间断缺血心停搏在冠脉搭桥术中的应用

１９９２～１９９３年间为１８０例冠脉病变的病人施行冠脉搭桥术，全部病人均采用核甙抑制剂利多氟嗪预处理和低温（２８℃）间断缺血心停搏进行术中心肌保护。平均每例病人作冠状动脉端吻合３～４个，每个吻合口用９分钟，主动脉阻断累加时间约２５分钟，体外循环时间９０分钟，术后医院死亡率１．６％（３／１８０），无术后心梗发生。作者认为，冠脉搭桥术的术中心肌保护可采用核甙抑制剂和间断缺血心停搏方法，而不用心肌停搏液。     

急性心肌梗死时房颤发生的时期及预后

目的 探讨急性心肌梗死(AMI)病人不同时期发生房颤(AF)的临床特点、治疗及预后。方法 采用非创伤性12导联心电图及心电监测法，监测460例AMI病人AF的发生率、原因、药物治疗反应及预后。其中40例病人发生AF，按发生时期分为两组：(1)早发组24例为发病24小时内出现AF；(2)晚发组16例为发病24小时后出现AF。结果 460例AMI病人中，发生AF40例(8．7％)。AF病人的住院病死率、心力衰竭、恶性心律失常发生率比无AF病人高(P＜0.05)。其中，晚期AF组病人住院病死率比早期AF组病人增加(P＜0．05)。结论 AMI病人并发AF，尤其并发晚发AF，提示病情重，预后不良。     

小儿癫痫持续状态心肌损伤的初步研究

目的　探讨小儿癫痫持续状态是否存在心肌损伤。方法　测定 2 4例全身性惊厥性癫痫持续状态患儿 (试验组 )血清心肌酶谱 (包括AST、CK MB、CK、LDH1、LDH)、心肌肌钙蛋白T(cTnT)、心电图 (ECG) ,并与 2 7例非惊厥持续状态的惊厥儿 (对照组 )进行比较。结果　试验组各心肌酶值 (u/L)为AST 2 77.9± 766.8,CK 1615 .8± 70 2 .3 ,CK MB 70 .3±70 .2 ,LDH1180 .0± 162 .0 ,LDH 619.8± 3 91.9;对照组为AST 83 .6± 163 .7,CK 13 4.6± 12 6.8,CK MB 2 5 .4± 13 .4,LDH171.9± 3 8.8,LDH 3 3 9.2± 2 14 .3 ,两组均值进行比较 ,CK ,CK MB ,LDH ,LDH1差异有统计学意义 ,AST差异无统计学意义 ;cTnT试验组测 13例 ,阳性 6例 ,对照组测 8例均阴性 ,两组比较差异有统计学意义 ;ECG试验组查 2 3例异常 15例 ,对照组查 2 4例异常 4例 ,两组比较差异有统计学意义。结论　小儿全身性惊厥性癫痫持续状态可引起心肌损伤     

兔心肌梗塞模型制备方法的改进及其在MRI中的应用

目的　对兔心肌缺血的模型制备方法进行改进 ,并探讨其在 MRI诊断研究中的价值。方法　分别采用高位结扎左冠状动脉前降支 (L AD)和同时低位结扎 L AD及左冠状动脉旋支 (L Cx)建立兔心肌梗塞模型 ,并在术后行 MRI检查 ,对取材后心肌标本行氯化三苯四氮唑 (TTC)及病理检查。结果　 1L AD组 2 0 % (5 / 2 5 )发生心室颤动导致死亡 ,L AD +L Cx组无一例发生室颤死亡。 2 L AD组 EKG改变明显者占 5 6 % (14 / 2 5 ) ,其中 2 1.4 3% (3/14 )在即刻就有 EKG明显改变 ,并在 30分钟后恢复正常 ;EKG改变不明显者占 4 4 % (11/ 2 5 ) ;L AD +L Cx组 10 0 %有 EKG明显改变 ,且 30分钟后亦无明显恢复。 3L AD组心肌梗塞范围较小 ,并均限于左室前壁 ,室间隔前部损害 ;而 L AD+L Cx组心肌梗塞范围较大 ,且累及左室前壁及侧壁 ,无一例有室间隔前部损害。4 L AD组中有 30 % (6 / 2 0 )不能显示小灶缺血局部心肌运动降低 ,16 .6 7% (3/ 18)无法分辨早期小梗塞灶的 MRI信号变化 ;而 L AD+L Cx组均能显示缺血局部心肌运动降低及梗塞灶早期的 MRI信号变化。结论　低位结扎兔心 L AD+L Cx,手术死亡率低 ,EKG改变明显 ,梗塞面积较大 ,是 MRI研究中一种较理想的心肌缺血动物模型制备方法。     

Combined evaluation of first pass radionuclide angiography and equilibrium radionuclide ventriculography in the diagnosis of coronary artery disease

Results of 203 patients who underwent first pass radionuclide angiography (FP) and quantitative equilibrium radionuclide ventriculography (qERNV) were stored in a data base system and evaluated statistically. Eighty eight of these patients also underwent exercise equilibrium radionuclide ventriculography (E-qERNV). In patients with coronary artery disease (CAD) without previous myocardial infarction (MI), evaluation of global and regional ejection fraction (gEF, rEF) at rest revealed a poor sensitivity of 64%, the specificity was about 71% (qERNV). FP at rest revealed similar values of sensitivity (69%) and specificity (83%). Additional assessment of stress induced changes of gEF, significantly (P<0.05) improved sensitivity of qERNV in CAD patients without a history of previous MI to 84% (specificity 86%). In patients with one previous MI, however, similar values of sensitivity were found (RFP: 87%, R-qERNV: 84%, E-qERNV: 93%). In patients with several MI's, sensitivity was above 90% at rest and during exercise (R-FP: 96%, R-qERNV: 93%, E-qERNV: 100%).     

