-36 scores as compared to the age-matched general Dutch population, and 84.2% (64/76) of the responders would choose surgery again if they would have a ruptured abdominal aortic aneurysm. Conclusions Survivors of ruptured abdominal aortic aneurysm have similar long-term quality of life scores compared to the age-matched general population. The majority of all survivors would choose to undergo acute abdominal aortic aneurysm repair again.

Impaired kidney function is associated with intraplaque hemorrhage in patients undergoing carotid endarterectomy.

BACKGROUND AND AIMS: Previously, we showed that patients undergoing carotid endarterectomy have an increased risk for major atherosclerotic events in the presence of moderate or poor kidney function. Acceleration of vascular inflammatory responses is considered to be causally involved in progression of atherogenesis and poor outcome in chronic kidney disease patients. The association between kidney function and plaque composition has not been thoroughly investigated yet. The aim of this study was to investigate the association between kidney function and atherosclerotic plaque composition in patients undergoing carotid endarterectomy. METHODS: Atherosclerotic plaques, harvested from 1796 patients who underwent carotid endarterectomy, were immunohistochemically stained for macrophages, smooth muscle cells, calcifications, collagen, microvessels, lipid core size and intraplaque hemorrhage. Cytokines were measured in plaque and plasma and associated with kidney function. Quantitative proteomics were performed on 40 carotid plaques and associated with kidney function. RESULTS: Decreased kidney function was associated with increased odds ratio of intraplaque hemorrhage, OR 1.15 (95% CI; 1.02-1.29 (p = 0.024)) and increased odds ratio of fibrous-atheromatous plaques (plaques with lipid core presenting more than 10% of total plaque surface) OR 1.21 (95% CI; 1.07-1.38 (p = 0.003)) per decrease of 20 points in eGFR. Proteomics revealed that decreased kidney function was associated with upregulation of the classical pathway of the complement system and the intrinsic pathway of the coagulation system. CONCLUSIONS: Decreased kidney function was associated with plaque hemorrhage but not with inflammatory plaque characteristics. Our data suggests that other pathways than the inflammation-pathway are involved in plaque vulnerability and poor outcome in patients with decreased kidney function.

Results of open pararenal abdominal aortic aneurysm repair: single centre series and pooled analysis of literature.

Objectives Endovascular treatment of pararenal abdominal aortic aneurysm has gained terrain over the past decade, despite the substantial need for reinterventions during follow-up. However, open repair is still a well-established treatment option. With the current study we report the results of a consecutive series of elective primary open pararenal abdominal aortic aneurysm repair in a tertiary vascular referral centre, combined with an overview of current literature and pooled data analysis of perioperative mortality of open and endovascular pararenal abdominal aortic aneurysm repair. Methods A retrospective analysis of a prospective database of all elective open pararenal abdominal aortic aneurysm repairs in the St. Antonius Hospital between 2005 and 2014 was performed. Primary endpoint was 30-day mortality. Secondary endpoints were 30-day morbidity, new onset dialysis, reintervention free survival, and overall survival during follow-up. Results Between 2005 and 2014, 214 consecutive patients underwent elective open pararenal abdominal aortic aneurysm repair. Mean age was 69.8 (±7.1) years, 82.7% (177/214) were men, and mean abdominal aortic aneurysm diameter was 62 (±11) mm. Thirty-day mortality was 3.4%. Thirty-day morbidity was 27.1%, which predominantly consisted of pneumonia (18.7% (40/214)), cardiac events (3.3% (7/214)), and new onset dialysis (2.8% (6/214)). Estimated five-year overall survival rate was 74.2%. 0.9% (2/214) of patients required abdominal aortic aneurysm-related reintervention, and an additional 2.3% (5/214) required surgical repair of an incisional hernia. Pooled analysis of literature revealed a 30-day mortality of 3.0% for open pararenal repair and 1.9% for fenestrated endovascular repair. Conclusion Open pararenal abdominal aortic aneurysm repair in the era of increasing endovascular options results in acceptable perioperative morbidity and mortality rates. Mid-term reintervention rate is low compared to fenestrated endovascular aneurysm repair. Expertise with open repair still remains essential for treatment of pararenal abdominal aortic aneurysms in the near future, especially for those patients that are declined for endovascular treatment.

Weight bearing or non-weight bearing after surgically fixed ankle fractures, the WOW! Study: study protocol for a randomized controlled trial.

