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Articles by S Sakai
Total Records ( 2 ) for S Sakai
  S Yokoyama , M Takano , M Yamamoto , S Inami , S Sakai , K Okamatsu , S Okuni , K Seimiya , D Murakami , T Ohba , R Uemura , Y Seino , N Hata and K. Mizuno
 

Background— Although coronary angiograms after bare-metal stent (BMS) implantation show late luminal narrowing beyond 4 years, the detailed changes inside the BMS have not yet been fully elucidated.

Methods and Results— Serial angiographic and angioscopic examinations were performed immediately (baseline), 6 to 12 months (first follow-up), and ≥4 years (second follow-up) after stenting without target lesion revascularization in 26 segments of 26 patients who received BMS deployment for their native coronary arteries. Angioscopic observation showed atherosclerotic yellow plaque crushed out by stent struts in 22 patients (85%) and mural thrombus in 21 patients (81%) at baseline. At first follow-up, white neointimal hyperplasia was almost completely buried inside the struts, and both yellow plaque and thrombus had decreased in comparison with baseline (12% and 4%, respectively; P<0.001). The frequencies of yellow plaque and thrombus increased from the first to second follow-ups (58% and 31%, respectively; P<0.05). All of the yellow plaques in the second follow-up were located not exterior to the struts but protruding from the vessel wall into the lumen. Late luminal narrowing, defined as an increasing of percent diameter stenosis between the first and second follow-ups, was greater in segments with yellow plaque than in those without yellow plaque (18.4±17.3% versus 3.6±4.2%, respectively; P=0.011).

Conclusions— This angiographic and angioscopic study suggests that white neointima of the BMS may often change into yellow plaque over an extended period of time, and atherosclerotic progression inside the BMS may contribute to late luminal narrowing.

  Y Hamamoto , M Kataoka , T Senba , K Uwatsu , Y Sugawara , T Inoue , S Sakai , S Aono , T Takahashi and S. Oda
  Objective

To find vertebral metastases with high risk of symptomatic malignant spinal cord compression (MSCC), features of vertebral metastases caused motor deficits of the lower extremities were examined.

Methods

From 2004 through 2006, 78 patients with metastases of the thoracic and/or the cervical spine were treated with radiation therapy (RT). Of these, 86 irradiated lesions in 73 patients were evaluable by magnetic resonance imaging and/or computed tomography at the initiation of RT and were reviewed retrospectively in this study. Twenty-eight patients (38%) had motor deficits at the initiation of RT. Assessed factors were age, sex, primary disease (lung, breast, digestive system and other cancer), lamina involvement, main level of tumor location and vertebral-body involvement.

Results

Incidence of motor deficits at the initiation of RT was 55% for lesions with lamina involvement and 5% for lesions without lamina involvement (P < 0.0001). Incidence of motor deficits was 15% for lesions located mainly in the cervical spine and/or the upper thoracic spine (Th1–4), 54% for lesions located mainly in the middle thoracic spine (MTS) (Th5–8) and 30% for lesions located mainly in the lower thoracic spine (Th9–12) (P = 0.0095). Age, sex, primary disease and vertebral-body involvement were not statistically significant factors for incidence of motor deficits due to MSCC (P > 0.9999, P = 0.7798, P = 0.1702 and P = 0.366, respectively).

Conclusions

Vertebral metastases with lamina involvement tended to cause symptomatic MSCC. Latent development of MSCC occurred more frequently in the MTS compared with other levels of the thoracic and the cervical spine.

 
 
 
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