Carotid stenting and endoloeaks discussed at SITE 2005


At the recent 6th SITE meeting on Endovascular Therapeutics in Barcelona, Spain, renowned experts from around the world gathered to discuss current questions as well as the future outlook of endovascular therapeutics.

Dr Martin Brown, Sheffield Vascular Institute, Northern General Hospital, Sheffield, UK, provided an update from the International Carotid Stenting Study (ICSS), which began recruitment in May 2001. Currently, there are 26 worldwide centers involved in the study and to date 463 patients have been recruited.

The study aims to randomise 1,500 patients with high-grade (>50% NASCET criteria), recently symptomatic (12 months), de-novo carotid disease already taking best medical therapy to either carotid artery stenting (CAS) or carotid endarterectomy (CEA), in equal proportions. The technical committee strongly suggested cerebral protection and has approved three stents and five protection systems. The primary outcome measure is stroke free survival at three years. “To date there remains a need for a large well-randomised trial of CAS versus CEA in symptomatic patients, we hope ICSS will fulfill this requirement,” said Gaines.

Gaines announced that centers are invited to apply which have a neurologist to assess suitability for inclusion and outcomes, and surgeons should have at least 50 CEA and a throughput of at least 10 per annum. The role of interventionalists has been discussed and to become involved in the study they must meet a certain criteria (they must have performed 50 CAS procedures away from the carotid artery and at least 10 in the carotid artery).

Also at SITE 2005, Dr Geoffrey Gilling-Smith, Royal Liverpool University Hospital, UK, discussed expansion of the aneurysm in the absence of endoleak and its consequences. He began by stating that it is a common misconception that expansion of an aneurysm is evidence of failure to isolate the aneurysm from the circulation, when such expansion merely indicates that the pressure within the aneurysm is greater than surrounding tissue pressure (25-35mm Hg). The pressure within the aneurysm may not in fact be sufficient to cause rupture while rupture in the absence of endoleak is in any case likely to be a relatively benign event since it is unlikely to result in hemorrhage and death. In many cases, therefore, the risks of secondary intervention may be greater than the risks of continued observation.

Gilling-Smith said that it is important to try and discover the cause of expansion and to determine the likelihood that the aneurysm is at systemic pressure. He said it is necessary to review X-rays to determine whether there is evidence of migration, impending dislocation of a modular graft limb or impending disengagement of graft limbs from the iliac arteries. He hypothesized that in such cases the seal around the graft anatomizes may be inadequate to isolate the aneurysm sac from systemic pressure and that expansion may be the first sign of impending late graft related endoleak. In such cases secondary intervention is advisable. The problem can often be solved with deployment of a cuff or extension limb although in some cases it may be necessary to reline the primary endograft or even convert to open repair.

Expansion may also be due to intermittent or low flow endoleak. These may be revealed on triple pass CT, contrast enhanced duplex or angiography and can be treated by secondary endografting, embolisation or laparoscopic clipping of the feeding vessel if there is concern that the leak may result in rupture and hemorrhage.

Expansion may result simply from transmission of pressure through thrombus sealing an endoleak or the interstices of a porous graft. In such cases, Gilling-Smith suggested measuring intrasac pressure directly by translumbar puncture under fluoroscopic control. If the pressure is high secondary conversion/open repair can be considered. If the pressure is low, he suggests continued observation as expansion of the aneurysm may result in expansion of the neck and late migration.

Gilling-Smith concluded by stating that expansion of the aneurysm in the absence of endoleak raises many questions to which there are too few answers.

Also discussing endoleaks at SITE was Dr Martin Malina, Associate Professor, Department of Vascular Surgery of Malm̦ University Hospital, Sweden. He asked the question at the meeting, ‘Do Type II endoleaks really matter?’ Malina pointed out that Type II endoleaks are associated with increased pressure within the aneurysm (pressure index approximately 60% compared to 20% in the successfully excluded sac), but do not necessarily cause a rupture.

Malina stressed that pressure inside the sac (i.e. endotension) rather than the presence of an endoleak is what matters because endotension may occur without evidence for an endoleak. This is based on his experience of more than 100 translumbar intrasac pressure measurements after EVAR. High intrasac pressure after EVAR is associated with increasing aneurysm diameter. The pressure may, however, vary between different parts of the sac which is a problem for adequate measurements. Endotension without evidence for endoleakage may be caused by low flow endoleak, intermittent endoleak, transmission of pressure through thrombus or porous graft, the pulsation of graft material within a closed space, the accretion of extracellular material (fribinolysis-> Sac hygroma) and infection.

Malina concluded that these Type II endoleaks can often be treated with superselective catheterization of the afferent vessels or by translumbar glue embolization of the circulated nidus within the sac.