顺行性/逆行同时灌注对缺血心肌灌注效果和能量代谢的影响

目的 应用磁共振成像(MRI)技术研究顺行性/逆行同时灌注(SARC)对缺血心肌的灌注效果和对能量代谢的影响.方法 将18头家猪切取猪心后,经猪心左前降支(LAD)、主动脉、心前静脉升支和冠状静脉窦建立灌注通路,其中6只猪心用于评估心肌灌注效果,12只用于评估心肌能量代谢.应用MRI观察顺行性/逆行注入磁共振造影剂[钆喷替酸葡甲胺(Gd-DTPA)]后其在心肌的分布,磷31磁共振图谱(31P MRS)比较顺行性灌注(AC)和SARC期间缺血心肌的灌注效果和能量代谢. 结果 AC经主动脉注入Gd-DTPA,缺血心肌的MRI信号无变化,但是SARC无论经主动脉还是经冠状静脉窦注入Gd-DTPA,在缺血区域均可以见到Gd-DTPA的分布.31P MRS图谱显示AC期间结扎LAD导致左室前壁心肌磷酸肌酸和三磷酸腺苷含量显著下降,而无机磷含量明显升高.但这些缺血反应可以被SARC灌注方法完全纠正.结论 SARC同时灌注缺血心肌,其血流供应足以维持缺血心肌的正常能量代谢.     

非停跳冠脉搭桥术中病人心脏形态和功能的变化

目的观察非停跳冠脉搭桥术（OPCAB）中病人心脏形态和功能的变化。方法择期行OPCAB病人30例，ASAll或Ⅲ级。麻醉诱导后气管插管，经右侧颈内静脉放置CCO／SVO，／CEDV导管，连续监测血液动力学参数，经口放人多平面经食管彩色超声诊断仪探头，监测食管超声心动图（TEE）参数。分别于打开心包时（基础值）、前降支（LAD）搭桥、回旋支（LCX）搭桥、右冠状动脉（RCA）搭桥、吻合完毕时测定TEE参数及血液动力学参数。结果与基础值比较，LAD搭桥时二尖瓣血流E波减速时间（DL）缩短，经过二尖瓣口的左心流量（Q；）降低，MAP、HR下降，CVP升高；LCX搭桥时左心室舒张末直径（LVEDD）、右心室舒张末直径（RVEDD）、三尖瓣环直径（TVD）、射血分数（EF）、Q，、经过中尖瓣口的右心流量（Q2）、左心室流出道舒张变化率[（DDL—SDL）／DDL]、三尖瓣血流E／A比值（E2／A2）、TVD降低，二尖瓣血流E／A比值（E1／A1）升高，DL、三尖瓣血流E波减速时间（DT2）缩短，HR、MAP、每搏量（sV）、混合静脉血氧饱和度（蹄01）、右心室舒张末容积（RVEDV）、右心室收缩末容积（RVESV）、右心室射血分数（RVEF）、右心室舒经末容积指数（RVEDVI）降低，CVP升高；RCA搭桥时LVEDD、LVESD、二尖瓣环直径、Q，、E2／A2、HR、MAP、平均肺动脉压、SV、SvO2、RVEVD、RVESV、RVEF、RVEDVI降低，CVP升高，DT1缩短，右心室流出道舒张直径（RVOTDD）、右心室流出道收缩直径（RVOTSD）增加（P＜0．05）；吻合完毕时各指标恢复到基础值水平（P＞0．05）。心脏形态学表明LAD、RCA搭桥时以左心室直接受压为主，LCX搭桥时以右心室受压为主。结论在OPCAB中LAD、LCX、RCA搭桥时左右心室同时受压，但左右心室受压的程度随着搭桥血管、心脏位置不同而不同；心功能呈一过性的损害，在完成血管搭桥后均能恢复。     

