無症候性心筋梗塞における心臓交感神経活性の役割—予後評価における有用性

Prognostic Value of Myocardial Sympathetic Activity in Patients with Asymptomatic Myocardial Infarction

　無症候性心筋梗塞（MI）32例を長期追跡調査し心事故出現に対する心臓交感神経イメージング（¹²³I-metaiodobenzylguanidine，BG）の有用性を臨床所見，心筋灌流イメージング，冠動脈造影所見，心エコー図，神経体液因子と比較検討した．BGの心筋への集積率（％UT），取り込み比（UR），洗い出し率（％WO）を求めた．平均19.9±10.3ヵ月経過観察期間中に10例（31％）で心不全（HF）が出現した．HF出現に関連した因子は糖尿病，心房細動の存在，左室拡張終期径≧54mm，BGの％UT，URの低下の5つで，MIの部位，広がり，％FSなどは関連しなかった．Cox多変量解析ではHF出現の予測因子はUR（p＝0.0007）のみで，URが0.58未満の群でのHF出現の相対リスクはUptake Ratio≧0.58の19.1倍であった．URは左室拡張終期径と相関を示し（r＝−0.578，p＝0.01），MI後の左室remodelingに交感神経活性が関連している可能性を示唆した．無症候性MIの予後の評価や病態解明において，BGによる心臓交感神経イメージングは有用な手がかりを与えてくれると考えられた．

　To clarify the significance of myocardial sympathetic activity in patients with asymptomatic myocardial infarction (MI). we performed ¹²³I-metaiodobenzylguanidine (MIBG) and ²⁰¹T1 imaging at rest.

　We calculated the ratio of cardiac uptake of the isotope to the total injected dose (%Uptake), percent washout of MIBG over 3 hours and the Uptake Ratio (UR, %Uptake of MIBG divided by %Uptake of ²⁰¹T1).We compared these indices with clinical findings, exercise stress - rest myocardial perfusion imaging with ^99mTc-methoxy-2-isobutyl isonitrile, coronary angiography, echocardiography and neurohumoral findings.

　During the follow-up period of 19.9±10.3 months in 32 patients, events (heart failure or cardiac death) developed in 10(31%). In univariate analysis, diabetes mellitus, atrial fibrillation, left ventricular end-diastolic dimension (LVDd) greater than 54 mm, and the %Up-take of MIBG and UR differed significantly between event and event-free groups. Cox proportional hazard model showed that the UR was a predictor of events (p= 0.0007). In patients with UR less than 0.58, the relative risk of events was 19.1 times greater than in patients with an UR greater than 0.58. UR was closely correlated to LVDd (r=-0.578, p=0.01) suggesting that myocardial sympathetic activity is related to LV remodeling after MI.

　MIBG imaging provides important information regarding the prognosis and the pathophysiologic process of asymptomatic MI.