浦西 歩美, 増田 佳純, 五十嵐 絵里奈, 澤田 智美, 浅沼 俊彦, 石蔵 文信, 別府 慎太郎

Ayumi URANISHI, Kasumi MASUDA, Erina IKARASH, Tomomi SAWADA, Toshihiko ASANUMA, Fuminobu ISHIKURA, Shintaro BEPPU

大阪大学大学院医学系研究科保健学専攻機能診断科学講座

Osaka University Graduate School of Medicine,Division of Health Sciences,Department of Functional Diagnostic Science

キーワード : contrast echo, coronary, infarction, microsphere, ATP

背景・目的：心筋血液量は心筋壊死の拡がり程度に応じて減ずる．しかし，心筋梗塞例で冠動脈狭窄がない場合，心筋壊死の程度に影響されることなく，冠微小循環血流速度は一定であるのかどうかはよく分かっていない．この関係を明らかにするために，マイクロスフェアを段階的に冠動脈注入し，均一な虚血巣を作成し，心筋コントラストエコー（MCE）法を用いて，心筋血液量，微小循環血流速度を検討した．方法：麻酔開胸犬8匹を用い，冠血流量をモニターしつつ，マイクロスフェア（平均径100μm）を左回旋枝より段階的に注入し，4段階の斑状心筋虚血モデルを作成した．各段階で安静時とATP負荷時にリアルタイムMCE法を施行した．関心領域を虚血領域と，対側の正常領域に設定し，輝度回復曲線y＝A（1-e^-βt）から，心筋血液量（A値）と心筋血流速度（β値）を算出した．結果：虚血領域では冠血流量は第4段階で初めて低下したが（コントロール，第1‐4段階でそれぞれ，20.8，21.8，19.0，13.4，9.2ml/min），ATP負荷時の冠血流量は漸次低下し（47.6，39.0，31.0，20.4，11.6ml/min），冠血流予備能も低下した（2.28，1.83，1.65，1.53，1.23）．A値は漸次低下した（前値111±8.7から104±9.5，90±11.9，74±19.2，56±31.9）．β値は当初は変動せず，実験後半で低下した（前値0.71±0.22から，0.89±0.27，0.65±0.25，0.62±0.33，0.29±0.18）．ATP負荷時のβ値は漸次低下し（前値2.07±1.34から，1.56±0.92，1.18±0.78，0.87±0.47，0.34±0.31），β予備能は漸次低下した．正常領域ではA値，β値とも変動はなかった．結語：斑状の心筋虚血モデルでは，冠動脈狭窄がなくとも，冠血流予備能が低下する．

Purpose: Myocardial blood volume should be decreased depending on the extent of myocardial necrosis. However, it is not known whether the flow speed remains constant in cases with myocardial infarction and without any coronary stenosis, independent from the severity of myocardial necrosis. To examine this relationship, diffuse myocardial infarction was modeled by stepwise injection of microspheres (MS) , and myocardial blood volume and blood flow velocity were evaluated by myocardial contrast echocardiography (MCE) . Methods: The subjects were eight open-chest dogs. MSs (average diameter 100亮m) were injected into the left circumflex artery to model four stages of diffuse myocardial infarction during monitoring of coronary flow volume. Real-time MCE was examined at rest and after ATP administration. The A and β values of the replenishment curve were measured at each stage. Results: Although coronary flow volume did not decrease until the 4^th stage at rest (20.8, 21.8, 19.0, 13.4, 9.2 ml/min at control and 1^st to 4^th stages, respectively) , it deteriorated stepwisely after ATP administration (47.6, 39.0, 31.0, 20.4, 11.6 ml/min) , resulting in deterioration of coronary flow reserve (2.28, 1.83, 1.65, 1.53, 1.23) . At rest, the A value decreased concomitantly with the dose of the MS injection, indicating the decrement of myocardial blood volume (111±8.7, 104±9.5, 90±11.9, 74±19.2, 56±31.9) . However, the β value did not change until a high dose of MSs (0.71±0.22, 0.89±0.27, 0.65±0.25, 0.62±0.33, 0.29±0.18) . On the other hand, after ATP administration, the β value decreased significantly with progression of MS load (2.07±1.34 at baseline, 1.56±0.92, 1.18±0.78, 0.87±0.47, 0.34±0.31) , indicating progressive deterioration of β reserve. Conclusions: Coronary flow reserve deteriorates concomitantly with progression of myocardial ischemia, even in the absence of coronary artery stenosis.