BACKGROUND: The optimal post-operative care regimen after surgically fixed Lauge Hansen supination exorotation injuries remains to be established. This study compares whether unprotected weight bearing as tolerated is superior to protected weight bearing and unprotected non-weight bearing in terms of functional outcome and safety. METHODS/DESIGN: The WOW! Study is a prospective multicenter clinical trial. Patients between 18 and 65 years of age with a Lauge Hansen supination exorotation type 2, 3 or 4 ankle fractures requiring surgical treatment are eligible for inclusion. An expert panel validates the classification and inclusion eligibility. After surgery, patients are randomized to either the 1) unprotected non-weight-bearing, 2) protected weight-bearing, or 3) unprotected weight-bearing group. The primary outcome measure is ankle-specific disability measured by the Olerud-Molander ankle score. Secondary outcomes are 1) quality of life (e.g., return to work and resumption of sport), 2) complications, 3) range of motion, 4) calf wasting, and 5) maximum pressure load after 3 months and 1 year. DISCUSSION: This trial is designed to compare the effectiveness and safety of unprotected weight bearing with two commonly used post-operative treatment regimens after internal fixation of specified, intrinsically stable but displaced ankle fractures. An expert panel has been established to evaluate every potential subject, which ensures that every patient is strictly screened according to the inclusion and exclusion criteria and that there is a clear indication for surgical fixation. TRIAL REGISTRATION: The WOW! Study is registered in the Dutch Trial Register ( NTR3727 ). Date of registration: 28-11-2012.

Symptomatic carotid atherosclerotic disease: correlations between plaque composition and ipsilateral stroke risk.

BACKGROUND AND PURPOSE: For symptomatic patients with carotid artery stenosis, the risk benefit for surgical intervention may vary among patient groups. Various modalities of plaque imaging have been promoted as potential tools for additional risk stratification, particularly in patients with moderate stenosis. However, it remains uncertain to what extent carotid plaque components predict risk of future ipsilateral ischemic stroke. METHODS: In 2 large atherosclerotic carotid plaque biobank studies, we related histological characteristics of 1640 carotid plaques with a validated risk model for the prediction of individual 1- and 5-year stroke risk. RESULTS: No significant heterogeneity between the studies was found. Predicted 5-year stroke risk (top versus bottom quartile) was related to plaque thrombus (odds ratio, 1.42; 95% confidence interval, 1.11-1.89; P=0.02), fibrous content (0.65; 0.49-0.87; P=0.004), macrophage infiltration (1.41; 1.05-1.90; P=0.02), high microvessel density (1.49; 1.05-2.11; P=0.03), and overall plaque instability (1.40; 1.05-1.87; P=0.02). This association was not observed for cap thickness, calcification, intraplaque hemorrhage, or lymphocyte infiltration. Plaques removed within 30 days of most recent symptomatic event were most strongly correlated with predicted stroke risk. CONCLUSIONS: Features of the vulnerable carotid plaque, including plaque thrombus, low fibrous content, macrophage infiltration, and microvessel density, correlate with predicted stroke risk. This study provides a basis for plaque imaging studies focused on stroke risk stratification.

Type 2 diabetes is not associated with an altered plaque phenotype among patients undergoing carotid revascularization. A histological analysis of 1455 carotid plaques.

AIMS: Diabetes accelerates progression of atherosclerotic disease, but data on associations between diabetes and advanced atherosclerotic plaque composition are scarce. METHODS AND RESULTS: We used one of the largest biobanks, the Athero-Express study (n=1455) at carotid endarterectomy (CEA). All plaques were subjected to histological analysis to assess lipid core size, collagen, macrophages, smooth muscle cells, micro-vessel density and calcifications. In addition, within a subset of patients cytokines and chemokines were assessed. The 295 patients (20%) with type-2 diabetes showed a higher proportion of previous cardiovascular interventions and more stringent treatment for hypertension and hypercholesterolaemia compared with patients without type-2 diabetes. Surprisingly, no associations between diabetes and histological plaque characteristics were observed. In addition, no differences were observed in the expression of inflammatory chemokines, cytokines or advanced glycation end products in plaques of diabetic and non-diabetic patients. CONCLUSION: In patients suffering from significant carotid artery disease, diabetes does not appear to be associated with specific atherosclerotic plaque characteristics.

Time-dependent changes in atherosclerotic plaque composition in patients undergoing carotid surgery.

