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123I-metaiodobenzylguanidine(MIBG)は心臓交感神経へのノルアドレナリンの取り込みと洗い出しを反映する放射性医薬品で,日本では1992年に臨床に供された。MIBG心筋シンチグラフィは循環器領域において虚血性心疾患1)2),不整脈,特発性拡張型心筋症,肥大型心筋症,糖尿病,腎不全や他の原因による心筋症に,そして,特に心不全の評価・治療適応の決定,予後評価のため用いられてきた3-5)。心不全では心ポンプ機能の低下に対する代償機序として交感神経機能の活性化が生じる。当初はカテコラミン刺激が心収縮機能を代償するが,長期にわたるカテコラミンへの曝露により心筋の構造と機能に障害をもたらし,カテコラミン濃度の上昇にもかかわらず心不全の代償ができなくなる。これは心筋内のノルエピネフリン濃度が減少し,β受容体の減少,ノルエピネフリン輸送体の減少によると報告されている4)5)。MIBGはノルアドレナリンの生理的なアナログで,心臓交感神経終末へuptake-1により取り込まれるが,心不全では比較的速やかに放出され心臓への集積は低集積となる。そして,心不全は適切に治療されるとMIBGの心臓集積が改善する可逆的な病態であると考えられる。
Recently. 123I-metaiodobenzylguanidine(MIBG)myocardial scintigraphy has been used to evaluate patients not only with heart failure but also parkinsonism.
We performed MIBG myocardial scintigraphy to observe the difference between two entities in 167 patients with severe decreased MIBG uptake(heart to mediastinum ratio:H/M less than 1.6). We considered these patients have severely reduced sympathetic nerve function in both entities. We divided these patients into heart failure group(65 patients)and parkinsonism group(102 patients)and compared MIBG indices obtained from heart, thyroid, and lung.
Early H/M(p=0.014), delayed H/M(p<0.001), early thyroid mediastinum ratio(p=0.020), and delayed thyroid mediastinum ratio(p=0.047)were more reduced in patients with parkinsonism than heart failure. Heart washout rate(p<0.001)and thyroid washout rate(p<0.001)were more increased in patients with parkinsonism than heart failure. These indices suggested sympathetic nerve function were more severely reduced in patients with parkinsonism than heart failure. Delayed lung mediastinum ratio(p=0.027)was more increased in patients with parkinsonism but early lung mediastinum ratio(p<0.001)was more increased in patients with heart failure. Thus, the clinical significance of MIBG lung uptake was unclear and needed further investigation.
Severe declined sympathetic nerve function in patients with parkinsonism than heart failure in MIBG indices may be caused by the different damage mechanisms between catecholamine drive induced by heart failure and nerve cell degeneration or omission of cell itself suffered from Lewy body disease.
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