The p48 Flow Modulation Device with Hydrophilic Polymer Coating (HPC) for the Treatment of Acutely Ruptured Aneurysms: Early Clinical Experience Using Single Antiplatelet Therapy

Abstract

Background: Flow diversion (FD) remains a potential treatment option following aneurysmal subarachnoid hemorrhage (aSAH) when standard options may not be feasible. However, it should not be considered a first-line treatment due to the need for dual antiplatelet therapy (DAPT). The hydrophilic polymer coating on the p48MW flow diverter (HPC, phenox) is a surface modification that inhibits platelet adhesion. This study aims to report on our early single-center experience using the p48MW HPC (phenox) flow diverter with single antiplatelet therapy (SAPT) following an aSAH.

Materials and methods: We retrospectively identified all patients who had been treated with the p48MW HPC for aSAH under SAPT. All patients treated within 30 days following an aSAH were included. Any occurrence of thromboembolic and hemorrhagic complications was recorded alongside angiographic and clinical follow-up details.

Results: Eight patients were identified. The mean interval between aSAH and FD was 6 days. Of the eight ruptured aneurysms, one was blister-like, one saccular, one mycotic, and the remaining five were dissecting aneurysms. Intraprocedural transient thrombus formation was observed in four patients (50%). Stent thrombosis was observed in one patient (12.5%) on day 3 with spontaneous recanalization after being switched onto DAPT. None of the aneurysms rebled after treatment. Two patients died due to cerebral vasospasm. Complete aneurysm occlusion had been achieved in all but one patient at angiographic follow-up (average 6 months).

Conclusions: This small series highlights the possibility and limitations of using the p48MW HPC with SAPT in ruptured aneurysms. Randomized trials with longer follow-up in larger cohorts are underway.

Keywords: Aneurysmal subarachnoid hemorrhage; Blister-like aneurysm; Dissecting aneurysm; Flow diverter; HPC; Ruptured aneurysm; Single antiplatelet therapy; Surface modification; p48MW HPC.

Fig. 1

A 50-year-old and drug-addicted male presented with subarachnoid hemorrhage from a left mycotic MCA aneurysm, who was treated by parent vessel occlusion (Patient #6). Four days later, and with the patient still intubated, he presented a sudden increase in the intracranial pressure. Head CT scan revealed a second subarachnoid hemorrhage, more prominent on the right side (A). A new diagnostic angiography showed a de novo right M2 mycotic aneurysm (B, circle), which was not present in the initial angiography (C). A single p48MW HPC (3 mm × 18 mm) was implanted after premedication with ASA (D). A total of 1500 mg ASA IV was needed to achieve sufficient platelet inhibition, tested by Multiplate and VerifyNow. After deployment, an incomplete opening of the distal end of the p48MW HPC with small thrombus formation was observed (E, circle). The complete opening of the device was achieved after crossing with an inverted microguidewire (F). The thrombus formation resolved after injection of eptifibatide (G). The most recent follow-up angiography performed 8 months after treatment showed the p48MW HPC following the contour of the fusiform vessel enlargement (H, arrow)

Fig. 2

A 58-year-old female presented with a sudden headache after impact with the trunk lid, followed by deterioration with nausea, vomiting, and unconsciousness (Patient #7). A cranial CT scan obtained on the day of admission revealed diffuse subarachnoid hemorrhage (Fisher grade 4) and hydrocephalus (A). Posterior–anterior arteriogram obtained with a right vertebral artery injection showing a fusiform dissecting aneurysm of the BA with the formation of a pseudoaneurysm (arrow) (B). Endovascular treatment was performed on day 1 after bleeding. Multiplate and VerifyNow tests confirmed sufficient platelet inhibition after premedication with 1000 mg ASA IV. Posterior–anterior projection obtained immediately after telescopic deployment of 5 p48MW HPC FDS (C). Insufficient platelet inhibition by ASA after treatment resulted in in-stent thrombosis on day 3 (D). The distal part of the BA was retrogradely perfused via the posterior communicating artery (E). T2WI MRI is showing a left pontine infarction due to the thrombosis of a pontine branch together with the dissecting aneurysm (F). Recanalization of the BA, including the aneurysm, was observed after the switch to DAPT plus eptifibatide IV (G). The patient was retreated with two p48MW HPC implanted distally before discharge. The most recent follow-up angiography performed 9 months after treatment shows complete exclusion of the pseudoaneurysm with total reconstruction of the previously dissected BA and patency of the FDS (H)

Fig. 3

A 49-year-old female presented with sudden onset of severe headache and subsequent obtundation (Patient #8). Cranial CT scan (A) showed diffuse subarachnoid hemorrhage (Fisher grade 4) and hydrocephalus. A diagnostic cerebral angiography (B, 3D-Volumen Rendering Technique; C, lateral view) demonstrated a fusiform, most likely dissecting left ICA paraclinoid aneurysm with a non-discernible neck (B, C, arrow). The aneurysm was treated with a single p48MW HPC (3 mm × 18 mm) after premedication with 30 mg prasugrel PO 3 h before the procedure (D). Multiplate and VerifyNow test confirmed sufficient platelet inhibition before and after treatment. Angiographic follow-up performed on day 2 after treatment showed the patency of the FDS and intracranial massive cerebral vasospasm (E). Refractory cerebral vasospasm resulted in large bilateral MCA and ACA infarction (F) and eventually, death