冠心病患者围术期内皮素变化的临床研究

目的研究冠心病患者围术期内皮素（ET）及血流动力学的改变,总结冠心病围术期的一些变化规律,为临床治疗提供参考。方法将37例冠心病患者及10例心瓣膜疾病患者依据不同的手术方式分为5组,冠状动脉旁路移植术＋室壁瘤切除术（CABG＋LVAN组）,体外循环冠状动脉旁路移植术（CABG组）,非体外循环冠状动脉旁路移植术（OPCAB组）,激光心肌打孔术（TMLR组）,对照组为风湿性心脏病行二尖瓣置换术患者。使用放射免疫分析法分别测定术前,主动脉阻断前（血管移植前或打孔前）,主动脉开放时（血管移植结束时或打孔后）,心肌再灌注后3h、6h、24h血ET值;并于术前、心肌再灌注后3h、6h、24h测定心排血指数（CI）。结果ET值组内比较：CABG＋LVAN组主动脉开放时（69．93±7．20pg／ml）,心肌再灌注后3h（89．99±5．76pg／ml）、6h（60．94±8．69pg／ml）、24h（68．99±10．30pg／ml）时ET值显著高于术前（40．17±13．37pg／ml,P〈0．05）;CABG组主动脉开放时（66．59±4．86pg／ml）,心肌再灌注后3h（95．97±10．72pg／ml）、6h（61．51±7．65pg／ml）、24h（57．85±6．34pg／ml）均显著高于术前（43．22±9．13pg／ml,P〈0．05）;OPCAB组血管移植结束时（66．47±5．90pg／ml）显著高于术前（44．80±6．51pg／ml,P〈0．05）;TMLR组打孔术后无显著升高;对照组主动脉开放时（69．92±10．80pg／ml）,心肌再灌注后3h（77．99±7．49pg／ml）、6h（46．76±7．61pg／ml）、24h（52．07±6．94pg／ml）显著高于术前（35．14±8．10pg／ml,P〈0．05）。组间比较：CABG组心肌再灌注后3h显著高于OPCAB组（95．97±10．72pg／ml vs．59．72±4．81pg／ml,P〈0．05）。心肌再灌注后各组CI均较术前明显增加,CABG组心肌再灌注后3h CI明显低于OPCAB组（2．17±0．46L／min·m^2 vs．3．25±0．05L／min·m^2,P〈0．05）。?     

肾缺血预处理对未成熟心肌的保护作用

目的探讨肾缺血预处理对未成熟心肌保护的影响，为未成熟心肌的保护提供新的方法。方法建立兔Langendorff灌注模型，将18只幼兔随机分为3组，缺血／再灌注组（I／R组）：灌注15min转为工作心15min，停灌45min，恢复灌注15min改为工作心30min；心脏缺血预处理组（CIP组）：灌注15min转为工作心15min，反复2次缺血5min再灌注5min，重复I／R组的方法；肾缺血预处理组（RIP组）：反复3次阻断左肾动脉血流5min再灌注5min，取离体心脏，灌注15min转为工作心15min，重复I／R组的方法。观察血流动力学、生化等指标。结果CIP组和RIP组的冠状动脉流量（CF）、心排血量（CO）、左心室收缩压（LVSP）恢复百分率均较I／R组升高，左心室舒张期末压（LVEDP）恢复率则较I／R组降低，差异有统计学意义（P〈0.01）；三组间比较，HR、AF恢复率差异无统计学意义（P〉0.05）；RIP组与CIP组比较各指标恢复率差异无统计学意义（P〉0．05）。RIP组与I／R组比较：心肌含水量（MWC）、血清肌酸激酶（cK）和乳酸脱氢酶（LDH）漏出率、ATP含量、丙二醛（MDA）含量、超氧化物歧化酶（SOD）活性、心肌细胞内Ca^2＋含量、心肌线粒体Ca^2＋-ATPase活性、心肌线粒体Ca^2＋含量、心肌线粒体合成ATP能力差异有统计学意义（P〈0.01），RIP组和CIP组比较各项指标差异无统计学意义（P〉0.05）。结论肾缺血预处理对未成熟心肌具有心肌保护作用。     

