Nobuyuki Komiyama

Faculty & Position:Cardiovascular Internal Medicine Department  doctor
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Last Updated: Sep. 09, 2019 at 11:48

Research Activities

Research Areas

  • Clinical internal medicine / Cardiovascular medicine

Research Interests

    , vulnerable plaque , integrated backscatter

Misc

  • Clinical relevance of dipyridamole stress Tc-99m-sestamibi myocardial SPECT for the early stage of acute myocardial infarction after reperfusion treatment
    Kinoshita Takahiko, Kuwabara Yoichi, Shikama Takeshi, Matsuno Koki, Kuroda Toru, Aouda Akira, Fujii Kiyotaka, Komiyama Nobuyuki, Masuda Yoshiaki
    Chiba medical journal 77(4) 207-212 Aug. 2001
    Objectives : This study aimed to evaluate coronary flow in acute myocardial infarction (MI) by stress myocardial perfusion imaging (MPI), and to compare that with metabolic status and perfusion at rest. Methods: Twenty-three patients with acute MI who received successful angioplasty within 12 hours were studied. All patients underwent dipyridamole stress or rest technetium (Tc)-99m-sestamibi and ^<123>I-BMIPP SPECT imaging in the acute phase (mean 3.8 and 7.3 days respectively). For each images, segmental accumulations were semi-quantitatively graded by 4-point scoring system (0=normal, 1=mild reduction, 2=severe reduction, 3=defect) for 14 segments to yield the total defect score (TDS). Results: [table] TDS in stress MPI was significantly bigger than that in rest MPI, although it was not significantly different from that in BMIPP. Conclusions: In the segments with infarction, dipyridamole stress MPI revealed to have greater defect than rest Tc in acute phase. This may indicate that the myocardium salvaged by reperfusion has disorder in coronary flow as well as metabolic disorder.
  • Thrombomodulin concentrations correlate inversely with the extent of coronary atheroscrelosis, and positively with tumor necrosis factor α, homocysteine, and vascular cell adhesion molecule-1 concentrations
    Yamamoto Masashi, Watanabe Shigeru, Komiyama Nobuyuki, Miyazaki Akira, Masuda Yoshiaki
    Chiba medical journal 77(4) 231-240 Aug. 2001
    We correlated the extent of coronary artery sclerosis with the serum concentrations of chemical risk factors for the development of atherosclerosis, especially soluble thrombomodulin (sTM). We hypothesized that extensive coronary artery endothelial damage decreases sTM expression. We also determined the relationships between sTM, tumor necrosis factor-α (TNF α), homocysteine (HC), and vascular cell adhesion molecule-1 (VCAM-1) serum concentrations in 48 patients (36 men and 12 women) with coronary artery disease. The angiographic extent of coronary atherosclerosis was evaluated based on 1) the number of major vessels with stenosis, 2) Gensini's severity score, and 3) the coronary extent score. No significant associations were observed between the number of diseased vessels and the serum concentrations of key factors. When patients were grouped according to Gensini's severity score, the HbAlc concentration was significantly higher and uric acid and sTM concentrations were significantly lower in the high score group (>40) than in the low score group. When patients were grouped based on the coronary extent score, the serum sTM concentrations were significantly higher in patients with one stenosis than patients with ≧2 stenoses. Furthermore, there were significant relationships between the sTM, HC, TNF α, and VCAM-1. We conclude that the progression of endothelial damage decreased the expression of sTM. In contrast, endothelial cell injury in the setting of increased HC concentrations was associated with increased TM and VCAM-1 expression. Furthermore, TNF α must also stimulate the expression of TM and VCAM-1.
  • Effect of Physical Training in Patients with Recent Myocardial Infarction Who Underwent Successful Percutaneous Transluminal Coronary Angioplasty : Exercise Tolerance and Left Ventricular Function
    KOIZUMI Tomomi, KOMIYAMA Nobuyuki, NAKASATO Takesi, YAMAMOTO Yutaka, MASUDA Yoshiaki
    日本臨床生理学会雑誌 = Japanese journal of applied physiology 30(6) 305-310 Dec. 2000


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