心肌缺血对QT间期离散度的影响

目的：探讨冠心病患者心肌缺血对ＱＴ间期离散度（ＱＴｄ）及校正后ＱＴ间期离散度（ＱＴｃｄ）的影响。方法：选取３０例冠心病患者，测定每例患者心肌缺血期、缺血缓解期及稳定期的ＱＴｄ及ＱＴｃｄ。结果：ＱＴｄ与ＱＴｃｄ在心肌缺血期为０．０９１３±０．０３２４秒、０．０１０６±０．０３７８秒；在缺血缓解期为０．０５２３±０．０３２８秒、０．０６１１±０．０３７３秒；在稳定期为０．０４９７±０．０２３０秒、０．０５６６±０．０２７１秒。心肌缺血期与缺血缓解期及稳定期相比，有显著性差异（Ｐ均＜０．０１）。而稳定期与缺血缓解期相比无显著性差异（Ｐ＞０．０５）。结论：心肌缺血可引起ＱＴｄ及ＱＴｃｄ的增大；心肌缺血期ＱＴｄ及ＱＴｃｄ增大，且显著高于缺血缓解期及稳定期。     

左旋卡尼汀对犬心房急性缺血诱发电生理变化的影响

目的观察左旋卡尼汀（L—CN）对犬心房急性缺血时心房肌电生理改变及心房颤动（房颤）诱发率的影响。方法2003—2005年将解放军总医院的12只健康杂种犬随机分为L—CN用药组和生理盐水对照组。结扎右冠状动脉心房分支，造成心房肌局部缺血。观察各组缺血前后右心房不同部位的有效不应期（AERP）、右心房内传导速度（CV）的变化，计算右心房内心房激动波波长（WL）和房颤的诱发率并行心房肌病理学检查。结果（1）结扎右冠脉后盐水组缺血区心肌AERP均明显缩短；L—CN组右冠脉结扎后AERP无显著缩短。（2）冠脉结扎前后，两组右心房内CV均无明显改变。（3）结扎冠脉后，盐水组右心房内WL明显缩短；L—CN组的WL无显著变化。（4）盐水组结扎右冠脉后在不同时间段测量时均诱发房颤，L—CN组结扎冠脉后均未诱发房颤。（5）盐水组可见不同程度的心肌缺血，以冠脉结扎处近端为显著；L—CN组不同部位心肌均未见缺血变化。结论L—CN能够有效防止心肌缺血诱发的电生理变化，从而有效减少房颤的发作。     

卡托普利对家兔急性缺血心肌室颤阈值和不应期离散度的影响

目的：观察卡托昔利对急性缺血心肌电生理特性和心室颤动(室颤)发生率的影响。方法：对在体兔心脏行冠状动脉左室支中点完全结扎，测定心肌室颤阈值(VFT)和不应期离散度(DRP)。结果：卡托普利提高缺血心肌VFT，降低DRP，并加速两者的恢复过程，缺血组室颤发生率为62．5%(n=8)，缺血干预组室颤发生率为11.1％(n=9)．差异有显著性。结论：提示卡托普利能稳定缺血心肌电生理，减少冠状动脉结扎后室颤发生，上述作用与其抑制血浆去甲肾上腺素(NE)、血管紧张素I(A1)水平和减少心肌缺血面积有关。     

自主神经系统对在体犬跨室壁三层心肌不应期不均一性影响的研究

为探讨自主神经系统对在体犬跨室壁三层心肌细胞不应期离散度的影响 ,分别在基础和缺血状态下 ,在交感神经和迷走神经刺激的过程中 ,用程序刺激法测定健康家犬在体心外膜心肌、中层心肌和心内膜心肌的不应期。结果 :在基础状态下 ,交感神经刺激能缩短三层心肌细胞的不应期 ,中层心肌细胞的不应期缩短最明显 ,跨室壁三层心肌不应期的离散度由 3± 2ms增加到 18± 6ms(P <0 .0 1) ;迷走神经刺激能延长三层心肌的不应期 ,心内膜心肌增加明显 ,跨室壁不应期离散度由 3± 2ms增加到 9± 4ms(P <0 .0 5 )。在急性缺血状态下 ,交感神经刺激延长三层心肌细胞的不应期 ,其中中层心肌细胞的不应期增加最明显 ,与刺激前相比 ,跨室壁不应期离散度由 4± 3ms增加到 16± 4ms(P <0 .0 1) ;迷走神经刺激对三层心肌细胞的不应期影响较小 ,与刺激前相比 ,跨室壁不应期离散度无显著变化。结论 :在基础及缺血状态下 ,交感神经刺激均能增加跨室壁不应期离散度 ;迷走神经刺激对跨室壁不应期离散度无显著影响。     