PI3K/AKT信号通路在异丙酚减轻离体大鼠心脏缺血再灌注损伤中的作用

目的 探讨PI3K／AKT信号传导通路在异丙酚减轻离体大鼠心脏缺血再灌注损伤中的作用。方法 成年SD大鼠32只，随机分为4组：缺血再灌注组（I／R组）、异丙酚组（P组）、渥曼青霉素组（W组）和异丙酚＋渥曼青霉素组（PW组），每组8只。建立Langendorff离体心脏灌注模型，灌注压10kPa,灌注速率7．10ml／min，I／R组用K-H液灌注，P组用含50μmol／L异丙酚的K-H液灌注，W组用含100nmol／L渥曼青霉素的K-H液灌注；PW组用含50μmol／L异丙酚＋100nmol／L渥曼青霉素的K-H液灌注，灌注15min，全心缺血30min，再灌注60min。测定再灌注10、40min时冠脉流出液中心肌肌钙蛋白（cTnI）浓度，再灌注60min时测定心肌组织丙二醛（MDA）含量、超氧化物歧化酶（SOD）活性，电镜下观察心肌细胞超微结构。结果 与I／R组比较，P组再灌注期间cTnI浓度明显降低，心肌组织SOD活性升高，MDA含量降低（P〈0．05），其余2组上述指标差异无统计学意义（P〉0．05）；与缺血前比较，P组再灌注40min时cTnI浓度升高，其余各组再灌注期间cTnI浓度均升高（P〈0．05或0．01）。P组电镜下心肌超微结构改变减轻。结论 异丙酚减轻离体大鼠心脏缺血再灌注损伤可能通过PI3K／AKT信号传导通路介导。     

异丙酚对心肌缺血再灌注损伤大鼠离体心脏脂质代谢的影响

目的观察异丙酚对心肌缺血再灌注损伤大鼠离体心脏脂质代谢的影响。方法雄性Wistar大鼠68只，体重350～450g，随机分为2组（n=34）：正常对照组（C组）和心肌缺血再灌注组（I／R组）。I／R组阻断左冠状动脉前降支，缺血30min，再灌注2h制备心肌缺血再灌注模型，取心脏在Langendorff灌注模型上用Krebs-Hemseleit（KBH）缓冲液灌注，将用放射性物质标记的（TAG）0．4mol/L加入循环回路中。分别用含不同浓度异丙酚[0（生理盐水）、0．1、1．0、5．0、10．0、500μmol／L]的灌注液进行灌注，监测平均动脉压、心率、主动脉流量（AFR）、冠状动脉血流（CFR），计算Hvdraulic work反映心肌作功情况。测定灌注液中TAG浓度，计算脂肪酸（FFA）氧化率，并测定心肌脂蛋白酶（LPL）活性。结果心肌缺血再灌可导致Hydraulic work降低，FFA氧化率和心肌LPL活性升高；与C组异丙酚浓度为0时比较，C组异丙酚浓度为10．0、50．0μmol／L时Hydraulic work降低，异丙酚浓度为5．0～50．0μmol／L时灌注液中TAG浓度升高，I／R组异丙酚浓度为10．0、50．0μmol／L时Hydraulic work降低，异丙酚浓度为5．0—50．0μmol／L时灌注液中TAG浓度升高，异丙酚浓度为10．0～50．0μmol／L时FFA氧化率和心肌LPL活性降低（P〈0．05）；与I／R组异丙酚浓度为0时比较，I／R组异丙酚浓度为0．1～10．0μmol／L时Hydraulic work升高，异丙酚浓度为5．0～50．0μmol／L时灌注液中TAG浓度升高，FFA氧化率及心肌LPL活性降低（P〈0．05）。结论异丙酚可减轻心肌缺血再灌注损伤大鼠心脏功能的降低，其机制与改善心肌脂质代谢有关。     

吗啡后处理抗心肌缺血再灌注损伤心肌细胞凋亡中的作用及机制

目的探讨吗啡后处理抑制心肌缺血／再灌注损伤大鼠心肌细胞凋亡的作用以及对信号通路P13K／AKT的影响。方法采用麻醉开胸大鼠在体心脏缺血模型。SD大鼠56只随机分成4组,每组14只：S组（假手术,只穿线,不结扎）,I／R组（单纯缺血再灌注）,M组（吗啡后处理＋缺血再灌注,再灌注前3min和再灌注后2min内静脉注入吗啡1．25mg／kg）,W＋M组（wortmannin＋吗啡后处理＋缺血再灌注,左冠状动脉前降支结扎前20min静脉注入15ug／kgwortmannin,特异性的P13K阻断剂）。除S组外,所有大鼠心脏都经历45min缺血和120min再灌注。再灌注120min时,各组随机取9只大鼠,TUNEL染色检测心肌细胞凋亡。其余5只大鼠采用Western Blot法测定心肌组织总AKT和磷酸化AKT的表达水平。结果再灌注120min,可在I／R组缺血区心肌检测到大量凋亡心肌细胞183=1．14％,吗啡后处理显著降低心肌细胞凋亡指数（10．83=1．24％,P〈0．01）;吗啡后处理使磷酸化AKT的蛋白表达明显增加。特异性的P13K阻断剂,wortmannin完全消除了吗啡后处理抑制缺血／再灌注损伤大鼠心肌细胞凋亡的作用,及抑制磷酸化AKT蛋白表达的增加。结论大鼠在体心脏缺血模型,吗啡后处理可通过P13K／AKT信号通路,抑制心肌缺血／再灌注损伤心肌细胞凋亡。     

