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Haruto Uchino, Daina Kashiwazaki, Naoki Akioka, Masaki Koh, Naoya Kuwayama, Kiyohiro Houkin and Satoshi Kuroda

OBJECTIVE

In this study the authors aimed to describe clinical features, surgical techniques, and long-term outcomes of repeat bypass surgery required for a certain subset of patients with moyamoya disease.

METHODS

The authors retrospectively reviewed a total of 22 repeat bypass surgeries for 20 patients (age range 1–69 years) performed during the last 20 years at their institutions. The patients were classified into 2 groups. Group A included 10 patients who underwent repeat bypass surgery for anterior circulation due to insufficient revascularization on the ipsilateral side. Group B included 10 patients who underwent repeat bypass surgery for posterior circulation due to the involvement of the posterior cerebral artery (PCA) after successful initial surgery for anterior circulation.

RESULTS

Preoperative symptoms included headache in 3 patients, transient ischemic attack in 10, cerebral infarction in 3, and intracranial hemorrhage in 4 patients. Intervals between the initial bypass surgery and repeat bypass surgery were 0.3–30 years (median 3 years). In group A, superficial temporal artery to middle cerebral artery (MCA) anastomosis and indirect bypass were performed on 7 hemispheres. Only indirect bypass was performed on 3 hemispheres because of the lack of suitable donor or recipient arteries. In group B, occipital artery (OA) to PCA anastomosis and indirect bypass were conducted on 4 hemispheres, and OA-MCA anastomosis and indirect bypass on 1 hemisphere. Only indirect bypass was conducted on 7 hemispheres because of the lack of suitable recipient arteries. All 22 repeat bypass surgeries were successfully conducted. During follow-up periods (median 4 years), none of the patients suffered repeat stroke except 1 patient who died of recurrent intracerebral hemorrhage 3 years after repeat bypass surgery for anterior circulation.

CONCLUSIONS

Repeat bypass surgery was feasible and effective to reduce further incidence of headache attack, transient ischemic attack, and ischemic/hemorrhagic stroke in moyamoya disease patients. Through precise radiological analysis, surgical procedures should be planned to yield maximal therapeutic effects.

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Daina Kashiwazaki, Masaki Koh, Haruto Uchino, Naoki Akioka, Naoya Kuwayama, Kyo Noguchi and Satoshi Kuroda

OBJECTIVE

The relationship between intraplaque hypoxia and intraplaque hemorrhage (IPH) has been reported, but the details remain obscure. In this study, the authors aimed to clarify the relationship among intraplaque hypoxia, endothelial progenitor cells (EPCs), and neovascularization, which causes IPH. The histological findings of specimens obtained from carotid endarterectomy were assessed.

METHODS

This study included 49 patients who underwent carotid endarterectomy. Magnetic resonance plaque imaging was performed to analyze the components of the carotid plaques, and surgical specimens were subjected to immunohistochemical analysis. The numbers of hypoxia-inducible factor-1 alpha (HIF-1α)–, CD34-, CD133-, and vascular endothelial growth factor receptor-2 (VEGFR-2)–positive cells in the carotid plaques were precisely quantified, as were the number and maximum diameter of CD31-positive microvessels.

RESULTS

Plaque components were judged as fibrous in 7 samples, lipid-rich in 22, and IPH in 20. The number of CD34-, VEGFR-2–, and CD133-positive cells as an EPC-specific marker was significantly correlated with the number of HIF-1α–positive cells (r = 0.9, r = 0.82, and r = 0.81, respectively). These numbers varied among the 3 plaque components (IPH > lipid-rich > fibrous). The number and maximum luminal diameter of CD31-positive microvessels were also significantly correlated with the number of HIF-1α–positive cells (r = 0.85 and r = 0.89, respectively) and varied among the 3 plaque components (IPH > lipid-rich > fibrous).