动态心电图对冠心病心肌缺血的定量诊断与疗效考核的评价（附128例分析）

本文应用动态心电图对１２８例已经确诊的冠心病心肌缺血患者进行时间定量监测，以指导选择不同的治疗方案，随后再监测考核其疗效。结果观察到显效：心肌缺血消失７９例；有效：心肌缺血时间显著缩短小于５分钟３６例；改善心缺血时间减少至１２０分钟以内１３例．考核结果表明，其疗效与缺血的程度和选择的治疗方案密切相关。从而，更加表明动态心电图在考核冠心病心肌缺血的诊治方面有着可靠的价值。     

慢径消融对快径正传有效不应期及房室传导时间的影响

目的研究房室结双径路折返性室上性心动过速慢径消融对快径正传有效不应期及房室传导时间的影响。方法83例房室结内折返性心动过速（AVNRT）者根据消融前HRAS，S2扫描刺激时房室跳跃值的不同分为：A组：〈50ms；B组：50—80ms；C组：〉81ms。行慢径消融，消融后均无慢径残留，测量消融前后快径有效不应期、房室传导时间的变化。结果消融后快径有效不应期及房宣传导时间均较消融前缩短，差异有统计学意义（P〈0．05）。消融前HRA程序刺激时房室跳跃值越大，消融后快径有效不应期缩短越明显，差异有统计学意义（P〈0．05）；房宣传导时间亦有类似结果。结论慢径消融后快径有效不应期及房宣传导时间均缩短，提示慢径消融可改善快径前向传导功能。     

室性心律失常,猝死及隐性心肌缺血

急性心肌缺血及室性心律失常的相关性已在实验动物得以证实。kaplinsky等发现狗冠状动脉闭塞30分钟内,早期室性心律失常的两个时期。Janse等描述了急性实验性心肌缺血时,心室节律异常的两种机制。他们发现,在缺血边缘的正常面存在一个病灶机制,可能由于正常浦肯野纤维内损伤电流所致,然而,在缺血心肌发现由大、小折返径而致的室性心律失常。猫冠状动脉闭塞后出现心肌及心外膜区域传导时间延长,非同步去极化及不应期缩短伴有室性心律失常。Kabell等证实:在实验动物,侧枝血流进入梗塞区减少而致的缺血可使梗塞区电图分级和延迟,以     

哌仑西平对兔急性心肌缺血心率变异与心电生理的影响

目的：观察小剂量哌仑西平对兔急性心肌缺血时心率变异与心电生理的影响,为临床应用提供实验理论依据。方法：建立兔急性心肌缺血模型,采用心率变异的时域指标及频域指标测定心肌缺血时心脏自主神经功能,应用心电生理研究方法测定心肌缺血时心电生理参数：心室有效不应期（VERP）,心室有效不应期离散度（VERPD）,QT离散度（QTD）,心室颤动阈值（VFT）的变化,比较哌仑西平预处理组与对照组各项指标。结果：兔急性心肌缺血时,哌仑西平预处理组较对照组心率变异时域指标增加,频域指标VLF,LF与LF／HF降低,HF增高;心电生理指标VERPD降低,QTD降低,VFT增高。相关性分析显示心率变异指标与VFT相关。结论：小剂量哌仑西平预处理能改善兔急性心肌缺血时的心电生理不稳定状态,增加心室颤动阈值,此作用与提高心脏迷走神经活性有关。     

降钙素基因相关肽对缺血心肌保护作用的实验研究

心肌缺血损伤会引起心律失常和缺血心肌局部代谢的异常,使用扩血管药物可以纠正或改善之。降钙素基因相关肽(CGRP)是含有37个氨基酸残基的神经多肽,是目前已知体内最强大的舒血管物质。在心肌缺血情况下,CGRP 亦能扩张冠状动脉,增加冠脉血流量。本文观察了心肌缺血后心电图ST-T 的变化及正常、缺血区心肌局部LDH、GOT、SOD 改变的影响,并观察CGRP 对缺血性心律失常的防治作用。     

心肌缺血早期室性心律失常发生机制的探讨

同步描记缺血和非缺血边缘区单相动作电位及体表心电图，探讨心肌缺血早期室性心律失常发生的可能机制。结果显示，不仅心室肌激动传导时间差异性延迟和复极化离散与心肌缺血性心律失常的发生有关，而且早期后去极化和触发活动也可能是缺血性心律失常启动的重要因素，并与折返机制互相影响。     

