Editor's Choice - Overview of Primary and Secondary Analyses From 20 Randomised Controlled Trials Comparing Carotid Artery Stenting With Carotid Endarterectomy.

OBJECTIVES: The aim of this review was to carry out primary and secondary analyses of 20 randomised controlled trials (RCTs) comparing carotid endarterectomy (CEA) with carotid artery stenting (CAS). METHODS: A systematic review and meta-analysis of data from 20 RCTs (126 publications) was carried out. RESULTS: Compared with CEA, the 30 day death/stroke rate was significantly higher after CAS in seven RCTs involving 3467 asymptomatic patients (odds ratio [OR] 1.64, 95% confidence interval [CI] 1.02-2.64) and in 10 RCTs involving 5797 symptomatic patients (OR 1.71, 95% CI 1.38-2.11). Excluding procedural risks, late ipsilateral stroke was about 4% at 9 years for both CEA and CAS, i.e., CAS was durable. Reducing procedural death/stroke after CAS may be achieved through better case selection, e.g., performing CEA in (i) symptomatic patients aged > 70 years; (ii) interventions within 14 days of symptom onset; and (iii) situations where stroke risk after CAS is predicted to be higher (segmental/remote plaques, plaque length > 13 mm, heavy burden of white matter lesions [WMLs], where two or more stents might be needed). New WMLs were significantly more common after CAS (52% vs. 17%) and were associated with higher rates of late stroke/transient ischaemic attack (23% vs. 9%), but there was no evidence that new WMLs predisposed towards late cognitive impairment. Restenoses were more common after CAS (10%) but did not increase late ipsilateral stroke. Restenoses (70%-99%) after CEA were associated with a small but significant increase in late ipsilateral stroke (OR 3.87, 95% CI 1.96-7.67; p < .001). CONCLUSIONS: CAS confers higher rates of 30 day death/stroke than CEA. After 30 days, ipsilateral stroke is virtually identical for CEA and CAS. Key issues to be resolved include the following: (i) Will newer stent technologies and improved cerebral protection allow CAS to be performed < 14 days after symptom onset with risks similar to CEA? (ii) What is the optimal volume of CAS procedures to maintain competency? (iii) How to deliver better risk factor control and best medical treatment? (iv) Is there a role for CEA/CAS in preventing/reversing cognitive impairment?

A Systematic Review and Meta-Analysis of the Presentation and Surgical Management of Patients With Carotid Body Tumours.

OBJECTIVES: The aim was to determine the mode of presentation and 30 day procedural risks in 4418 patients with 4743 carotid body tumours (CBTs) undergoing surgical excision. METHODS: This is a systematic review and meta-analysis of 104 observational studies. RESULTS: Overall, 4418 patients with 4743 CBTs were identified. The mean age was 47 years, with the majority being female (65%). The commonest presentation was a neck mass (75%), of which 85% were painless. Dysphagia, cranial nerve injury (CNI), and headache were present in 3%, while virtually no one presented with a transient ischaemic attack (0.26%) or stroke (0.09%). The majority (97%) underwent excision, but only 21% underwent pre-operative embolisation. Overall, 27% were Shamblin I CBTs; 44% were Shamblin II; and 29% were Shamblin III. The mean 30 day mortality was 2.29% (95% CI 1.79-2.93). The mean 30 day stroke rate was 3.53% (95% CI 2.91-4.29), while the mean 30 day CNI rate was 25.4% (95% CI 24.5-31.22). The prevalence of persisting CNI at 30 days was 11.15% (95% CI 8.42-14.64). Twelve series (544 patients) correlated 30 day stroke with Shamblin status. Shamblin I CBTs were associated with a 1.89% stroke rate (95% CI 0.92-3.82), increasing to 2.71% (95% CI 1.43-5.07) for Shamblin II CBTs and 3.99% (95% CI 2.34-6.74) for Shamblin III tumours. Twenty-six series (1075 patients) correlated CNI rates with Shamblin status: 3.76% (95% CI 2.62-5.35) for Shamblin I CBTs, 14.14% (95% CI 11.94-16.68) for Shamblin II, and 17.10% (95% CI 14.82-19.65) for Shamblin III tumours. The prevalence of neck haematoma requiring re-exploration was 5.24% (95% CI 3.45-7.91). The proportion of patients with a neck haematoma requiring re-exploration was not reduced by pre-operative embolisation (5.92%; 95% CI 2.56-13.08) vs. no embolisation (5.82%; 95% CI 2.76-11.88). Pre-operative embolisation did not reduce drainage losses (639 mL vs. 653 mL). CONCLUSIONS: This is the largest meta-analysis of outcomes after CBT excision. Procedural risks associated with tumour excision were considerable, especially with Shamblin III tumours where 4% suffered a peri-operative stroke and 17% suffered a CNI.

