Refined filter-type protection devices would lower stroke-rate

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At SITE 2005, Dr Sumaira Macdonald, consultant vascular radiologist and honorary clinical senior lecturer, Freeman Hospital, Newcastle, UK, discussed the limitations of filter-type cerebral protection devices. She began by stating that of the three philosophies in mechanical cerebral protection; balloon occlusion (distal or proximal to the index lesion), flow reversal and distal filtration, the latter is utilized in over 90% of procedures. Whilst flow reversal and balloon occlusion devices significantly reduce microembolization, according to Macdonald they do so at the expense of continuous procedural cerebral perfusion. Up to 10% of patients may not tolerate this type of cerebral protection due to inadequacies of the Circle of Willis plus/minus contralateral high-grade carotid stenosis.

Macdonald told Vascular News that recent communications with Juan Parodi suggest that more patients may be rendered tolerant of flow reversal by maintaining the systolic blood pressure above 140mmHg and that patients may be generally more tolerant of flow reversal than of distal balloon occlusion, because the former promotes collateral through-flow.

Filtration devices collect debris that has been liberated from the site of the bifurcation lesion during endovascular manipulation. Previous studies have indicated that 88% of the total procedural embolic load is trapped. However, the actual in-vivo % is unknown as particles smaller than the pores may pass through or around the filter (current devices have pore sizes ranging from 100-150 microns). Procedural transcranial Doppler (TCD) has demonstrated that more high-intensity transients (HITS) are generated with a filter-type device than during unprotected carotid artery stenting (CAS). In-vivo cases have indicated that a substantial proportion of these HITS correspond to particulate matter and cannot be dismissed as air.

Furthermore, this corresponded to more new white lesions on magnetic resonance imaging (MRI) of the brain in the protected limb of a randomized trial (conducted by Macdonald in her PhD thesis) comparing unprotected CAS with CAS protected by means of a filter-type device. The literature highlights that there is a 15-29% incidence of new white lesions detected on diffusion-weighted MRI of brain following protected CAS.

Macdonald stated that the pragmatic approach is to continue to use a filter-type device that protects the brain from macroemboli (of clinical significance), accepting that the trade-off would be the production of more microemboli than are detected during unprotected CAS. However, she maintained that the clinical significance of this increased burden of microemboli is not clear as there is no evidence of deficit in protected patients compared with unprotected patients on a comprehensive neuropsychometric test battery within a randomized trial setting, albeit in the acute time-frame (30 days).

In addition to protection devices, confounding variables such as refinements in technique (to include monorail low-profile systems and dedicated carotid stents), advances in pharmacological support and learning curve have had a profound affect on outcomes. The dual antiplatelet regime has been shown to have significant benefits over the herapin infusion/asprin regime (CAVATAS). All these variables have developed during the same time-line as the evolution in cerebral protection.

Other considerations include the spasm, dissection, filter-occlusion by debris with flow limitation and difficulties with deployment and retrieval, which may all contribute to the procedural adverse event-rate. However, protection devices offer no benefit outside of the procedural time-frame and may cause intimal damage at the site of deployment which has the potential for late complications. Moreover, other mechanisms of neurological damage, for example haemodynamic injury following CAS, are often overlooked and will not be addressed by the use of the available protection devices.

Macdonald concludes that current filtration devices could be more effective than they are and further reductions in the procedural stroke-rate will require refinements in protection device technology and attention to non-embolic causes of stroke during CAS. Moreover, an improved understanding of platelet activation may promote further advances in pharmacological support and may further reduce procedural and possibly late embolic stroke.

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