Search Results

You are looking at 1 - 9 of 9 items for

  • Author or Editor: Kenji Yoshida x
  • All content x
Clear All Modify Search
Restricted access

Naoki Toma, Satoshi Matsushima, Kenichi Murao, Kenji Kawaguchi, Kyoko Imanaka-Yoshida, Toshimichi Yoshida, and Waro Taki

✓ Despite the high technical success rates and the acceptable morbidity and mortality rates that are associated with carotid artery (CA) stent implantation, morphological changes in the vessel wall after this procedure are still unknown. The authors describe histopathological findings of the CA after stent implantation in a human autopsy specimen.

A 75-year-old man with asymptomatic CA stenosis underwent successful CA stent implantation, but died 8 months afterward of complications surrounding treatment of a thoracic aortic artery aneurysm. The stented CA was isolated from the autopsy specimen and was analyzed macroscopically and with the aid of scanning electron microscopy and histopathological methods.

Although there was focal persistence of a chronic inflammatory reaction around the stent struts, a stabilized neointima overlying the stent, which was principally composed of cells that stained positively for α—smooth muscle actin and collagen deposition with complete reendothelialization of the luminal surface, was confirmed in the internal CA. In contrast, residual mural thrombus around the stent struts in the common CA led to a concern about the potential risk for distal embolism in the future. The present case provides supportive evidence of stabilized neointima overlying the stent and valuable information regarding morphological characteristics useful for selecting a stent of an appropriate size.

Full access

Wataru Yanagihara, Kohei Chida, Masakazu Kobayashi, Yoshitaka Kubo, Kenji Yoshida, Kazunori Terasaki, and Kuniaki Ogasawara

OBJECTIVE

Some adult patients with moyamoya disease (MMD) undergoing revascularization surgery show an improvement or decline in cognition postoperatively. Revascularization surgery for ischemic MMD augments cerebral blood flow (CBF) and improves cerebral oxygen metabolism. However, cerebral hyperperfusion, which is a short-term, major increase in ipsilateral CBF that is much greater than the metabolic needs of the brain, sometimes occurs as a complication. Cerebral hyperperfusion produces widespread, minimal injury to the ipsilateral white matter and cortical regions. The aim of the present prospective study was to determine how changes in CBF due to arterial bypass surgery affect cognitive function in adult patients with symptomatic ischemic MMD and misery perfusion.

METHODS

Thirty-two patients with cerebral misery perfusion, as determined on the basis of 15O gas positron emission tomography, underwent single superficial temporal artery–middle cerebral artery (M4 in the precentral region) anastomosis. Brain perfusion single-photon emission computed tomography (SPECT) studies were performed preoperatively, on the 1st postoperative day, and 2 months after surgery. Neuropsychological tests were also performed preoperatively and 2 months after surgery.

RESULTS

Postoperative neuropsychological assessments demonstrated cognitive improvement in 10 cases (31%), no change in 8 cases (25%), and decline in 14 cases (44%). Based on brain perfusion SPECT and symptoms, 10 patients were considered to have cerebral hyperperfusion syndrome, and all of these patients exhibited a postoperative decline in cognition. Relative precentral CBF on the 1st postoperative day was significantly greater in patients with postoperative cognitive decline (167.3% ± 15.3%) than in those with improved (105.3% ± 18.2%; p < 0.0001) or unchanged (131.4% ± 32.1%; p = 0.0029) cognition. The difference between relative precentral CBF 2 months after surgery and that before surgery was significantly greater in patients with postoperative cognitive improvement (17.2% ± 3.8%) than in those with no postoperative change (10.1% ± 2.4%; p = 0.0003) or with postoperative decline (11.5% ± 3.2%; p = 0.0009) in cognition.

CONCLUSIONS

Cerebral hyperperfusion in the acute stage after arterial bypass surgery impairs cognitive function. An increase in CBF in the chronic stage without acute-stage cerebral hyperperfusion improves cognitive function in adult patients with symptomatic ischemic MMD and misery perfusion.

Restricted access

Kenji Yoshida, Kuniaki Ogasawara, Masakazu Kobayashi, Junichi Tsuboi, Hitoshi Okabayashi, and Akira Ogawa

Object

Scar formation in the carotid sheath is often identified during carotid endarterectomy (CEA) in patients with previous cardiac surgery, and dissection of the carotid sheath and exposure of the carotid arteries in such patients are difficult. The purpose of the present study was to investigate factors related to scar formation identified during CEA in patients with previous cardiac surgery.