高胸段硬膜外阻滞对猪急性心肌缺血/再灌注损伤的保护作用

目的：探讨高胸段硬膜外阻滞（HTEA）对心肌缺血／再灌注损伤的保护作用。方法：20只家猪随机分为两组，结扎左冠状动脉前降支（LAD）造成造血40min后再灌注6h，实验组（n=10)结扎前硬膜外腔注入0．5％布比卡因2ml;对照组（n=10)结扎前硬膜外腔注入生理盐水2ml。测定心率（HR）、平均动脉压（MAP）、中心静脉压（CVP）、血浆超氧化物歧化酶（SOD）活性、血清丙二醛（MDA）浓度、心肌乳酸（LA）释放量。结果：（1）实验组硬膜外阻滞的HR减慢22％，MAP、CVP分别降低25％和28％，而对照组血液动力学无明显变化。（2）实验组SOD活性变化不显著，再灌注5h、6h活性升高（P＜0．01）；MDA浓度在4h降至最低点（P＜0．05）；对照组SOD活性明显降低（P＜0．05），MDA含量明显增加（P＜0．05）。（3）两组心肌LA释放量在开放前达到高峰，之后随着供血、供氧的恢复逐渐下降，但实验组明显低于对照组（P＜0．01）。（4）开始再灌注时由于发生室颤实验组死亡1只，对照组死亡只（P＜0．05）。结论：HTEA可以减轻心肌缺血／再灌注损伤，其机制与保护SOD活性，降低心肌氧耗及脂质过氧化程度有关。     

KATP通道在参附注射液减轻大鼠心肌缺血再灌注损伤中的作用

目的研究KATP通道在参附注射液（SFI）减轻大鼠心肌缺血再灌注损伤中的作用。方法24只SD大鼠,雌雄不拘,体重240～320 g,随机分为4组（n=6）：对照组（C组）、缺血再灌注组（I/ R组）、SFI组和SFI＋KATP通道阻滞剂格列苯脲组（SG组）。C组仅穿线不结扎左冠状动脉前降支,穿线后静脉输注生理盐水8 ml/kg。采用结扎左冠状动脉前降支40 min再灌注120 min制备心肌缺血再灌注损伤模型。SFI组缺血前15 min静脉输注SFI 8 ml/kg,SG组给予格列苯脲0．33 mg/kg和SFI 8 ml/ kg。再灌注120 min后从心尖穿刺抽血,测定血清cTnI与IL-6浓度,抽血后立即取心肌组织,测定心肌组织SOD活性、MDA含量、TNF-α表达,并在电镜下观察心肌超微结构。结果与C组比较,I/R组心肌SOD活性降低,心肌MDA、TNF-α和血清IL-6、cTnI水平升高（P＜0．05）;与I/R组比较,SFI组、SG组心肌SOD活性升高,心肌MDA、TNF-α和血清cTnI、IL-6水平降低（p＜0．05）;SG组与SFI组比较上述指标差异无统计学意义（P＞0．05）。SFI组与SG组心肌超微结构损伤程度明显轻于I/R组。结论参附注射液可以减轻大鼠心肌缺血再灌注损伤,其作用机制与KATP通道的激活无关。     

异丙酚预先给药对心肌缺血再灌注损伤大鼠炎性反应的影响

目的探讨异丙酚预先给药对心肌缺血再灌注损伤大鼠炎性反应的影响。方法健康雄性SD大鼠48只，随机分为4组（n=12）：假手术组（S组）、缺血再灌注组（I／R组）、低剂量异丙酚组（L组）、高剂量异丙酚组（H组）。结扎左冠状动脉前降支（LAD）30min、再灌注120min，建立大鼠心肌缺血再灌注损伤模型。分别于再灌注30min（T1）、120min（T2）时采集股动脉血1ml，ELISA法测定血浆肿瘤坏死因子-α（TNF-α）、白细胞介素-10（IL-10）的浓度，再灌注120min时TTC法测心肌梗死面积，电镜下观察心肌细胞超微结构。结果与S组比较，I／R组、L组、H组在T1、T2时TNF-α、IL-10浓度升高（P〈0．05）；与I／R组比较，L组、H组在T1、T2时TNF-α浓度降低（P〈0.05），IL-10浓度升高（P〈0．05），心肌梗死面积减小（P〈0．05）；L组比较，H组T1、T2时，TNF-α浓度降低，IL-10浓度升高，心肌梗死面积减小（P〈0.05）。电镜下观察I／R组心肌细胞超微结构改变严重，L组、H组心肌细胞超微结构改变程度较I／R组轻。结论异丙酚预先给药通过抑制再灌注诱发的炎性反应减轻了大鼠心肌缺血再灌注损伤。     