BACKGROUND: Time-dependent trends in the incidence of cardiovascular disease have been reported in high-income countries. Because atherosclerosis underlies the majority of cardiovascular diseases, we investigated temporal changes in the composition of atherosclerotic plaques removed from patients undergoing carotid endarterectomy. METHODS AND RESULTS: The Athero-Express study is an ongoing, longitudinal, vascular biobank study that includes the collection of atherosclerotic plaques of patients undergoing primary carotid endarterectomy in the province of Utrecht from 2002 to 2011. Histopathologic features of plaques of 1583 patients were analyzed in intervals of 2 years. The analysis included quantification of collagen, calcifications, lipid cores, plaque thrombosis, macrophages, smooth muscle cells, and microvessels. Large atheroma, plaque thrombosis, macrophages, and calcifications were less frequently observed over time, with adjusted odds ratios of 0.72 (95% confidence interval, 0.650-0.789), 0.62 (95% confidence interval, 0.569-0.679), 0.87 (95% confidence interval, 0.800-0.940), and 0.75 (95% confidence interval, 0.692-0.816) per 2-year increase in time, respectively. These changes in plaque characteristics were consistently observed in patient subgroups presenting with stroke, transient ischemic attack, ocular symptoms, and asymptomatic patients. Concomitantly, risk factor management and secondary prevention strategies among vascular patients scheduled for carotid endarterectomy significantly improved over the past decade. CONCLUSIONS: In conclusion, over the past decade, atherosclerotic plaques harvested during carotid endarterectomy show a time-dependent change in plaque composition characterized by a decrease in features currently believed to be causal for plaque instability. This appears to go hand in hand with improvements in risk factor management.

Histological features of carotid plaque in patients with ocular ischemia versus cerebral events.

BACKGROUND AND PURPOSE: Patients with carotid artery stenosis and ocular ischemic events have a much lower risk of future ipsilateral ischemic stroke on medical treatment and lower procedural risks for endarterectomy and stenting than patients with cerebral ischemic events, and are closer in risk to patients with asymptomatic stenosis. The reasons for this difference in prognosis are not fully understood, but may reflect differences in carotid plaque pathology. METHODS: In consecutive patients undergoing carotid endarterectomy for recently symptomatic stenosis (Oxford Plaque Study, Athero-Express Study), we compared carotid plaque histology (using validated semiquantitative scales) in those who had cerebral events within the last 6 months (n=1317) versus those with ocular events only (n=323). RESULTS: Compared with plaques from patients with ocular events only, those from patients with cerebral events had significantly more large lipid core (odds ratio [OR], 1.38; 95% confidence interval [CI], 1.05-1.82; P=0.02), inflammation (OR, 1.32; 95% CI, 1.02-1.72; P=0.04) and overall plaque instability (OR, 1.37; 95% CI, 1.05-1.80; P=0.02), and less fibrous content (OR, 0.71; 95% CI, 0.54-0.92; P=0.01), and calcification (OR, 0.70; 95% CI, 0.54-0.91; P=0.008). The overall number of histological features known to be associated with vulnerable plaque was greater in patients with cerebral events than in those with ocular events (P=0.002). CONCLUSIONS: Carotid plaques from patients undergoing endarterectomy for previous ocular ischemic events have fewer vulnerable plaque features than those from patients with recent cerebral ischemic events, possibly explaining some of the differences in risk of stroke between these groups.

Platelets enter atherosclerotic plaque via intraplaque microvascular leakage and intraplaque hemorrhage: a histopathological study in carotid plaques.

BACKGROUND: Platelets foster an inflammatory environment that influences atherosclerotic lesion progression and facilitates plaque rupture, in addition to their role in acute thrombus formation. The route of entry of platelets into the atherosclerotic plaque and their exact location inside the plaque are however not completely understood. METHODS AND RESULTS: 188 carotid plaques were examined for the presence of platelets using immunohistochemistry (CD42b), and 76/188 (40.4%) were platelet positive. Platelets were observed in intraplaque hemorrhages, around plaque microvessels, mostly without leakage of erythrocytes; and in mural thrombi. Platelet positive staining was associated with a higher plaque microvessel density, and elevated plaque-levels of interleukin-8. CONCLUSION: Due to their short life span, platelets reflect recent bleeding. It can be hypothesized that platelets might serve as a marker for leaky microvessels inside atherosclerotic plaques that are at risk for development, or progression of plaque hemorrhage.

Clinical prediction rule to estimate the absolute 3-year risk of major cardiovascular events after carotid endarterectomy.