Methods

Twenty-three patients with internal carotid artery stenosis (≥ 70%) and previous cardiac surgery underwent CEA. A patient was prospectively defined as having scar formation during CEA when scissors were required throughout dissection of the carotid sheath and exposure of the carotid arteries.

Results

Scar formation was identified during dissection of the carotid sheath in 7 patients (30.4%). In all 7 patients, the side of CEA was identical to the side on which the Swan-Ganz catheter was inserted during cardiac surgery, and the incidence of previous ipsilateral Swan-Ganz catheter insertion was significantly higher in patients with the scar formation (100%) than in those without (31.3%). Seven (58.3%) of 12 patients with a history of ipsilateral Swan-Ganz catheter insertion had scar formation. Two of the 7 patients with scar formation experienced complications after CEA, including one patient with hemiparesis due to artery-to-artery embolism during surgery, and another patient with transient vocal cord paralysis.

Conclusions

A history of Swan-Ganz catheter insertion during previous cardiac surgery is associated with the presence of scar tissue in the ipsilateral carotid sheath and a higher risk of complications during CEA.

Restricted access

Kuniaki Ogasawara, Keiko Yamadate, Masakazu Kobayashi, Hidehiko Endo, Takeshi Fukuda, Kenji Yoshida, Kazunori Terasaki, Takashi Inoue, and Akira Ogawa

Object. Cognitive impairment occurs in 20 to 30% of patients following carotid endarterectomy (CEA). The purpose of the present study was to determine whether postoperative cerebral hyperperfusion is associated with impairment of cognitive function in patients undergoing that procedure.

Methods. Cerebral blood flow (CBF) was measured using single-photon emission computerized tomography scanning before and immediately after CEA and on the 3rd postoperative day in 92 patients with ipsilateral internal carotid artery stenosis of 70% or greater. Hyperperfusion post-CEA was defined as a 100% increase or greater in CBF compared with preoperative values. Neuropsychological testing was also performed preoperatively and at the 1-, 3-, and 6-month follow-up examinations.

At the 1-month postoperative neuropsychological assessment, 11 patients (12%) displayed evidence of cognitive impairment. In addition, the incidence of postoperative cognitive impairment in patients with post-CEA hyperperfusion (seven [58%] of 12 patients) was significantly higher than that in patients without post-CEA hyperperfusion (four [5%] of 80 patients; p < 0.0001). A logistic regression analysis demonstrated that post-CEA hyperperfusion was the only significant independent predictor of postoperative cognitive impairment. Of the seven patients in whom post-CEA hyperperfusion and cognitive impairment were identified 1 month postoperatively, four (including three patients with hyperperfusion syndrome) remained cognitively impaired at the 3- and 6-month follow-up examinations.

Conclusions. Postoperative cerebral hyperperfusion is associated with impairment of cognitive function in patients undergoing CEA. Furthermore, the development of hyperperfusion syndrome is associated with the persistence of postoperative cognitive impairment.

Restricted access

Suguru Igarashi, Toshihiko Ando, Tatsuhiko Takahashi, Jun Yoshida, Masakazu Kobayashi, Kenji Yoshida, Kazunori Terasaki, Shunrou Fujiwara, Yoshitaka Kubo, and Kuniaki Ogasawara

OBJECTIVE

A primary cause of cognitive decline after carotid endarterectomy (CEA) is cerebral injury due to cerebral hyperperfusion. However, the mechanisms of how cerebral hyperperfusion induces cerebral cortex and white matter injury are not known. The presence of cerebral microbleeds (CMBs) on susceptibility-weighted imaging (SWI) is independently associated with a decline in global cognitive function. The purpose of this prospective observational study was to determine whether cerebral hyperperfusion following CEA leads to the development of CMBs and if postoperative cognitive decline is related to these developed CMBs.

METHODS

During the 27-month study period, patients who underwent CEA for ipsilateral internal carotid artery stenosis (≥ 70%) also underwent SWI and neuropsychological testing before and 2 months after surgery, as well as quantitative brain perfusion SPECT prior to and immediately after surgery.

