Is microcatheter-associated plastic debris the primary cause of non-ischemic cerebral enhancing (NICE) lesions in endovascular procedures?

I read with great interest the recent case series by Atanasio et al. (1) and have thoroughly investigated the phenomenon of foreign body emboli [or non-ischemic cerebral enhancing (NICE) lesions] following endovascular treatment of intracranial aneurysms. This phenomenon, associated with endovascular therapy, has been observed for approximately 15 years, yet it remains a rare finding overall (2). Notably, attention has primarily focused on the type of endovascular procedure and the implanted devices. The question arises why these lesions seem to occur more frequently after aneurysm interventions compared to angiography or thrombectomy procedures.

Aneurysm procedures tend to be longer, more technically complex, and often done under elective settings, where minor neurological changes can be more readily detected (3). In contrast, in acute stroke cases, existing deficits and comorbidities often obscure new findings, making subtle changes less noticeable (4).

Another key difference between aneurysm treatment and thrombectomy lies in the use of different microcatheters—typically softer and smaller ones for coils, or larger ones for flow disruption devices.

With prolonged manipulation or deformation, some of these microcatheters may release particles (5), which could explain microemboli as well as NICE lesions. Furthermore, clinically silent infarcts observed after flow diverter implantation appear to depend on the type of microcatheter used and on the difficulty of intracranial navigation (6). These aspects are largely absent from most publications regarding NICE lesions. Therefore, it would be particularly relevant to know which microcatheters were used, whether they were pre-shaped or deformed—either mechanically or by exposure to hot air or steam—and what the procedure durations were in the few known cases. Given the small number of documented NICE lesion cases, further multicenter research is warranted to investigate these contributing factors.

Other sources of hydrophilic polymer emboli have also been described, including fragments originating from guiding catheters (7), guide wires (8) as well as pusher wires (9). A recent scoping review further emphasized that hydrophilic coatings from multiple device components may delaminate and lead to embolic complications (10).

Additionally, multi-axial catheter systems, particularly when intermediate catheters are used, create additional friction interfaces and mechanical strain during navigation, which may in turn increase particulate shedding and polymer delamination.

I wish to highlight that, within the broader discussion of NICE lesions, the potential role of microcatheters has so far been only rarely mentioned. In summary, the overall pathogenesis of NICE lesions is likely multifactorial, integrating procedural duration, catheter manipulation, device type, delivery systems, and procedural complexity as interacting co-factors.

Acknowledgments

None.

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References

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