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論文
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Gamou, Tadatsugu ; Sakata, Kenji ; Tada, Hayato ; Konno, Tetsuo ; Hayashi, Kenshi ; Ino, Hidekazu ; Yamagishi, Masakazu ; Kawashiri, Masa-aki ; on behalf of the MILLION Study Group ; 坂田, 憲治 ; 多田, 隼人 ; 今野, 哲雄 ; 林, 研至 ; 井野, 秀一 ; 山岸, 正和 ; 川尻, 剛照
概要:
Background:The MILLION study, a prospective randomized multicenter study, revealed that lipid and blood pressure (BP)-lo
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wering therapy resulted in regression of coronary plaque as determined by intravascular ultrasound (IVUS). In the present study we performed additional analysis to investigate the associated factors with regression of coronary plaque. Methods and Results:We investigated serial 3D IVUS images from 68 patients in the MILLION study. Standard IVUS parameters were assessed at both baseline and follow-up (18–24 months). Volumetric data were standardized by length as normalized volume. In patients with plaque regression (n=52), plaque volumenormalizedsignificantly decreased from 64.8 to 55.8 mm3(P<0.0001) and vessel volumenormalizedsignificantly decreased from 135.0 to 127.5 mm3(P=0.0008). There was no difference in lumen volumenormalizedfrom 70.1 to 71.8 mm3(P=0.27). There were no correlations between % changes in vessel volume and cholesterol or BP. On the other hand, negative correlations between % change in vessel volume and vessel volumenormalizedat baseline (r=−0.352, P=0.009) or plaque volumenormalizedat baseline (r=−0.336, P=0.01) were observed. Conclusions:The current data demonstrated that in patients with plaque regression treated by aggressive lipid and BP-lowering therapy, the plaque regression was derived from reverse vessel remodeling determined by vessel volume and plaque burden at baseline irrespective of decreases in lipids and BP.<br />出版者照会後に全文公開
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論文
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蒲生, 忠雄 ; Gamou, Tadatsugu
概要:
金沢大学附属病院<br />QT延長症候群（LQTS）90症例中27症例（30%）に、若年発症徐脈58症例中7症例（12%）に、孤立性心房細動90症例8症例（9%）に遺伝子変異が認められた。同定された遺伝子変異に対して機能解析を行ったところ
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、QT延長症候群で同定された12遺伝子変異、若年発症の徐脈の2変異，孤立性心房細動の2変異は機能喪失変異であり、孤立性心房細動3変異は機能亢進変異であった。ゼブラフィッシュ初期胚にLQTSの原因遺伝子の一つであるKCNH2のアンチセンスモルフォリノ単独を導入したところ房室ブロックを認めた。また、野生型ヒトKCNH2 mRNAを同時に注入したところ房室ブロックの改善が認められた。<br />Gene analysis showed mutations were found in 27 out of 90 patients with long QT syndrome, 7 out of 58 patients with inherited bradyarrhythmia, 8 out of 90 patients with lone atrial fibrillation. We performed cellular electrophysiological study for detected mutations. Sixteen mutations were loss of function mutations and 2 mutations were gain of function mutations. Morpholino KCNH2 knockdown in zebrafish embryos displayed a AV block and WT hHERG RNA injection restored normal repolarization.<br />研究課題/領域番号:23591078, 研究期間(年度):2011-2013
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