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症例は61歳,男性で,早朝の胸部圧迫感を訴え受診した.冠動脈内のエルゴノビン負荷試験などにより多枝冠攣縮性狭心症と診断した.201T1 SPECTでは前壁と下壁で集積低下がみられたが,123I-β-methyl-iodophenylpentadecanoic acid(123I-BMIPP)の心筋集積はみられなかった.フローサイトメトリー法によるCD36はI型CD36欠損であった.
CD36は長鎖脂肪酸の輸送蛋白として知られているので,123I-BMIPPの心筋への取り込みにCD36が重要な因子となる.CD36欠損,特にI型CD36欠損が123I-BMIPP心筋無集積の重要な一因子であるとわれわれは考えている.また,本症例は冠攣縮に遺伝的因子も関与する可能性が示唆された.
A 61-year-old male visited our hospital complaining of chest oppression in the morning. He was diagnosed as multivessel-vasospastic angina by ergonovine intraco-ronary arterial provocation. 201T1 SPECT showed areas with decreased accumulation in the anterior and inferior walls, but no myocardial accumulation of 123I-β-methyl -p-iodophenylpentadecanoic acid (123I-BMIPP) was ob-served. We analyzed CD36 expression in blood cells using a flow cytometer and found there was a type I CD36 deficiency.
The CD36 molecule of human blood cells is known as a transporter of long-chain fatty acids. Hense, CD36 may have an important role for myocardial uptake of long-chain fatty acids as well as 123I-BMIPP. The absence of myocardial 123I-BMIPP uptake may be due to CD36 deficiency, especially type I . This case demon-strated that a genetic factor may be involved in coro-nary vasospasm.
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