CONCLUSIONS

The present findings suggest that intraplaque hypoxia may accelerate abnormal microvessel formation derived from EPCs, which in turn promotes IPH. The results also suggest that microvessel enlargement is a pivotal characteristic of IPH and these enlarged microvessels are immature endothelial tubes with disorganized branching and are fragile and prone to rupture.

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Shusuke Yamamoto, Satoshi Hori, Daina Kashiwazaki, Naoki Akioka, Naoya Kuwayama and Satoshi Kuroda

OBJECTIVE

This study aimed to assess longitudinal changes in the collateral channels originating from the lenticulostriate artery (LSA), posterior communicating artery (PCoA), and anterior and posterior choroidal arteries (AChA and PChA, respectively) during disease progression and/or aging. The impact of collateral channels on onset type was also examined.

METHODS

This study included 71 involved hemispheres in 41 patients with moyamoya disease. The disease was categorized into 6 stages according to Suzuki’s angiographic staging system. The degree of development of each moyamoya vessel was categorized into 3 grades.

RESULTS

The LSA started to dilate in stage 2, showed the most prominent development in stage 3, and decreased in more advanced stages (p < 0.001). The AChA most notably developed in stage 3 and gradually shrank (p = 0.04). The PCoA started to dilate in stage 3 and showed the most prominent development in stage 4 (p = 0.03). The PChA started to dilate in stage 3 and showed the most prominent development in stages 4 to 5 (p < 0.001). Patient age was negatively related to LSA development (p = 0.01, R = 0.30) and was positively associated with the abnormal dilation and extension of the PCoA (p = 0.02, R = 0.28) and PChA (p < 0.001, R = 0.45). The PCoA, AChA, and PChA more distinctly developed in hemispheres with intracerebral or intraventricular hemorrhage than in hemispheres with ischemic stroke or transient ischemic attack (p < 0.001, p = 0.03, and p = 0.03, respectively).

CONCLUSIONS

This study suggests that the collateral channels through moyamoya vessels longitudinally shift from the anterior to posterior component during disease progression and aging, which may be closely related to the onset of hemorrhagic stroke in adult moyamoya disease.

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Daina Kashiwazaki, Naoki Akioka, Naoya Kuwayama, Tomohide Hayashi, Kyo Noguchi, Kortaro Tanaka and Satoshi Kuroda

OBJECTIVE

The roles of endothelial progenitor cells (EPCs) in the development of carotid plaque are still obscure. This study aimed to clarify this by assessing the histological findings of specimens obtained from carotid endarterectomy.

METHODS

This study included 34 patients who underwent carotid endarterectomy. MR imaging was performed to semiquantitatively analyze the components of the carotid plaques in all patients. The surgical specimens were subjected to immunohistochemistry. The distributions of the CD34-, CD133-, VEGF-2R–positive cells in the carotid plaques were precisely analyzed, and their number was quantified. Simultaneously, the CD34-positive microvessels were localized.

RESULTS

The plaque component was judged as lipid-rich plaque in 19 patients, intraplaque hemorrhage (IPH) in 11 patients, and fibrous plaque in 4 patients. The CD34-positive microvessels were densely distributed in the plaque shoulder and interface-to-media regions. The CD34-, CD133-, and VEGF-2R–positive cells were mainly localized around the CD34-positive microvessels. The number of CD34-positive microvessels significantly correlated with the number of CD34-, CD133-, and VEGF-2R–positive cells (R = 0.308, p = 0.009; R = 0.324, p = 0.006; and R = 0.296, p = 0.013, respectively). Vulnerable plaques (lipid-rich and IPH) had significantly higher numbers of the CD34-positive microvessels (p = 0.007) and CD34-, CD133-, and VEGF-2R–positive cells than fibrous plaques (p = 0.031, p = 0.013, and p = 0.002).

CONCLUSIONS

These findings strongly suggest that neovascularization in the plaque shoulder and interface-to-media regions may play a key role in delivering EPCs from the peripheral blood to the carotid plaque, promoting the growth of carotid plaque. Furthermore, the invaded EPCs, especially the CD133-positive immature EPCs, may be related to plaque vulnerability.