A New Concept to Help Deal With Dissections in Peripheral Angioplasty

Peripheral Arterial Disease (PAD) affects nearly a fifth of those over the age of 60 in the Western World</div

Ilio-ureteric Fistula: A Rare Cause of Haematuria

Ilio-ureteric Fistula: A Rare Cause of Haematuri

Cardiovascular risk in patients with small abdominal aortic aneurysms

Background: Abdominal aortic aneurysm (AAA) is a cardiovascular health problem. Ultrasound screening has been shown to reduce the risk of AAA-related, but not all-cause, mortality. The recent introduction of screening in several countries has meant that thousands of patients with a small AAA (<5·5cm) that does not require immediate treatment are diagnosed annually. We sought to investigate the cardiovascular profiles of patients with ectatic aortas and assess whether participation in screening reduces cardiovascular risk. Methods: We used three sets of data: from the National Health Service AAA Screening Programme (NAAASP) during the 2013–14 round that were linked with Health Episode Statistics (HES) (235 409 individuals); a subset of the Framingham Study population who had an abdominal CT scan in 2004–05 and were followed up for 10 years (1383 individuals); and data for patients with a small AAA who had been in surveillance for at least 1 year in the UK Aneurysm Growth Study (UKAGS) (384 individuals) or from a national UK audit (1538 individuals), to assess cardiovascular risk and events. Findings: In the linked NAAASP–HES cohort, cardiovascular mortality was 0·30% (95% CI 0·28–0·32) for individuals with an abdominal aortic diameter of less than 2·5 cm; 0·81% (0·51–1·11) for those between 2·5 and 2·9 cm; and 1·30% (0·90–1·71) for those less than 3·0 cm. Death from a cardiovascular event was more likely for individuals with a small AAA than for those without AAA (risk ratio 4·33, 95% CI 3·15–5·97). In the Framingham cohort, abdominal aortic diameter was independently associated with cardiovascular events (hazard ratio [HR] 1·1, 95% CI 1·02–1·18; p<0·0001). An abdominal aortic diameter of more than 2·5 cm was also associated with cardiovascular events (HR 7·6, 95% CI 5·1–11·3; p<0·0001). In the UKAGS and audit populations, patients were not more likely to take antiplatelet agents or statins after entering screening surveillance; cholesterol concentrations and blood pressure also increased. Interpretation: In these contemporary large cohorts of patients with small AAA, cardiovascular events and death were common and were the leading cause of death. The implication is that patients are not more likely to receive cardiovascular protection if they enter screening or surveillance with existing protocols. Cardiovascular risk reduction interventions should be implemented in screening programmes in the future

Overview of Primary and Secondary Analyses From 20 Randomised Controlled Trials Comparing Carotid Artery Stenting With Carotid Endarterectomy

Objectives Overview of primary and secondary outcomes from 20 randomised controlled trials (RCTs) comparing carotid endarterectomy (CEA) with carotid artery stenting (CAS). Methods Systematic review and meta-analysis of data from 20 RCTs (126 publications). Results Peri-operative death/stroke was significantly higher after CAS. Excluding procedural risks, ipsilateral stroke was about 4% at 9-years for CEA/CAS, ie CAS was durable. To improve 10-year survival; peri-operative stroke/myocardial infarction must be prevented, mandating greater emphasis on risk factor control and best medical therapy (BMT). Reducing procedural death/stroke after CAS may be achieved through emerging CAS technologies, but better case selection is essential; eg perhaps preferentially performing CEA in; (i) symptomatic patients aged >70yrs; (ii) interventions <14 days of symptom onset and (iii) situations where stroke risk after CAS is higher (segmental/remote plaques, plaque length >13mm, heavy burden of white matter lesions (WML), avoiding situations where 2 or more stents need to be deployed). New WMLs are significantly more common after CAS and may be associated with higher rates of late stroke/TIA, requiring better risk factor control and BMT in patients with new, post-operative WMLs. There is no evidence that new WMLs predispose to cognitive impairment. Restenoses are more common after CAS, but do not increase late ipsilateral stroke. CEA is associated with a small, but significant increase in stroke ipsilateral to 70-99% restenoses, but procedural risks need to be Conclusions Questions to be answered include; (i) can CAS be undertaken <14 days of symptom-onset with outcomes similar to CEA; (ii) will emerging stent technologies and improved cerebral protection prevent stroke after CAS; (iii) what is the optimal volume of CAS procedures to maintain competency; (iv) how to deliver better risk factor control and BMT, and (v) is there a role for CEA/CAS in preventing/reversing cognitive impairment? What this paper adds to the literature? This is the first paper to provide a comprehensive overview of primary and secondary outcome data from 20 RCTs comparing CEA with CAS. It includes separate meta-analyses for peri-operative risks and late ipsilateral stroke. Secondary analyses include risk factors for stroke after CEA/CAS and its prevention; the effect of peri-operative stroke or myocardial infarction on long-term survival; non-stroke complications after CEA/CAS (cranial nerve injury, haematoma, arrhythmias and hypertension/hypotension); the significance of new white matter lesions on late stroke and cognitive impairment and whether asymptomatic 70-99% restenoses increase the risk of ipsilateral stroke after CEA and CAS.</p

Endovascular Repair for a Ruptured AAA due to a Combined Type IIIb and Ia Endoleak.

We report a case of a ruptured abdominal aortic aneurysm (AAA) caused by a combined type IIIb and Ia endoleak. Also, we propose the mechanism that resulted in this combined endoleak. Specifically, a 71-year old-man, with a previous history of endovascular aneurysm repair (EVAR) for an AAA, was diagnosed with a contained rupture. CT scan depicted a type Ia endoleak and a migrated Talent endograft. A proximal aortic cuff sealed the endoleak, but intraoperative angiography revealed that a type IIIb endoleak coexisted due to fabric tear close to the Talent bifurcation. A second aortic cuff could not seal the fabric tear; so, in-lay parallel limbs were sequentially deployed as a "kissing endograft" technique inside the cuff. Simultaneous treatment of combined type IIIb and Ia endoleaks has not yet been described. Maybe the type IIIb endoleak is the primary entity causing sac enlargement, neck recontouring, proximal migration, and ultimately type Ia endoleak, which leads to huge enlargement and rupture. Placement of an aortic cuff to seal the proximal endoleak/migration and kissing endografts limbs for the fabric tear seems a safe option in such patients