Effect on myocardial perfusion of simultaneous delivery of cardioplegic solution through a single coronary artery and the coronary sinus.

OBJECTIVE: This study was to determine whether simultaneous antegrade-retrograde cardioplegia through a single coronary artery and the coronary sinus provides sufficient and homogeneous perfusion to the heart. METHODS: Simultaneous antegrade-retrograde cardioplegia was conducted in 7 isolated pig hearts through the coronary sinus in conjunction with the left anterior descending artery, the left circumflex artery, and the right coronary artery, respectively. The efficacy of simultaneous antegrade-retrograde cardioplegia for myocardial perfusion was assessed by monitoring the distribution of magnetic resonance contrast agent and measuring the effluent from the venting coronary arteries. RESULTS: Injection of contrast agent into a perfusing artery during simultaneous antegrade-retrograde cardioplegia resulted in increased image signal intensity not only in the territory of the perfusing artery but also in the areas normally served by the other 2 venting arteries (including the right ventricular wall). The myocardium in the territories of the 2 venting arteries was lightened with contrast agent given into the coronary sinus during simultaneous antegrade-retrograde cardioplegia. Myocardium in the perfusing artery territory and right ventricular wall remained dark. Moreover, a significant amount of effluent was collected from the venting arteries during simultaneous antegrade-retrograde cardioplegia: 4.7 to 7.8 mL/min from the right coronary artery; 10.5 to 17.7 mL/min from the left anterior descending artery; and 9.7 to 15.2 mL/min from the left circumflex coronary artery. CONCLUSIONS: Simultaneous antegrade-retrograde cardioplegia through a single coronary artery and the coronary sinus provides homogeneous perfusion to the entire heart. During simultaneous antegrade-retrograde cardioplegia, arterial flow supports its own designated myocardium, as well as adjacent myocardium normally served by the venting arteries; the arterial route also supports the right ventricular free wall when the right coronary artery is vented. Venous perfusion of simultaneous antegrade-retrograde cardioplegia mainly supports myocardium in the territories of the venting arteries and does not perfuse the right ventricular free wall. Blood flow delivered to myocardium normally supported by the venting arteries is believed to be sufficient to prevent ischemic injury.     

Complete occlusion both left main coronary artery and right coronary artery

A 67-year-old man, who had complete occlusion both of left main coronary artery (LMCA) and right coronary artery (RCA), underwent coronary revascularization. He had been suffering from severe angina pectoris preoperatively. Exercise electrocardiogram (single Master) showed myocardial ischemia. On cardiac catheterization, he showed extensive collaterals from right main coronary artery, and well-preserved left ventricular function. At operation, coronary arteries revealed severe sclerosis, especially in RCA, but there was no evidence of old myocardial infarction. Three saphenous vein grafts were bypassed to LAD, LCX, and RCA. Postoperatively, he remained free of angina pectoris at 6 months after uneventful surgery.     

川崎病冠状动脉病变及搭桥手术

目的 探讨川崎病后严重冠状动脉病变及搭桥手术（ＣＡＢＧ）后的近期及远期效果。方法随访发现,６例川崎病后严重冠状动脉病变的病儿均有左冠状动脉前降支（ＬＡＤ）病变,右冠状动脉（ＲＣＡ）病变５例,左冠状动脉回旋支（ＬＣＸ）病变３例,左冠状动脉主干（ＬＭＴ）病变２例,心肌梗死３例。共行１５支ＣＡＢＧ;单支２例,３支３例,４支１例;左胸廓内动脉（ＬＩＴＡ）至ＬＡＤ６例;右胸廓内动脉（ＲＩＴＡ）至ＬＡＤ１例。     

Phasic coronary blood flow pattern during a continuous flow left ventricular assist support.

