Commentary

Optimal Renal Artery Stenting: Does Size Matter?

Michael C. Nguyen, MBBS and Lawrence A. Garcia, MD
Michael C. Nguyen, MBBS and Lawrence A. Garcia, MD
Renal artery stenosis is mainly a disease of progressive atherosclerosis involving the ostium and proximal third of the main renal artery and the peri-renal aorta. Atherosclerosis accounts for 90% of cases of renal artery stenosis (RAS).1 The prevalence of atherosclerotic RAS increases with age, particularly in patients with diabetes, hyperlipidemia, diffuse type of peripheral arterial occlusive disease, coronary artery disease or hypertension.2–6
Most authorities consider blood pressure control, preservation or salvage of kidney function and prevention of flash pulmonary edema to be important treatment goals for patients with atherosclerotic RAS. Treatment options include medication alone (usually involving combination therapy), or revascularization of the stenosed artery or arteries. Some clinicians also use antiplatelet agents such as aspirin or clopidogrel to reduce the risk for thrombosis. The current standard for revascularization in most patients is percutaneous transluminal angioplasty with stent placement. Angioplasty without stenting is less commonly used due to higher rates of vessel recoil and lesion restenosis.
Balloon angioplasty achieves technical success in only 25–30% of cases in ostial RAS.7,8 Meanwhile, stenting for RAS has become an established technique that leads to a satisfactory morphologic result in most cases. A meta-analysis of 678 patients from 14 studies found a technical success rate (residual stenosis < 20%–50%) of 98%.9 In addition to singlecenter cohorts,10–14 a randomized study showed renal stenting to be technically and functionally superior to conventional balloon angioplasty in the treatment of atherosclerotic ostial RAS.15 Acute success rates were 57% versus 88% for balloon angioplasty and stenting, respectively. The 6-month restenosis rates were 48% and 15% in favor of stenting. The predictors of in-stent restenosis include renal artery size and stent diameter with increasing restenosis rates related to decreasing vessel or stent size,13,16,17 with no relationship to stent design. There are significantly more restenoses (36%) in vessels smaller than 4.5 mm than in vessels treated with stent diameters of more than 4.5 mm (12%).17 Optimal stent deployment defined by the post-stenting minimal lumen area (MLA) or minimal lumen diameter (MLD) has been shown to be an important predictor of late stent patency in the coronary circulation18–20 and it is reasonable to assume that similar biological effects would apply to the renal vasculature. Up to now, a major drawback to the assessment of restenosis involves the lack of uniform criteria within these studies due to varying definitions and imaging modalities used for restenosis detection (contrast angiography, duplex ultrasound, magnetic resonance angiography, computed tomographic angiography).
Given the significance of restenosis, Aqel et al report in the current issue on underdeployed renal stents and the possible effects on restenosis in a small series of patients. They test the hypothesis that optimal stent deployment during renal artery interventions can be achieved using the Metricath (MC) system, a balloon-catheter sizing device. Results from 20 renal artery lesions found that MC guidance resulted in adjunctive intervention in 90% of the treated lesions, increasing the MLD from 4.40 ± 0.77 mm to 5.17 ± 0.82 mm (p < 0.001) after the adjunctive intervention. The study highlights the deficiencies with single-balloon inflation during stent deployment. This has been demonstrated in the coronary vasculature where routine postdilatation has become the standard of care. The use of routine postdilatation during coronary intervention ensures adequate stent apposition and reduces the incidence of in-stent thrombosis.21 The rate of stent thrombosis in the renal vasculature remains small in the current literature, even with the current study suggesting inadequate stent apposition in the majority of cases despite acceptable angiographic results. However, optimal stent expansion remains a key goal to limit future restenosis.
Rocha-Singh et al reported a stent thrombosis rate of 1% in 208 patients undergoing renal stenting following failed balloon angioplasty.22 The low reported rate of stent thrombosis may be due to inherent difficulties with diagnosis, since events tend to be either associated acutely with the procedure or manifest late, often with symptoms of vague pain or reduction in creatine clearance, rather than the catastrophic acute presentation seen in coronary stent thrombosis. Even though the current study by Aqel et al23 has several limitations, including low numbers and a single operator, the report does, however, highlight the need to be vigilant and perform optimal stent sizing and postdilatation for all endovascular procedures to include renal revascularization. The drawbacks with routine postdilatation in “all” renal revascularization patients relate to the higher risk of complications that may occur, including dissection/perforation and atheroemboli. Therefore, identifying those with poor stent apposition requiring adjuvant intervention is necessary. The study showed safety and feasibility of the MC system, however long-term clinical data and follow up are needed to assess the efficacy and benefit of this strategy. Furthermore, the potential need to use thisdevice compared with other devices such as intravascular ultrasound needs to be addressed. What has been suggested in this current report is that for improved outcomes in renal artery endovascular stenting, optimal stent deployment is required.

 

References

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