Embolic Protection and Antiplatelet Use for Renal Artery Stenting

Embolic Protection and Antiplatelet Use for Renal Artery Stenting

Colyer William R, Cooper Christopher J
Interventional Cardiology - Volume 3 - Issue I
Published: November 2008
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Atherosclerotic renal artery stentosis (RAS) is a frequently recognised cause of secondary hypertension and chronic kidney disease.1–4 Revascularisation of RAS with angioplasty and stenting is often performed with the goals of improved blood pressure control and preserving or improving renal function.5 However, renal artery stenting is sometimes associated with acute worsening of renal function.6 Possible mechanisms of renal artery injury following stent placement include toxicity from iodinated contrast and distal embolisation. Atheroembolisation is well documented as a cause of renal disease, although definitive diagnosis requires a renal biopsy and therefore is rarely confirmed pathologically.7–10 The use of embolic protection devices (EPDs) has been shown to improve outcomes of percutaneous revascularisation procedures in saphenous vein grafts and carotid arteries.11–13 Although currently no EPDs are approved for use during renal artery stenting, data are emerging that suggest a role for these devices in this setting.

Atheroembolisation During Renal Artery Stenting
In an ex vivo study, Hiramoto et al. demonstrated that renal artery stenting is associated with the release of atheroembolic particles.14 In this study, explanted aorto-renal artery specimens from renal artery endarterectomy procedures were used, along with polytetrafluroethylene grafts, to create a model for renal artery stenting. This demonstrated that each step of the procedure, including passage of the guidewire, was associated with embolisation of thousands of particles, with the particle number inversely related to particle size. This ex vivo evidence of atheroembolisation is supported by several clinical studies that demonstrated the retrieval of embolic material following renal stenting with the adjunctive use of an EPD.15–24

Embolic Protection Devices
Currently, several EPDs are commercially available. These devices can be divided into three broad categories: proximal protection devices, distal occlusive devices and distal filter devices. Due to the fact that the overwhelming majority of atherosclerotic RAS lesions are ostial, proximal protection devices are not practical and will not be discussed here.

Distal Occlusion
The GuardWire® (Medtronic, Minneapolis, MN, US) is a system that utilises a temporary occlusion balloon to prevent antegrade flow during a stent procedure. Following stent deployment, an aspiration catheter is used to remove any embolised material before balloon deflation and the restoration of antegrade flow to the kidney. The use of the GuardWire in conjunction with renal artery stenting has been reported.16–19,22–24

A potential advantage of distal occlusion is its low crossing profile. Indeed, given that guidewire passage leads to the embolisation of large numbers of atheromatous particles, a lower profile may help to decrease this number, particularly in the case of high-grade stenoses.14 In addition, the technique of occlusion and aspiration prevents the embolisation of particles of all sizes. This may be important, given that the majority of embolised particles are smaller than 100ìm.14,16 Although the clinical significance of the embolisation of small particles, particularly those smaller than 60ìm, is unknown, particles in the size range of 20–40ìm may be large enough to obstruct the afferent arteriole.14 Consistent with this possibility, it has been demonstrated that embolic particles smaller than 100ìm may lead to cerebral injury.25,26

One potential disadvantage of distal occlusion is that imaging between procedural steps, such as balloon pre-dilatation and stent deployment, is limited due to the static column of contrast. A second potential disadvantage of distal occlusion is the induction of renal ischaemia. Henry et al. reported a mean renal artery occlusion time of 6.46 minutes.19 Whether this duration of ‘warm’ renal ischaemia may lead to a decline in renal function is not known.

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