OBJECTIVE: Continuous flow left ventricular assist devices (LVADs) have been introduced and tested as a bridge to heart transplantation, bridge to recovery, and destination therapy, and several studies have been conducted to assess the physiologic effects of continuous flow LVADs. However, the effect of reduced pulsatility on the phasic coronary blood flow pattern is unknown. The aim of this study was to investigate the phasic coronary blood flow patterns during continuous flow LVAD support. METHODS: Phasic coronary blood flow patterns and hemodynamic data were analyzed using three flow probes placed around the left anterior descending coronary artery (LAD), left circumflex coronary artery (LCX), and the right coronary artery (RCA) in 16 pigs before and after initiating the LVAD support with or without creating LAD stenosis. RESULTS: The total coronary blood flow (TCBF, 112.8+/-31.4 mL/min) gradually decreased when the continuous flow LVAD support increased to 2.0 L/min (110.7+/-29.0 mL/min, P = 0.571), 2.5 L/min (103.7+/-26.1 mL/min, P = 0.079), and 3.0 L/min (101.5+/-27.2 mL/min, P = 0.027) because of decreases in LAD flow and LCX flow. LVAD support caused decrease in systolic and peak systolic LAD flow, LCX flow, and RCA flow, whereas diastolic RCA flow increased. In the presence of LAD stenosis, the TCBF (97.7+/-36.1 mL/min) decreased when the continuous flow LVAD support increased to 2.0 L/min (83.9+/-22.1 mL/min, P = 0.029), 2.5 L/min (83.2+/-25.2 mL/min, P = 0.012), and 3.0 L/min (87.6+/-23.4 mL/min, P = 0.005) because of decreases in LCX flow. CONCLUSION: Use of a continuous flow LVAD decreased TCBF, LAD flow, and LCX flow secondary to reduced systolic LAD flow and LCX flow, and decreased TCBF and LCX flow in the presence of LAD stenosis. These findings are potentially relevant to understanding the physiology of myocardial blood perfusion during continuous flow LVAD support especially in patients with coronary artery disease.     

A comparison of the results of A-C bypass grafting in collateral and non-collateral groups

Ninety patients who had aorto-coronary bypass grafting were divided into two groups: a collateral group, which had coronary arterial stenosis or occlusion with collateral circulation, and a non-collateral group, which had coronary arterial stenosis or occlusion without collateral circulation. The number of coronary arteries visualized through collateral circulation in coronary angiograms (CAG) was 32, left anterior descending arteries (LAD) 17, right coronary arteries (RCA) 11, and left circumflex arteries (LCX) 4. The results of A-C bypass grafting in the collateral and non-collateral groups were compared. Surgical mortality was 0% in the collateral group, and 5.4% in the non-collateral group. The differences in graft patency and graft flow between the two groups were not statistically significant. However, left ventricular ejection fraction and myocardial perfusion, which was estimated by thallium-201 myocardial perfusion scintigram, were significantly improved after A-C bypass in the collateral group. Although the coronary arteries visualized through collateral vessels seemed too narrow to undergo graft anastomosis, they were, in fact, large enough. A-C bypass grafting was achieved with more satisfactory results in the collateral group than in the non-collateral group.     

Coronary artery bypass grafting in two patients with single coronary artery

We experienced two patients with single coronary artery who underwent CABG using arterial grafts successfully. In two patients coronary angiography demonstrated a single coronary artery which was originated in left coronary sinus and was bifurcated to LAD and LCx, and then RCA branched off proximal LAD, passing in front of the right ventricular out flow tract (Sharbaugh Type L-IIa). To the first patient, a 52-year-old man who had angina on exertion due to long stenosis of RCA, CABG to RCA using RITA was carried out. To the second patient, a 57-year-old man who had inferior myocardial infarction due to 90% stenosis of proximal LAD, CABG to RCA using RITA and LAD using LITA was carried out. Single coronary artery without additional congenital cardiac anomalies may lead to myocardial ischemia, necessitating CABG as coronary reconstructions.     

