Abstract

Intracranial arterial stenosis is a frequent cause of major stroke [1]. Medical treatment with either platelet antiaggregation or anticoagulation may be an option for asymptomatic patients and for those not suitable for endovascular therapy. In patients with high-grade symptomatic stenoses, balloon dilatation using coronary stents [2], neurovascular variants thereof [3], or self-expanding stents [4] offers better protection from stroke. In dedicated centers, these procedures are carried out safely and efficiently. The long-term course, however, remains a concern. The dilemma is that drug-eluting stents (DES) provide good long-term results, but are just too stiff for elongated vessels. For all bare-metal stents (BMS), no matter if balloon-expandable, self-expanding, stainless steel, cobalt-chromium or nickel-titanium, in-stent restenosis (ISR) rates of 30% and higher have been reported. Since ISR of > 50% lumen loss may again cause cerebral ischemia, treatment of these patients is mandatory. In the past, conventional balloon dilatation or the deployment of a second stent was established clinical practice. Some years ago, Scheller et al. could show in pigs that a short-term exposure of the vessel wall to the antiproliferative drug paclitaxel is able to inhibit vascular smooth muscle cell proliferation for several days [5]. Angioplasty of coronary ISR performed with iopromide- and paclitaxel-coated balloons (drug-eluting balloon [DEB]) prevents restenosis more frequently and longer than the use of bare-surface balloons [6]. We report the clinical history of a young patient with a symptomatic, presumably inflammatory proximal middle cerebral artery (MCA) plaque, which was treated by balloon dilatation and self-expanding stent deployment, followed by recurrent intracranial ISR. Three retreatments with conventional balloons were again followed by severe intimal hyperplasia. After angioplasty with a DEB, no further ISR occurred.

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