Effects of a thromboxane A2 synthetase inhibitor on ventricular fibrillation threshold during coronary artery occlusion and reperfusion

The effects of a new thromboxane A2 synthetase inhibitor (DP-1904) on electrical stability of the heart were tested in anesthetized, open chest dogs. The incidence of spontaneous ventricular arrhythmias, ventricular refractory period and ventricular fibrillation threshold (VFT) during ligation of the left anterior descending coronary artery (LAD) for 180 min and after reperfusion were measured as indices of stability. Ventricular fibrillation and ventricular tachycardia occurred spontaneously after ligation of LAD in 56% of 9 control dogs and 29% of 7 dogs which received intravenous DP-1904 (100 mg) before ligation of LAD (n.s.). In the control group, the ventricular refractory period decreased in the ischemic region; consequently, the difference in refractory period duration between the ischemic and non-ischemic regions (i.e., dispersion) increased 30 min after coronary ligation (7 +/- 9 ms vs 32 +/- 17 ms, p less than 0.05). The dispersion at 30 min after coronary ligation, though, was not affected in the DP-1904 treated group (2 +/- 4 ms vs 10 +/- 9 ms, n.s.). The VFT (determined with pulse trains) decreased from 28 +/- 5 mA to 15 +/- 11 mA (p less than 0.05) 30 min after coronary ligation in the control group, but was not affected (30 +/- 0 mA vs 27 +/- 4 mA) in the DP-1904 group. The plasma concentration of thromboxane B2 decreased after DP-1904 administration (baseline vs 30 min after coronary ligation: 475 +/- 165 pg/ml vs 165 +/- 74 pg/ml, n = 3, p less than 0.05), while the concentration of 6-keto-prostaglandin F1 alpha increased gradually. In conclusion, DP-1904 prevents a decline in electrical stability in the ischemic region of the canine heart during coronary occlusion.     

KATP通道阻断剂对兔缺血心室肌跨壁离散度的影响

目的探讨免冠脉结扎前后缺血区心室肌单相动作电位时程（MAPD100）和跨壁离散度（TDR）的动态变化,观察阻断KATP通道后缺血区心室肌的单相动作电位（MAP）参数变化。方法30只家兔随机分为单纯缺血组（n=15）和GLB（glibenclamide）组（n=15）。单纯缺血组开胸,制作缺血模型,利用整合的3层心肌同步记录MAP电极,并结合程控刺激技术,测量结扎前、结扎后5 min、30 min、1 h、1 d、2 d的缺血区3层心肌MAPD100并计算TDR。GLB作为KATP通道阻断剂预处理实验组,制作缺血模型,相同时间点记录3层心肌MAPD100并计算TDR。结果与结扎前比较,单纯缺血组冠脉结扎后5 min1 h 3层心肌MAPD100均缩短有统计学意义,以MAPDmid100缩短最为显著,TDR与结扎前比较增大有统计学意义。在1 d、2 d的时间点上与结扎前比较TDR变化无统计意义。GLB组结扎后5 min1 h Mid、Epi层MAPD与单纯缺血组比较增大有统计学意义,TDR减小有统计学意义。结论使用KATP通道阻断剂GLB可减小冠脉结扎后初期心室肌TDR增大程度。     

Computer simulation of ventricular tachyarrhythmias during coronary artery ligation and release.

A computer (PDP-10) simulation model was constructed using rapid, simultaneous measurements of effective refractory period (ERP), ERP dispersion (RPD), premature ventricular beat (PVB) thresholds, and multi-directional conduction times during coronary artery ligations and release in the anesthetized dog. In addition, estimates of currents of injury between ischemic and non-ischemic electrodes were included based on published data from electromagnetic recordings in dogs. Propagated PVB's were inscribed by the model when criteria for excitation, dispersion, and conduction were met based on known electrophysiological characteristics of heart muscle. The model correctly predicts high vulnerability to arrhythmias at three to seven minutes of ligation, stabilization at 10 to 15 minutes of ligation, and decreased vulnerability by lidocaine during ischemia. There was no arrhythmia when ischemic thresholds were increased by the drug before significant RPD and conduction prolongation developed. Vulnerability to arrhythmias was also predicted by the model after release of short (five minute) and long (15 minute) ligation. Since (experimentally) arrhythmias occurred much more frequently after long ligations, additional yet unknown factors other than those considered in the model must be operative in the genesis of reperfusion arrhythmias. This conclusion is supported by the observations that high ischemic thresholds induced by lidocaine returned to normal slowly after ligation release, and despite this protective effect, experimentally, lidocaine failed to abolish reperfusion arrhythmias.     