BACKGROUND AND PURPOSE: Prognosis after carotid endarterectomy is mainly determined by the occurrence of major adverse cardiovascular events (MACEs). Optimal medical treatment to reduce risk is the mainstay of MACE prevention. The level of risk of MACE may determine the initiation and aggressiveness of medical treatment, yet a prediction rule to assess that absolute MACE risk after carotid endarterectomy is currently unavailable. METHODS: The prediction model was developed in a consecutive cohort of 1138 patients who underwent carotid endarterectomy between 2002 and 2009. Primary end point was MACE and encompassed myocardial infarction, stroke, and cardiovascular death. Fourteen potential clinical predictors were entered into a Cox proportional hazard model. After backward stepwise regression, internal validation was conducted with bootstrapping techniques to correct for overfitting. To provide an easily applicable clinical tool, a score chart was constructed, dividing patients into 4 risk groups. Model performance was assessed in terms of discrimination, calibration, and risk stratification. RESULTS: During a mean follow-up of 2.28 (± 0.95) years, 148 events occurred, corresponding to a cumulative incidence of 13%. Clinical predictors in the final model were age, history of coronary or peripheral artery disease, smoking, systolic blood pressure, use of antihypertensive drugs, clinical presentation, presence of contralateral carotid stenosis, and serum creatinine levels. Discrimination of the final model, in terms of a C statistic, was 0.69 (0.64-0.73) and calibration showed a good overall fit (Gronnesby and Borgan, P=0.39). The observed incidence of MACE in the 4 risk groups was 6%, 9%, 19%, and 35%, respectively, indicating good overall risk stratification. CONCLUSIONS: The clinical prediction model for MACE in the first 3 years after carotid endarterectomy may be used to identify high-risk patients to help optimize medical treatment and risk factor management as part of secondary prevention to increase life expectancy free from MACE. Despite our success in stratifying risk among these patients, even the lowest stratum remains at high risk and all of these patients should receive maximal secondary preventive measures.

Different stages of intraplaque hemorrhage are associated with different plaque phenotypes: a large histopathological study in 794 carotid and 276 femoral endarterectomy specimens.

BACKGROUND AND PURPOSE: Intraplaque hemorrhage (IPH) is an important determinant of progression and destabilization of atherosclerotic plaque. We recently demonstrated that IPH is an independent predictor of cardiovascular events. IPH has become more clinically relevant since magnetic resonance imaging (MRI) technique is able to visualize IPH in vivo. Different stages of IPH have been described. However, etiology of the different stages is not known and it is unclear if these detected different stages are all associated with the vulnerable plaque phenotype. METHODS AND RESULTS: 1070 patients who underwent a carotid (n=794) or femoral (n=276) endarterectomy were included. Histopathological presence of IPH was determined and divided into 3 types: recent, organized and amorphous IPH. Carotid IPH was observed in 644/794 (81%) plaques, divided into 14 (2%) recent, 70 (11%) organized and 560 (87%) amorphous. Femoral IPH was observed in 175/276 (63%) plaques, divided into 2 (1%) recent, 89 (51%) organized and 84 amorphous (48%). Overall presence of carotid IPH was associated with a large lipid core, no or minor staining of smooth muscle cells, no or minor calcification and high microvessel density. Overall presence of femoral IPH was associated with moderate to heavy staining of macrophages. Plaques with organized IPHs revealed more macrophages, a larger lipid core, less smooth muscle cells, less calcification and higher microvessel density than plaques with amorphous IPHs. CONCLUSIONS: IPH is a significant characteristic of carotid and femoral atherosclerotic plaque and can be classified into different types. Organized IPH is associated with unstable and amorphous IPH with stable plaque characteristics.

Atherosclerotic plaque vulnerability as an explanation for the increased risk of stroke in elderly undergoing carotid artery stenting.

BACKGROUND AND PURPOSE: Recent randomized trials showed an increased periprocedural risk for stroke with increasing age in patients undergoing carotid artery stenting. Manipulation of atherosclerotic plaques during carotid artery stenting can result in plaque rupture with subsequent superimposed thrombus formation, embolization, and cerebrovascular events. We hypothesized that atherosclerotic plaques become more unstable with increasing age and thereby might provide insight into the age-related increased risk of cerebrovascular events during carotid artery stenting. METHODS: Carotid atherosclerotic plaques were harvested from 1385 consecutive patients undergoing carotid endarterectomy between 2002 and 2010. Carotid plaques were quantitatively analyzed for macrophages, smooth muscle cells, and microvessels; and semiquantitatively analyzed for collagen, calcifications lipid cores, and intraplaque hemorrhages. Patients were divided in 4 groups by age: <60, 60 to 69, 70 to 79, and ≥80 years. Measures of association between age as a continuous variable and histological characteristics were also calculated. RESULTS: Increasing age was associated with a decrease in the amount of smooth muscle cells in the carotid plaque. More plaques with large atheroma and heavy plaque calcifications were observed among elderly patients. After correction for baseline differences, risk factors, and medication use, age was independently associated with a more vulnerable carotid plaque composition. CONCLUSIONS: Plaque stability decreases gradually with age. Older patients with carotid stenosis have relatively unstable plaques with low smooth muscle cell content, a high amount of large lipid cores, and more calcified plaques as compared with younger patients. The underlying vulnerable plaque composition in the elderly might be an important contributing factor to the increased risk of stroke for older patients undergoing carotid artery stenting.