Known knowns, known unknowns and unknown unknowns: a 2010 update on carotid artery disease.

The management of carotid artery disease never ceases to attract controversy. The last 12 months has seen publication of a number of important studies which have informed debate and 2010 holds the prospect of much more. This update offers a personal review of a number of contemporary issues including; (i) guidelines for non-invasive imaging in rapid access clinics, (ii) whether improvements in best medical therapy have rendered many of the conclusions from ACAS and ACST obsolete, (iii) is carotid disease really just a marker for increased stroke risk following cardiac surgery (rather than being an important cause), (iv) what is the current status of endarterectomy and stenting in patients with symptomatic carotid disease and (v) why we must offer expedited interventions to TIA/minor stroke patients. The available evidence suggests that while most 'known knowns' will endure, quite a few may be returning to the category of 'known unknowns' once again. Who knows what 'unknown unknowns' await us in 2010 and beyond.

Laparoscopic ligation of splenic artery aneurysm.

Splenic artery aneurysms are rare and often asymptomatic; however, rupture may prove fatal. Although many can be treated with percutaneous embolization, tortuosity of the artery may render this approach impossible. Presented is a case report describing laparoscopic ligation of a splenic artery aneurysm after failed attempt at embolization.

Platelet inhibition by aspirin is diminished in patients during carotid surgery: a form of transient aspirin resistance?

The majority of patients who suffer peri-operative thromboembolic complication while undergoing vascular procedures do so despite taking aspirin. This study examined the antiplatelet effect of aspirin during surgery in patients undergoing carotid endarterectomy (CEA). Fifty patients undergoing CEA were standardised to 150 mg aspirin daily for > or =2 weeks. Platelet aggregation in response to arachidonic acid (AA) was measured in platelet rich plasma prepared from blood taken prior to, during, and at the end of surgery. Spontaneous platelet aggregation was also studied, as was the role of physiological agonists (ADP, collagen, thrombin, and epinephrine) in mediating the in vivo and in vitro responses to AA. Eighteen patients undergoing leg angioplasty, also on 150 mg aspirin, without general anaesthesia, served as a control group. In the CEA patients aggregation induced by AA (5 mM) increased significantly from 7.6 +/- 5.5% pre-surgery to 50.8 +/- 29.5% at the end of surgery (p <0.0001). Aggregation to AA was even greater in samples taken mid-surgery from a sub-set of patients (73.8+/-7.2%; p = 0.0001), but fell to 45.9 +/- 7.4% by the end of surgery. The increased aggregation in response to AA was not due to intra-operative release of physiological platelet agonists since addition of agents that block/neutralise the effects of ADP (apyrase; 4 micro g/ml), thrombin (hirudin; 10 units/ml), or epinephrine (yohimbine; 10 micro M/l) to the samples taken at the end of surgery did not block the increased aggregation. The patients undergoing angioplasty also showed a significant rise in the response to AA (5 mM), from 5.6 +/- 5.5% pre-angioplasty to 32.4 +/- 24.9% at the end of the procedure (p <0.0001), which fell significantly to 11.0 +/- 8.1% 4 hours later. The antiplatelet activity of aspirin, mediated by blockade of platelet arachidonic acid metabolism, diminished significantly during surgery, but was partially restored by the end of the procedure without additional aspirin treatment. This rapidly inducible and transient effect may explain why some patients undergoing cardiovascular surgery remain at risk of peri-operative stroke and myocardial infarction.