Assessment of the size and distribution of the coronary artery selected for bypass grafting using myocardial contrast echocardiography during coronary artery bypass surgery]

We assessed the size and distribution of the native coronary artery selected for bypass grafting, using myocardial contrast echocardiography by injection of sonicated agents into a saphenous vein graft, during surgical revascularization. A total of 69 saphenous vein grafts (LAD, 16; D1, 10; OM, 13; PL, 13; RCA, 17) were performed in 36 patients with right dominant system at preoperative coronary angiogram. The size of the area of revascularized myocardium was quantified with the ratio of its circumference to a full circle depicted on the left ventricular short-axis view at the mid-papillary level. The extents of the revascularized area to LAD stenosing at the proximal portion was 28 +/- 6% and stenosing at the intermediate portion was 23 +/- 6%. D1, 10 +/- 2%; OM, 17 +/- 3%; PL, 22 +/- 6%, RCA, 17 +/- 5%. The extent of the areas perfused by the totally occluded coronary arteries with collateral vessels was similar to those perfused by the partially occluded coronary arteries. In conclusion, myocardial contrast echocardiography enabled the intraoperative assessment of the geometry of regional myocardial perfusion, and was very useful for the intraoperative evaluation of the effectiveness of the indicated surgical procedure.     

Intraoperative blood-flow responses in coronary artery bypass grafts.

Intraoperative graft flow responses in 15 patients who underwent coronary artery bypass grafting (CABG) were studied systematically. The mean blood flow for 13 left anterior descending (LAD) coronary artery grafts was 64 +/- 20 ml/min and for 12 right coronary artery (RCA) grafts was 53 +/- 13 ml/min. Of these, systolic flow was dominant in one LAD and three RCA grafts, suggesting the perfusion of the right ventricle or the noncontractile left ventricle segment, or both. Five LAD and two RCA grafts had a negligible reactive hyperemic response, and the underlying cause for this can be futher examined by observing their phasic flow patterns. Temporary occlusion of the coronary artery proximal to the site of anastomosis produced increased flow in 8 grafts, indicating the presence of competitive flow; decreased flow was observed in 15 grafts, indicating the presence of proximal retrograde flow which may play a role in the proximal occlusion of the bypassed artery later. Thus intraoperative flow studies supplement the preoperative angiographic findings in elucidating the pathophysiology involved and are useful in evaluating CABG operations.     

Myocardial perfusion and right ventricular function.

Objective: Maximal right ventricular (RV) performance is influenced by left heart hemodynamics and hence coronary perfusion. We examined the role of myocardial perfusion of the right ventricle as potential determinant of maximal RV function. Materials and methods: In 6 canine isovolumic right heart preparations, incremental volumes were introduced into a high compliance RV balloon until RV failure occurred. Maximal RV developed pressure (RVDP) and maximal positive RV dP/dt were determined at a constant controlled left ventricular (LV) output of 2 l/min and at controlled mean arterial pressures of 50, 80 and 120 mmHg. Right coronary artery (RCA) flow was measured. Results: Maximal RVDP increased significantly with increasing mean arterial pressures (44.8+/-11.2 vs 57.2+/-15.5 vs 75.4+/-2.5 mmHg for systemic pressures of 50, 80 and 120 mmHg respectively, p < 0. 05). With increasing mean arterial pressures RCA flow increased significantly (33.1+/-11.0 vs 46.1+/-20.4 vs 79.6+/-35.3 ml/min). At the onset of RV failure, RCA blood flow significantly decreased in all preparations compared to the maximal flow in the RCA (1.9+/-1.0 vs 33.1+/-11.0 ml/min at 50 mmHg; 13.6+/-10.2 vs 46.1+/-20.4 ml at 80 mmHg and 18.7+/-8.0 vs 79.6+/-35.3 ml/min at 120 mmHg; p < 0.05). Conclusions: These results suggest that coronary perfusion is a major determinant of maximal RV function. The coronary artery driving pressure must be sufficient to avoid the onset of RV failure. Maintaining systemic pressure and hence RV myocardial blood flow may thus extend RV function.     

Patient with pseudo-retrograde coronary flow in the normal right coronary artery and left circumflex artery: pitfall of retrograde coronary flow to detect coronary artery occlusion

A 75-year-old lady with hypertension and paroxysmal atrial fibrillation underwent echocardiography to evaluate cardiac function. Transthoracic Doppler echocardiography revealed retrograde coronary flow in the right coronary artery (RCA) and left circumflex artery (LCX). Computed tomographic coronary angiography demonstrated normal but tortuous coronary arteries. This tortuosity of the coronary arteries was thought be a cause of pseudo-retrograde coronary flow in the RCA and LCX. The present case demonstrates a pitfall of retrograde coronary flow for the detection of coronary artery occlusion in daily practice.