Electrophysiologic effects of partial coronary occlusion and reperfusion

Electrophysiologic changes caused by partial coronary occlusion have not previously been examined. In nine dogs, refractory periods and conduction times were determined using the extrastimulus method after a 50 percent reduction in coronary blood flow. In another five dogs, ventricular automaticity was studied after the production of complete heart block. After 5 minutes of partial coronary occlusion the refractory period in the ischemic zone shortened from 164.6 ± 4.2 (mean ± standard error of the mean) to 149.6 ± 5.8 msec (P < 0.001); after 60 minutes it shortened further to 142.5 ± 5.6 msec, resulting in a dispersion of refractoriness. Intramyocardial conduction time from the ischemic to the non-ischemic zone was prolonged from 48.6 ± 1.6 to 60.0 ± 3.3 msec (P < 0.01), whereas conduction time from the nonischemic to the ischemic zone remained unchanged. No significant changes were observed in ventricular automaticity after partial coronary occlusion (idioventricular rate 56.0 ± 6.4 versus 51.2 ± 6.6 beats/min). Reperfusion 1 hour after partial occlusion resulted in a return of the refractory period and conduction time to preocclusion values, but there were no changes in idioventricular rate. Thus, after a 50 percent reduction in coronary blood flow, the decrease in local refractory period and prolongation of conduction time result in underlying electrical instability predisposing to reentrant arrhythmias whereas automaticity is unchanged. These abnormalities are fully abolished when reperfusion is instituted after 60 minutes of partial coronary occlusion.     

Alterations in electrophysiological properties during canine myocardial ischemia--variation with location in the ischemic zone in vivo

We examined electrophysiological properties of the ischemic myocardium of the canine heart. Multiple bipolar electrodes for stimulation or for recording electrograms were placed on the epicardial surface and at the endocardium of the ventricle. The time course of changes in excitability threshold, in effective refractory period and in local conduction time during ischemia was estimated at the epicardial and endocardial sides of the central ischemic zone, at the epicardial side of the peripheral ischemic zone and at both sides of the normal zone. Soon after left anterior descending coronary artery occlusion, a rise of excitability threshold, a lengthening of effective refractory period and a prolongation of conduction time consistently occurred in all portions of the ischemic zone. The degree of changes, however, was not uniform: it was greater at the epicardial side of the central ischemic zone. In most experiments, the changes reached maximum within 10 min after occlusion. Then, altered electrophysiological properties recovered to some extent or stabilized. The results indicate that electrophysiological properties deteriorate momentarily after coronary occlusion but then recover or stabilize, and that their changes during acute ischemia are not uniform in the ischemic region but severer at the central zone and epicardial side.     

Effect of acute subendocardial ischemia on ventricular refractory periods

OBJECTIVES: To investigate the impact of acute subendocardial ischemia on the dispersion of ventricular refractory periods. METHODS: Acute subendocardial ischemia was induced in sheep by partial ligation of the left circumflex coronary artery and rapid pacing of the left atrium. The ventricular effective refractory period (ERP) was measured in five areas of the left ventricle by a programmed premature stimulation technique. RESULTS: The average ERP and ERP dispersion remained unchanged in the control group (n=5, P>0.05). In the study group (n=5), the ERP was shortened following subendocardial ischemia. ERP dispersion decreased significantly from 48+/-9 ms to 36+/-13 ms 30 min after the ischemia (P=0.02). There was neither spontaneous nor stimulation-induced ventricular arrhythmia after ischemia. CONCLUSION: Acute subendocardial ischemia leads to a homogenous reduction of ventricular ERP. This may partially explain why subendocardial ischemia is associated with a low incidence of ventricular arrhythmia.     

左旋卡尼汀对犬心房急性缺血诱发电生理变化的影响

目的观察左旋卡尼汀(L-CN)对犬心房急性缺血时心房肌电生理改变及心房颤动(房颤)诱发率的影响。方法2003～2005年将解放军总医院的12只健康杂种犬随机分为L-CN用药组和生理盐水对照组。结扎右冠状动脉心房分支,造成心房肌局部缺血。观察各组缺血前后右心房不同部位的有效不应期(AERP)、右心房内传导速度(CV)的变化,计算右心房内心房激动波波长(WL)和房颤的诱发率并行心房肌病理学检查。结果(1)结扎右冠脉后盐水组缺血区心肌AERP均明显缩短;L-CN组右冠脉结扎后AERP无显著缩短。(2)冠脉结扎前后,两组右心房内CV均无明显改变。(3)结扎冠脉后,盐水组右心房内WL明显缩短;L-CN组的WL无显著变化。(4)盐水组结扎右冠脉后在不同时间段测量时均诱发房颤,L-CN组结扎冠脉后均未诱发房颤。(5)盐水组可见不同程度的心肌缺血,以冠脉结扎处近端为显著;L-CN组不同部位心肌均未见缺血变化。结论L-CN能够有效防止心肌缺血诱发的电生理变化,从而有效减少房颤的发作。     

Electrophysiological and antiarrhythmic effects of propranolol in canine acute myocardial ischemia.