Restenosis after carotid surgery: the importance of clinical presentation and preoperative timing.

BACKGROUND AND PURPOSE: Carotid endarterectomy (CEA) of stable atherosclerotic plaques is associated with an increased risk for restenosis. Patients with transient ischemic attack and patients with and stroke have relatively unstable atherosclerotic plaques. However, carotid plaques stabilize over time after a cerebrovascular event due to plaque repair after rupture. These findings raised 2 questions: (1) Is preoperative clinical presentation related to restenosis after CEA? (2) Does delayed revascularization result in a higher risk for restenosis compared with CEA in the short term after a cerebrovascular event? METHODS: Between 2002 and 2009, 1203 patients undergoing CEA were included. The impact of clinical presentation on the occurrence of restenosis 1 year after CEA was investigated and corrected for cardiovascular risk factors, medication use, and type of arteriotomy closure. Patency was assessed with standardized duplex ultrasound imaging at 1 year after CEA. Restenosis was defined as recurrent luminal narrowing ≥50% at the endarterectomy site. RESULTS: At 1 year of follow-up, restenosis was observed more frequently in asymptomatic patients than in patients with transient ischemic attack and patients with stroke. The adjusted odds ratio (95% CI) for restenosis was 0.56 (0.35 to 0.89) for patients with transient ischemic attack and 0.49 (0.27 to 0.87) for patients with stroke compared with asymptomatic patients. Subgroup analysis showed an increased risk for restenosis if CEA was performed >30 days after stroke (adjusted OR, 2.23; 1.02 to 5.73). CONCLUSIONS: Asymptomatic patients have an increased risk for restenosis at 1 year after CEA compared with patients with transient ischemic stroke and patients with stroke. CEA within 30 days after stroke is associated with a decreased risk of restenosis, which supports the current strategy for early surgical intervention after stroke.

Is age of 80 years a threshold for carotid revascularization?

BACKGROUND AND PURPOSE: Carotid Angioplasty and Stenting (CAS) has emerged as an alternative to Carotid Endarterectomy (CEA) in treatment of carotid stenotic disease. With increasing life expectancy clinicians are more often confronted with patients of higher age. Octogenarians were often excluded from randomized trials comparing CAS to CEA because they were considered high-risk for revascularization. Conflicting results on the peri-procedural outcome of carotid revascularization in these patients have been reported. In order to objectively evaluate whether age above 80 years should be an upper limit for indicating carotid revascularization we systematically reviewed the currently available literature. METHODS: Literature was systematically reviewed between January 2000 and June 2010 using Pubmed and Embase, to identify all relevant studies concerning CAS and CEA in octogenarians. Inclusion criteria were 1) reporting outcome on either CEA or CAS; and 2) data subanalysis on treatment outcome by age. The 30-day Major Adverse Event (MAE) rate (disabling stroke, myocardial infarction or death) was extracted as well as demographic features of included patients. RESULTS: After exclusion of 23 articles, 46 studies were included in this review, 18 involving CAS and 28 involving CEA. A total of 2.963 CAS patients and 14.365 CEA patients with an age >80 years were reviewed. The MAE rate was 6.9% (range 1.6 - 24.0%) following CAS and 4.2% (range 0 - 8.8%) following CEA. A separate analysis in this review included the results of one major registry 140.376 patients) analyzing CEA in octogenarians only reporting on 30-day mortality and not on neurological or cardiac adverse events. When these data were included the MAE following CEA is 2.4% (range 0 - 8.8%) CONCLUSIONS: MAE rates after CEA in octogenarians are comparable with the results of large randomized trials in younger patients. Higher complication rates are described for CAS in octogenarians. In general, age > 80 years is not an absolute cut off point to exclude patients from carotid surgery. In our opinion, CEA should remain the golden standard in the treatment of significant carotid artery stenoses, even in the very elderly.

