Pipeline Embolization Device for the Treatment of Unruptured Intracranial Dissecting Aneurysms

Background: Intracranial dissecting aneurysms (IDAs) are rare but pose significant challenges to treatment. The pipeline embolization device (PED) has been demonstrated to be an effective treatment option with excellent outcomes. Herein, we report our experience with patients treated with the PED for unruptured IDAs.Methods: We retrospectively reviewed our hospital database and identified patients who were treated with PEDs for unruptured IDAs between March 2016 and September 2020. Data including demographics, clinical presentation, aneurysm characteristics, procedural details, intra- or peri-procedural complications, and follow-up details were collected.Results: Eighty patients (61 men, 76.25%) were treated with PED for unruptured IDAs. The most common symptoms were headache (34, 42.5%), dizziness (29, 36.25%), and nausea or vomiting (15, 18.75%). Of these patients, 73 had one aneurysm, and seven harbored two aneurysms. All of them achieved successful PED deployment. Six patients experienced intra- or peri-procedural complications including perforator artery occlusion, thromboembolic, hemorrhagic events, and falling of the stent into the aneurysm sac. Follow-up with digital subtractive angiography was available for 29 patients with a median of 6 months, and 28 (96.56%) patients had aneurysm occlusion. Late thrombosis occurred in four patients, and two of them had unfavorable outcomes. Clinical follow-up showed that a favorable clinical outcome was achieved in 76 (95%) patients, and the mortality rate was 3.75%.Conclusion: Treating unruptured IDAs is safe and effective with long-term favorable clinical and angiographic outcomes. However, the complications of this treatment should be noted. Careful selection of appropriate patients and individualized antiplatelet therapy might be needed.

A heparin–rosuvastatin-loaded P(LLA-CL) nanofiber-covered stent inhibits inflammatory smooth-muscle cell viability to reduce in-stent stenosis and thrombosis

Background An endovascular covered-stent has unique advantages in treating complex intracranial aneurysms; however, in-stent stenosis and late thrombosis have become the main factors affecting the efficacy of covered-stent treatment. Smooth-muscle-cell phenotypic modulation plays an important role in late in-stent stenosis and thrombosis. Here, we determined the efficacy of using covered stents loaded with drugs to inhibit smooth-muscle-cell phenotypic modulation and potentially lower the incidence of long-term complications. Methods Nanofiber-covered stents were prepared using coaxial electrospinning, with the core solution prepared with 15% heparin and 20 µM rosuvastatin solution (400: 100 µL), and the shell solution prepared with 120 mg/mL hexafluoroisopropanol. We established a rabbit carotid-artery aneurysm model, which was treated with covered stents. Angiography and histology were performed to evaluate the therapeutic efficacy and incidence rate of in-stent stenosis and thrombosis. Phenotype, function, and inflammatory factors of smooth-muscle cells were studied to explore the mechanism of rosuvastatin action in smooth-muscle cells. Result Heparin–rosuvastatin-loaded nanofiber scaffold mats inhibited the proliferation of synthetic smooth-muscle cells, and the nanofiber-covered stent effectively treated aneurysms in the absence of notable in-stent stenosis. Additionally, in vitro experiments showed that rosuvastatin inhibited the smooth-muscle-cell phenotypic modulation of platelet-derived growth factor-BB induction and decreased synthetic smooth-muscle-cell viability, as well as secretion of inflammatory cytokines. Conclusion Rosuvastatin inhibited the abnormal proliferation of synthetic smooth-muscle cells, and heparin–rosuvastatin-loaded covered stents reduced the incidence of stenosis and late thrombosis, thereby improving the healing rates of stents used for aneurysm treatment. Graphic abstract

Heparin- and Rosuvastatin- loaded Poly(L-lactide-co-caprolactone) Nanofiber Aneurysm Covered Stent Inhibits Inflammatory Smooth Muscle Cell in Reducing in-stent Stenosis and Thrombosis

Background: Endovascular covered-stent has unique advantages in treating complex intracranial aneurysms. However, in-stent stenosis and late thrombosis have become the main factors affecting the efficacy of covered-stent treatment. Smooth-muscle-cell phenotypic modulation plays an important role in late in-stent stenosis and thrombosis. Thus, covered stents loaded with drugs that can inhibit smooth-muscle-cell phenotypic modulation may lower the incidence of long-term complications. Methods: Nanofiber covered stents were prepared using coaxial electrospinning. A rabbit-carotid-artery aneurysm model was established and treated with covered stents. Angiography and histology were performed to evaluate the therapeutic efficacy and incidence rate of in-stent stenosis and thrombosis. Phenotype, function, and inflammatory factors of smooth-muscle cells were studied to explore the mechanism of rosuvastatin in smooth-muscle cells. Result: Heparin–rosuvastatin-loaded nanofiber scaffolds inhibited the proliferation of synthetic smooth-muscle cells. Heparin–rosuvastatin-loaded nanofiber covered stent effectively treated aneurysms without showing any notable in-stent stenosis. In vitro experiments showed that rosuvastatin could inhibit the smooth muscle cell phenotypic modulation of platelet-derived growth factor-BB induction. The inflammatory cytokines secretion and cell viability were inhibited after rosuvastatin treatment.Conclusion: Rosuvastatin could inhibit the abnormal proliferation of synthetic smooth-muscle cells. Heparin–rosuvastatin-loaded covered stents could reduce the incidence of stenosis and late thrombosis and improve the healing rates of stents used for aneurysm treatment.

Incidental Finding of Strut Malapposition Is a Predictor of Late and Very Late Thrombosis in Coronary Bioresorbable Scaffolds

Malapposition is a common finding in stent and scaffold thrombosis (ScT). Evidence from studies with prospective follow-up, however, is scarce. We hypothesized that incidental observations of strut malapposition might be predictive of late ScT during subsequent follow-up. One hundred ninety-seven patients were enrolled in a multicentre registry with prospective follow-up. Optical coherence tomography (OCT), performed in an elective setting, was available in all at 353 (0–376) days after bioresorbable scaffold (BRS) implantation. Forty-four patients showed evidence of malapposition that was deemed not worthy of intervention. Malapposition was not associated with any clinical or procedural parameter except for a higher implantation pressure (p = 0.0008). OCT revealed that malapposition was associated with larger vessel size, less eccentricity (all p < 0.01), and a tendency for more uncovered struts (p = 0.06). Late or very late ScT was recorded in seven of these patients 293 (38–579) days after OCT. OCT-diagnosed malapposition was a predictor of late and very late scaffold thrombosis (p < 0.001) that was independent of the timing of diagnosis. We provide evidence that an incidental finding of malapposition—regardless of the timing of diagnosis of the malapposition—during an elective exam is a predictor of late and very late ScT. Our data provide a rationale to consider prolonged dual antiplatelet therapy if strut malapposition is observed.