心脏跳动下修补小儿室间隔缺损的临床研究

目的　探讨在浅低温体外循环心脏跳动下完成小儿室间隔缺损修补术的可行性。方法　 18例小儿室间隔缺损随机分为观察组和对照组 ,观察组在浅低温体外循环心跳下修补室间隔缺损 ,对照组为常规心脏停跳下修补室间缺损。测定心肌同功酶释放和三磷酸腺苷 ,观察左室压力 ,评价术野显露及气栓预防效果等。结果　观察组心肌同功酶释放明显低于对照组 ,三磷酸腺苷含量明显高于对照组 ,心肌超微结构基本正常 ,术中左室压力低于主动脉压力 ,术后无气栓发生。结论　浅低温体外循环心脏跳动下行小儿室间隔缺损修补术能更好地保护心肌。术野显露技术和防气栓的方法简便可行。     

Toxic effects of Fusarium mycotoxin butenolide on rat myocardium and primary culture of cardiac myocytes.

Mycotoxin toxicosis has been implicated in the etiopathogenesis of Keshan disease (KD), an endemic cardiomyopathy prevailing in some regions of China. Butenolide (4-acetamido-4-hydroxy-2-butenoic acid gamma-lactone, CAS No. 16275-44-8), a mycotoxin produced by several Fusarium species such as Fusarium tricinctum and Fusarium graminearum, is frequently detected from the cereals in the endemic areas of KD. The present study is undertaken to investigate whether this mycotoxin can induce myocardial damage. Exposure of primary culture of cardiac myocytes to butenolide resulted in significant cytotoxicity, manifested by changes in cell morphology and decreases in cell viability. Consistent with the in vitro findings, distinct myocardial toxicity in vivo was observed after administration of rats by gavage with butenolide (10 and 20 mg/kg/day) for 2 months, and the myocardial injuries were characterized by focal necrosis of myocardium and fragmentation of myofiber. Butenolide also induced significant oxidative damage to the myocardium in vitro evidenced by a concentration-dependent lipid peroxidation in the myocardial homogenates, whereas antioxidants superoxide dismutase (SOD), N-acetylcysteine (NAC) and glutathione (GSH) provided significant protections against this oxidative effect. Taken together, these results clearly reveal that butenolide possesses the potential to induce myocardial toxicity. The present findings may reinforce the hypothesis that toxicosis by mycotoxins is one of the etiological factors for KD.     

Scintigraphic evaluation of myocardial uptake of thallium 201 and technetium 99m pyrophosphate utilizing a rat model of chronic doxorubicin cardiotoxicity

To evaluate the usefulness of myocardial scintigraphy as a monitoring tool for chronic doxorubicin (DXR) cardiotoxicity, a rat model was used to investigate the relationship between the myocardial uptake of thallium 201 (Tl) or rechnetium 99m pyrophosphate (^99mTc-PPi) and histological changes of the heart. Although there was no significant difference in myocardial Tl uptake between control and DXR-treated rats at an early phase after Tl injection, late-phase Tl uptake was significantly higher in the DXR-treated rats than in the control rats, indicating a slow wash-out of Tl from the myocardium. The wash-out rate calculated from scintigraphic examination of DXR-treated rats was significantly decreased with increasing degree of cardiomyopathy. Since the Tl wash-out rate was sharply decreased even in animals with minimal histological changes, it may be a possible monitoring tool for the early detection of chronic DXR cardiotoxicity. On the other hand, myocardial^99mTc-PPi images could be obtained only in rats with severe myocardial changes and hence would not useful for early detection.     

The effects of altering time delays of coupled pacing during acute atrial fibrillation

BACKGROUND: Coupled pacing (CP), which consists of delivering a premature electrical stimulation to the heart after the effective refractory period of ventricular activation, is a novel method for controlling ventricular rate during atrial fibrillation (AF). It also has been established that CP improves pump function by enhancing external cardiac work and myocardial efficiency. OBJECTIVE: The purpose of the present study was to determine if two time delays for CP (short and long) would result in similar improvements in ventricular function. METHODS: In a canine model, we applied CP at two time delays (CP-S and CP-L) during two stages: sinus rhythm (SR) and acute AF. The cardiac responses to CP during SR served as the nontachycardic and nondepressed control. During both rhythms, we shortened the coupling interval until we obtained maximal contractility, designated CP-S. Next, we increased the delay until we started to see a measurable secondary contraction (left ventricular pressure development of approximately 20 mmHg). These longer delays were designated CP-L. RESULTS: Our results showed that the ventricular rate of intrinsic activation (VRIA) remained decreased despite prolongation of the time delay of CP during both AF and SR. Also, both delays of CP increased left ventricular systolic pressure (LVSP) and dLVP/dt, which are indices of myocardial contractility. In contrast, CP increased external cardiac work only during AF. Prolonging this time delay did not markedly decrease the improvement in external cardiac work. Myocardial O(2) consumption (MVO(2)) did not significantly change as the result of CP during either SR or AF. Finally, myocardial efficiency improved during AF as the result of CP at both time delays. CONCLUSIONS: In conclusion, shorter time delays for CP increased contractile strength during both SR and AF. However, extending the time delay of CP had minimal effects on diminishing the improved ventricular pump function and energetics that resulted from CP during AF. Thus, the maximal enhancement of myocardial contractility via CP-S was not needed to maintain the improved ventricular function during acute AF when CP is applied.