RESULTS

According to quantitative brain perfusion SPECT and SWI before and after surgery, 12 (16%) and 7 (9%) of 75 patients exhibited postoperative cerebral hyperperfusion and increased CMBs in the cerebral hemisphere ipsilateral to surgery, respectively. Cerebral hyperperfusion was associated with an increase in CMBs after surgery (logistic regression analysis, 95% CI 5.08–31.25, p < 0.0001). According to neuropsychological assessments before and after surgery, 10 patients (13%) showed postoperative cognitive decline. Increased CMBs were associated with cognitive decline after surgery (logistic regression analysis, 95% CI 6.80–66.67, p < 0.0001). Among the patients with cerebral hyperperfusion after surgery, the incidence of postoperative cognitive decline was higher in those with increased CMBs (100%) than in those without (20%; p = 0.0101).

CONCLUSIONS

Cerebral hyperperfusion following CEA leads to the development of CMBs, and postoperative cognitive decline is related to these developed CMBs.

Full access

Koji Yoshida, Kuniaki Ogasawara, Hiroaki Saura, Hideo Saito, Masakazu Kobayashi, Kenji Yoshida, Kazunori Terasaki, Shunrou Fujiwara, and Akira Ogawa

OBJECT

Cognitive function is often improved or impaired after carotid endarterectomy (CEA) for patients with cerebral hemodynamic impairment. Cerebral glucose metabolism measured using positron emission tomography (PET) with 18F-fluorodeoxyglucose (FDG) correlates with cognitive function in patients with neurodegenerative diseases. The present study aimed to determine whether postoperative changes in cerebral glucose metabolism are associated with cognitive changes after CEA.

METHODS

In patients who were scheduled to undergo CEA for ipsilateral internal carotid artery (ICA) stenosis (≥ 70% narrowing), cerebral blood flow (CBF) and cerebrovascular reactivity (CVR) to acetazolamide were assessed preoperatively using brain perfusion single-photon emission computed tomography (SPECT). CBF measurement using SPECT was also performed immediately after CEA. For patients with reduced preoperative CVR to acetazolamide in the cerebral hemisphere ipsilateral to surgery, cerebral glucose metabolism was assessed using FDG-PET before surgery and 3 months after surgery and was analyzed using 3D stereotactic surface projection. Neuropsychological testing was also performed preoperatively and 3 months postoperatively.

RESULTS

Twenty-two patients with reduced preoperative CVR to acetazolamide successfully underwent FDG-PET studies and neuropsychological testing before and after CEA. Seven, 9, and 6 patients were defined as showing improved, unchanged, and impaired postoperative cognition, respectively, based on the neuropsychological assessments. The cortical area with increased postoperative glucose metabolism was greater in patients with improved postoperative cognition than in those with unchanged (p < 0.001) or impaired (p < 0.001) postoperative cognition. The cortical area with decreased postoperative glucose metabolism was greater in patients with impaired postoperative cognition than in those with improved (p < 0.001) or unchanged (p < 0.001) postoperative cognition. All 7 patients with improved cognition exhibited postoperative hemispheric increases in glucose metabolism, while 5 of the 6 patients with impaired cognition exhibited postoperative hemispheric decreases in glucose metabolism. Brain perfusion SPECT revealed that the latter 6 patients experienced postoperative cerebral hyperperfusion, and 2 of the 6 patients exhibited cerebral hyperperfusion syndrome. The cortical area with decreased postoperative glucose metabolism in these 2 patients was greater than that in other patients.

CONCLUSIONS

Postoperative changes in cerebral glucose metabolism, as measured using FDG-PET, are associated with cognitive improvement and impairment after CEA.

Restricted access

Hiroshi Kashimura, Kuniaki Ogasawara, Yoshitaka Kubo, Shunsuke Kakino, Kenji Yoshida, Masayuki Sasoh, Hajime Takahashi, Kenji Suzuki, and Akira Ogawa

✓ A technique for exposing the vertebrobasilar junction with traction of the dentate ligament is described for treatment of large vertebral artery (VA) aneurysms via the far lateral suboccipital approach with partial condylar resection. The most rostral attachment of the dentate ligament is divided above the site where the VA pierces the dura mater. A traction suture is placed into the dentate ligament and gently retracted using mosquito forceps. As a result, the medulla oblongata is lifted dorsally and slightly rotated by the divided and retracted dentate ligament, allowing an approach from a more superior or inferior direction. The present technique is useful for the treatment of large thrombosed VA aneurysms.

