摘要：

To the Editor: In their publication in Stroke, Quan et al conducted a novel investigation of unruptured intracranial aneurysms regarding to vascular inflammation via high-resolution vessel wall magnetic resonance imaging (HR-VW MRI) and immunofluorescence staining. However, by lacking of spontaneously ruptured aneurysm as control, further investigation should be done to identify the relationship between infiltrated immune cells and aneurysm rupture. In this publication, authors draw the conclusion that HR-VW MRI could be used to detect the enhancement of vessel wall by atherosclerosis, which plays an important role in intracranial aneurysm rupture. Nevertheless, insufficient evidence was provided to support their conclusion that rupture of intracranial aneurysm was sequentially induced by atherosclerosis. This assumption, however, is also not well demonstrated by the given histological evidence from hematoxylin and eosin or Masson's trichrome staining. In fact, heterogeneous structure and atherosclerosis of intracranial aneurysm have been described in previously study. It is well documented that the presence of atherosclerosis increased certain surgical risk for intracranial aneurysm, as well as the positive signals from MRI. But, whether it triggers the aneurysm rupture has not been determined yet. Therefore, whether the enhanced signal of HR-VW MRI could be identified as an indication for aggressive surgical management is still open to question. Moreover, the following results regarding to accumulation of infiltrated macrophages in enhanced vessel wall is also worth to deliberation. As different types (M1 and M2) of macrophages play alternative roles of functions, such as destruction and remodeling the vascular structure, formation of new collagen fibers, as well as composition of vessel cells. Here, except the colocalization of NLRP3 (nod-like receptor protein 3) and CD68, no clearly evidence indicated the potential phenotypes of macrophages. Meanwhile, as a marker from scavenger receptor, CD68 is not only expressed on macrophages but could also be found on circulating monocytes and even vascular smooth muscle cells. Besides, the functional and morphological transformation of vascular smooth muscle cells to macrophage-like phagocytes in intracranial aneurysm in other vascular disease had been well described in both in vivo and in vitro studies. Overall, we believe CD68 alone is not a suitable marker for identifying the function and phenotypes of macrophages in vascular diseases. More importantly, it diminished the credibility of the conclusion that the HR-VW MRI enhanced vessel wall is associated with severe inflammation that could potentially result in aneurysm rupture. On the contrary, based on the studies from Ollikainen et al, the enhanced signal of vessel wall from HR-VW MRI could be also induced by lysed erythrocytes produces like iron deposition, which usually happened in focal chronic bleeding and thrombosis, especially the adventitia layer of aneurysm. However, whether existence of iron depositions triggers aneurysm rupture is still mystery. Therefore, without further evidences on both pathological and clinical follow-up studies, it is difficult to convince the audience to believe that enhanced HR-VW MRI with single time point could totally reflect the process of inflammation process. Taking together, due to considerable impact of the artifact in the tissue, unconvincing immunologic analysis on macrophages and lack of evidence to support the association between atherosclerosis and aneurysm rupture, it is very difficult for us to be convinced that current observation represents a new insight in clinical application of HR-VW MRI.

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