Decreased kidney function: an unrecognized and often untreated risk factor for secondary cardiovascular events after carotid surgery.

BACKGROUND AND PURPOSE: Chronic kidney disease is an important risk factor for development and progression of atherosclerosis. The objective of the current study was to investigate the contribution of moderate kidney failure to cardiovascular (CV) mortality and morbidity after carotid endarterectomy (CEA). In addition, we investigated which proportion received optimal medical treatment or underwent diagnostic workup of the kidneys prior to CEA. METHODS: Between 2002 and 2009, 1085 patients undergoing CEA were included in this study. Estimated glomerular filtration rate (eGFR) was assessed at baseline. Moderate kidney failure was defined as an eGFR 30-59 and compared with normal or mildly reduced kidney function (eGFR ≥60). Primary endpoint was CV death, composed of fatal myocardial infarction, fatal stroke, and ruptured abdominal aneurysm. Secondary endpoints were CV morbidity. RESULTS: Moderate kidney failure (eGFR 30-59) was observed in 26.5% (288/1085) of the patients. During a median follow-up of 2.95 years (0.0 to 3.0 years), the adjusted hazard ratio for CV death with an eGFR 30-59 was 2.22 (1.27 to 3.89). Adjusted hazard ratio for MI with an eGFR 30-59 was 1.90 (1.04 to 3.47). No higher risk for stroke and peripheral interventions was observed. Of all patients with an eGFR 30-59, 38.3% (105/274) received angiotensin-converting enzyme inhibitors, 74.5% (204/274) received statins, and 34.4% (99/288) visited a nephrologist. CONCLUSIONS: Patients with an eGFR 30-59 have a 2.2-fold increased risk for CV death and 1.9-fold increased risk for myocardial infarction the 3 three years after CEA compared with patients with an eGFR ≥60, independent of other CV risk factors. A minority of these patients receive optimal medical treatment, which might explain the increased risk for progression of chronic kidney disease and CV morbidity and mortality.

Pleiotropic effects of statins in atherosclerotic disease.

Statins have an established role in the treatment of hypercholesterolemia and the prophylactic treatment of patients with atherosclerotic disease, and have been found to prevent secondary cardiovascular events and thereby reduce morbidity and mortality. Nevertheless, the pathophysiologic effect of statins on inflammatory responses and local atherosclerotic plaque morphology in humans remains a matter of debate. In particular the question is unanswered whether statin-induced alterations in plaque composition can be ascribed to LDL lowering or an anti-inflammatory pleiotropic effect. We will discuss the results of a recent study by Puato et al. concerning the effect of two different atorvastatin dosages and a nonstatin lipid-lowering drug on atherosclerotic plaque morphology.

Long-term follow-up of secondary interventions after endovascular aneurysm repair with the AneuRx endoprosthesis: a single-center experience.

PURPOSE: To evaluate initial and long-term results of secondary interventions after endovascular aneurysm repair (EVAR) with an AneuRx endoprosthesis. METHODS: Between 1996 and 2003, an AneuRx device was used primarily in 212 patients (197 men; mean age 71+/-7.0 years). Sixty-two (29%) patients (58 men; mean age 73+/-7.2 years) required a secondary intervention (percutaneous, endovascular, or open repair) after EVAR and were prospectively followed after their secondary interventions. Data were analyzed retrospectively. RESULTS: Of the 212 AneuRx patients, 59 (28%) required secondary interventions for endoleaks (28 type Ia, 6 type Ib, 8 type II, and 17 type III) and 3 (1%) for obstruction of the endoprosthesis. The mean interval between primary EVAR and secondary intervention was 39+/-30 months. The yearly risk of requiring a secondary intervention after receiving a primary AneuRx graft was 3.7%. Overall 30-day morbidity after a secondary intervention was 18% (11/62); the 30-day mortality was 5% (3/62). Short endovascular extender cuffs were used for type Ia endoleaks in 23 of 28 patients. Over a mean follow-up of 81+/-34 months after the secondary intervention, the success of short endovascular cuffs for treatment of type Ia endoleak was 52% (12/23); the remaining 11 (48%) patients required additional reinterventions for recurrent endoleak or persistent aneurysm growth. CONCLUSION: Patients with a primary AneuRx stent-graft had an acceptable yearly risk of requiring a secondary intervention following EVAR, but 30-day morbidity and mortality rates were significant and must be taken into account during primary decision making for endovascular or open repair. Proximal extender cuffs may not be a durable treatment for type Ia endoleak.