To correlate the antiarrhythmic and electrophysiological effects of propranolol in acute myocardial ischemia, we examined the effects of temporary (15-minute) ligations of the left anterior descending coronary artery in studies on 15 dogs. We recorded bipolar electrograms and monophasic action potentials from the ischemic and normal zones and measured the intervals from the onset of QRS in a standard electrocardiogram lead to the major deflection of electrograms recorded from the ischemic and normal zones. We also determined monophasic action potential duration (APD) and effective refractory period (ERP). Data for control ligations were compared to those during which propranolol, 40 mug/kg, was administered intravenously immediately after ligation. Propranolol reduced the mean number of ventricular beats per minute (from 15 to 6) (P less than 0.01). Propranolol slowed conduction in the ischemic zone (by 10 msec at peak effect, P less than 0.01) and had no or only a very slight effect (by 1-msec at 15 minutes, P less than 0.05) on conduction in the normal zone. Propranolol also prolonged APD in the ischemic (32-msec) and normal (14-msec) zones (P less than 0.01), prolonged ERP in the ischemic (41-msec) and normal (20-msec) zones (P less than 0.01), and reduced the APD/ERP ratio in the ischemic (1.62 to 1.47) (P less than 0.01) and normal (1.62 to 1.55) (P less than 0.05) zones. During the control ligation, APD in the ischemic zone was 25 msec shorter than in the normal zone (P less than 0.01), but with propranolol the difference was not significant. The effects of propranolol in slowing conduction in the ischemic zone, in prolonging refractoriness, in reducing APD/ERP, and in reducing the disparity in APD between ischemic and normal zones may explain its demonstrated antiarrhythmic effects in acute myocardial ischemia.     

Regional myocardial ischemia: characterization of temporal, transmural and lateral flow interfaces in the porcine heart

The three-dimensional distribution of coronary flow and tissue adenosine triphosphate was characterized in the anaesthetized open pig chest after 10, 15, 30, 45, 60 and 120 min of coronary artery ligation. Radioactive microspheres were given at the onset (153-gadolinium) and end (113-tin) of ischemia. A simultaneous multiple biopsy device was used to obtain 50 contiguous transmural biopsies from each heart over an area (40 mm X 28 mm) of tissue which incorporated the centre of the ischemic zone, a lateral interface of injury and normally perfused tissue. Frozen biopsies were lyophilized, subfractionated into 2 mm transmural sections, and taken for radioactive counting. There was little or no detectable collateral flow in the ischemic zone. There was a sharp lateral flow interface which fell from 2.2 +/- 0.04 mL/min/g in normally perfused tissue to less than 2% of this value over a transition zone of less than 2 mm width. Myocardial adenosine triphosphate content showed a similar sharp interface and was severely depressed throughout the ischemic zone at all the ischemic times studied. During the 2 h ischemic period there was no increase in flow to any part of the ischemic zone and there was no change in the position, or sharpness, of the lateral interface. The absence of either lateral or transmural borderzones of intermediate injury in the pig makes pharmacological infarct size limitation highly improbable in this species.     

Effects of procainamide on the dispersion of recovery of excitability during coronary occlusion.

In 14 mongrel dogs, refractory periods were determined in nonischemic and acutely ischemic zones of myocardium during control conditions, 15 minutes after coronary ligation, and 10 and 20 minutes after a procainamide infusion. Following coronary ligation, refractory periods in the nonischemic area remained unchanged (100.8% of control) while in the ischemia area they decreased to 88.6% of control (P less than 0.02) causing a dispersion of refractoriness of 12.2%. After the administration of procainamide, refractory periods lengthened in the nonischemic as well as in the ischemic areas but the changes were such that the temporal dispersion caused by the coronary ligation was reduced from 12.2% to 5.5% (P less than 0.01) after 10 minutes, and to 5.0% (P less than 0.02) after 20 minutes of drug infusion. It is concluded that procainamide exerts different overall effects on the nonischemic and acutely ischemic canine myocardium. It is postulated that this action may play a role in the suppression of re-entrant arrhythmias.