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拡張型心筋症(以下DCMと略す)は原因不明の収縮能低下をきたす予後不良の疾患であるが,その一因にと同時に,心筋代謝賦活剤による代謝面からの改善も試みられている。1957年Craneら1)によりウシの心筋のミトコンドリアから分離され,Lesterら2)によりCoen—zyme Q (以下CoQと略す)と名づけられた補酵素は,電子伝達系に関与して細胞呼吸に重要な役割を持ち,ヒトでは側鎖のイソプレノイド基の数nが10であるため,Coenzyme Q10(CoQ10)と呼ばれる。心不全患者ではこのCoQの心筋での欠乏3)が報告されており,また心不全に対するCoQの臨床的有用性も数多く報告されている4〜9)。
我々は心不全をきたす疾患のうちでも最も予後不良な疾患の1つであるDCMに対するCoQ10の有用性を心エコー法を用いて検討した。
To evaluate the chronic effect of coenzyme Q10 (CoQ10) to dilated cardiomyopathy (DCM), sixteen patients with DCM were studied by echocardio-graphy. Seven of sixteen patients were received CoQ10 45 mg per day for five months (CoQ10 group). Nine of them were followed without CoQ10, for five months (non-CoQ10 group). Blood pressure and heart rate were not significantly changed in both groups. In echocardiographic findings, left ventricular end-diastolic dimension (Dd) was not significantly changed, end-systolic dimension (Ds) was increased from 52±5 mm to 55±6 mm and percent fractional shortening (%FS) decreased from 22±5% to 18±6% (p<0.05) in non-Co10 group. In CoQ10 group, Dd and Ds tended to increase slightly (n. s.) and %FS tended to increase (21±5% to 23±5%, n. s.). Although symptom of heart failure was deteriorated in three of nine patients in non-CoQ10 group, it was aggra-vated in one and was improved in two of seven patients in CoQ10 group. That is to say, although in non-CoQ10 group cardiac contractility decreased progressively for five months, it was not significantly changed in CoQ10 group. These results suggested that CoQ10 might prevent the progression of my-ocardial lesion in DCM.
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