In this report, we present the fatal spontaneous delayed rupture of a previously unruptured large PICA aneurysm following treatment with the PED. Pathology at postmortem examination has supported the theory that intra-aneurysmal thrombus may acutely destabilize the aneurysm wall. Aneurysms with an anatomic arrangement that promote continued flow into the neck may not be optimal candidates for the flow-diversion treatment strategy.
BACKGROUND AND PURPOSE:Some patients are at high risk of aneurysm recurrence after endovascular treatment: patients with large aneurysms (Patients Prone to Recurrence After Endovascular Treatment PRET-1) or with aneurysms that have previously recurred after coiling (PRET-2). We aimed to establish whether the use of hydrogel coils improved efficacy outcomes compared with bare platinum coils.
We 1 read with great interest the recent publication by Cebral et al entitled "Aneurysm Rupture Following Treatment with Flow-Diverting Stents: Computational Hemodynamics Analysis of Treatment." 1 The postprocedural rupture of previously unruptured aneurysms after flow diversion (FD) is an uncommon but devastating complication. Correspondingly, any analysis that would allow operators to identify aneurysms at high risk for rupture after FD could improve the safety profile of the treatment strategy. Cebral et al 1 used a computational fluid dynamics (CFD) model to generate results, which suggest that FDs, in selected cases, may induce dramatic elevations of intra-aneurysmal pressure leading to postprocedural rupture. The authors further suggested that their numeric simulations would allow them to prospectively identify those aneurysms at risk for rupture after FD. They present 7 aneurysms, 3 with postprocedural rupture and 4 that were treated successfully. The selected aneurysms and arterial segments, along with assumptions about flow through the segments, constant pressure at the outlet of the segments, and rigid arterial walls, were evaluated within a CFD model. Using this model, their calculations showed that all 3 aneurysms which went on to rupture after FD demonstrated severe increases in intra-aneurysmal pressure (Ͼ20 mm Hg) after treatment, while those aneurysms that did not rupture after FD did not exhibit such dramatic pressure rises (Ͻ3 mm Hg). While this hypothesis is very attractive, the modeling upon which these conclusions are based, seems flawed. The article underscores the general need to critically evaluate the results and carefully parse the pictures output by CFD programs, especially when pressures are reported. Given that the concepts are presented within the context of a complex mathematical argument, it may be difficult for readers who are inexperienced in fluid mechanics or CFD to fully appreciate the details of what the authors are proposing. The major problems with the study include the following: 1) a vast overestimation of the physiologic pressure gradients occurring across short, tapered, and/or tortuous vascular segments; and 2) a selective invocation of cerebral autoregulation.
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