Restricted access

Ryounoshin Hirooka, Kuniaki Ogasawara, Makoto Sasaki, Keiko Yamadate, Masakazu Kobayashi, Yasunori Suga, Kenji Yoshida, Yasunari Otawara, Takashi Inoue, and Akira Ogawa

Object

Cerebral hyperperfusion after carotid endarterectomy (CEA) impairs cognitive function and is often detected on cerebral blood flow (CBF) imaging. The purpose of the present study is to investigate structural brain damage seen on magnetic resonance (MR) images obtained in patients with cerebral hyperperfusion and cognitive impairment after CEA.

Methods

One hundred and fifty-eight patients with ipsilateral internal carotid artery stenosis (≥ 70%) underwent CEA. Neuropsychological testing was performed preoperatively and at the 1st postoperative month. Cerebral blood flow was measured using single-photon emission computed tomography before, immediately after, and 3 days after surgery. Magnetic resonance imaging was performed before and 1 day after surgery. In patients with post-CEA hyperper-fusion (defined as a CBF increase ≥ 100% compared with preoperative values) on CBF imaging, MR images were also obtained on the 3rd postoperative day, the day on which hyperperfusion syndrome developed, and 1 month after the operation.

Results

The incidence of postoperative cognitive impairment was significantly higher in patients with post-CEA hyperperfusion on CBF imaging (12 [75%] of 16 patients) than in those without (6 [4%] of 142 patients; p < 0.0001). Only 1 of 5 patients with cerebral hyperperfusion syndrome developed reversible brain edema in the cerebral hemisphere ipsilateral to the CEA on MR images obtained on the day hyperperfusion syndrome occurred. However, postoperative cognitive impairment developed in all 5 patients with cerebral hyperperfusion syndrome regardless of the presence or absence of new lesions on MR images. In addition, postoperative cognitive impairment developed in 5 (45%) of 11 patients with asymptomatic cerebral hyperperfusion on CBF imaging despite the absence of new lesions on any postoperative MR images.

Conclusions

Although cerebral hyperperfusion syndrome after CEA sometimes results in reversible brain edema visible on MR imaging, postoperative cerebral hyperperfusion—even when asymptomatic—often results in impaired cognitive function without structural brain damage on MR imaging.

Restricted access

Taro Suzuki, Kuniaki Ogasawara, Ryonoshin Hirooka, Makoto Sasaki, Masakazu Kobayashi, Daiya Ishigaki, Shunro Fujiwara, Kenji Yoshida, Yasunari Otawara, and Akira Ogawa

Object

Preoperative impairment of cerebral hemodynamics predicts the development of new cerebral ischemic events after carotid endarterectomy (CEA), including neurological deficits and cerebral ischemic lesions on diffusion weighted MR imaging. Furthermore, the signal intensity of the middle cerebral artery (MCA) on single-slab 3D time-of-flight MR angiography (MRA) can assess hemodynamic impairment in the cerebral hemisphere. The purpose of the present study was to determine whether, on preoperative MR angiography, the signal intensity of the MCA can be used to identify patients at risk for development of cerebral ischemic events after CEA.

Methods

The signal intensity of the MCA ipsilateral to CEA on preoperative MR angiography was graded according to the ability to visualize the MCA in 106 patients with unilateral internal carotid artery stenosis (≥ 70%). Diffusion weighted MR imaging was performed within 3 days of and 24 hours after surgery. The presence or absence of new postoperative neurological deficits was also evaluated.

Results

Cerebral ischemic events after CEA were observed in 16 patients. Reduced signal intensity of the MCA on preoperative MR angiography was the only significant independent predictor of postoperative cerebral ischemic events. When the reduced MCA signal intensity on preoperative MR angiography was defined as an impairment in cerebral hemodynamics, MR angiography grading resulted in an 88% sensitivity and 63% specificity, with a 30% positive- and a 97% negative-predictive value for the development of postoperative cerebral ischemic events.

Conclusions

Signal intensity of the MCA on preoperative single-slab 3D time-of-flight MR angiography is useful for identifying patients at risk for cerebral ischemic events after CEA.