双相电震致心律失常性的降低及其与高效除颤的关系

双相电震比单相电震除颤更有效，但其机制未明。除颤的易损性上限（ＵＬＶ）假说认为一个无效电震是由于它再次诱发了心室颤动（ＶＦ），因此研究ＶＦ诱发的机制可能有助于理解除颤的机制。单、双相电震以电震强度（ＳＳ）与偶联间期（ＣＩ）及波形随机结合的方式施加于Ｌａｎｇｅｎｄｏｒｆ灌流的兔离体心脏上，比较心脏对单、双相电震的ＶＦ易损性。结果心脏对双相电震的反应有如下几点不同于其对单相电震的反应：①易损区（ＡＯＶ）小（８．９±４．２个区域单位ｖｓ１３．９±６．０个区域单位，Ｐ＜０．０５）。②易损区与非心律失常反应区之间的过渡区窄（１４．７±４．８个区域单位ｖｓ２９．９±６．４个区域单位，Ｐ＜０．００１）。③双相电震将整个ＡＯＶ向更长的ＣＩ移动（左边界右移了１１．０±８．８ｍｓ，右边界右移了６．０±５．２ｍｓ，Ｐ均＜０．０１）。这种双相电震致心律失常性的降低可有助进一步解释双相电震除颤阈值降低的现象。     

Inoue气囊经皮瓣膜成形术治疗成人肺动脉瓣狭窄

１９８５年１２月至１９９４年８月，５３例成人先天性肺动脉瓣狭窄（ＰＳ）患者用Ｉｎｏｕｅ气囊进行经皮肺动脉瓣成形术（ＰＢＰＶ），成功率为１００％，无严重并发症。术后ＰＶＤ口压力阶差从９０．９±４５．９ｍｍＨｇ减至３８．１±３２．３ｍｍＨｇ（Ｐ＜０．００１）。ＰＶ口直径从８．９±３．６ｍｍ增至１７．４±４．６ｍｍ（Ｐ＜０．００１）。在６．４±２．８（０．８至９．５）年的随访期，心功能保持在Ⅰ级至Ⅱ级，其中９例重行心导管术检查，术前术后及随访的ＰＶ压力阶差分别为１０６．９±４７．７ｍｍＨｇ、５０．１±２９．２ｍｍＨｇ及２９．６±１６．０ｍｍＨｇ（术前比术后及随访Ｐ＜０．０５）；ＰＶ口径分别为８．２６±１．４、１７．２±２．０５及１８．７±１．３ｍｍ（Ｐ＜０．００１）（术前比术后及随访Ｐ＜０．０５）．认为Ｉｎｏｕｅ气羹ＰＢＰＶ对ＰＳ是有效和安全的方法，远期疗效满意。     

心肌梗塞病人心室晚电位与电程序刺激的相关性及其预后意义

对４８例心肌梗塞（ＭＩ）病人的心室晚电位（ＶＬＰ）检测与自发和心室电程序刺激（ＥＰＳ）诱发单形性持续性室性心动过速（ＳＭＶＴ）的相关性的研究表明：（１）临床无自发持续室速者ＶＬＰ和ＥＰＳ阳性率分别为１９％和２６％；（２）ＥＰＳ诱发ＳＭＶＴ者ＶＬＰ检出率（６２．５％）高于未诱发者（９。４％）；（３）ＶＬＰ阳性者ＥＰＳ－ＳＭＶＴ诱发率（７６．９％）高于ＶＬＰ阳性者（１７．１％）（Ｐ〈０．０５）。结果显     

一次口服单硝酸异山梨酯对心力衰竭患者的急性血液动力学效应

对９他心力衰竭患者（冠心病４例，高血压性心脏病１例，扩张型心肌病４例）一次口服单硝酸异山梨酯２０ｍｇ后，采用有创检查观察急性血液动力学效应，发现用药后半小时显效，１小时效应达高峰时，平均肺动脉压，肺毛细血管嵌压分别从服药前的４．６５±１．１７ｋＰａ（３４．９±８．８ｍｍＨｇ），２．８１±０．９２ｋＰａ（２１．１±６．９ｍｍＨｇ）降至３．００±１．０３ｋＰａ（２２．５±７．７ｍｍＨｇ）及１．７６±０．５４ｋＰａ（１３．２±４．１ｍｍｇ，Ｐ＜０．００１），中心静脉压从１．１９±０．６２ｋＰａ（８．９±４．７ｍｍＨｇ）降至０．６９±０．４６ｋＰａ（５．２±３．５ｍｍＨｇ，Ｐ＜０．０１），肺血管阻力由２９，２２±１４．８９ｋＰａ·ｓ／Ｌ降至１６．９６±８．６６ｋＰａ·ｓ／Ｌ（Ｐ＜０．０１）。药物最大效应持续至少６小时。在服药后０．５～２小时，平均动脉压明显下降（Ｐ＜０．０５）。心率无变化。一次口服未见副作用。提示单硝酸异山梨酯是治疗心力衰竭有前途的新药。     

64例老年人高血压性脑出血外科治疗临床分析

目的分析老年人高血压性脑出血临床特点，探讨其外科治疗的预后。方法采用局麻下小骨窗开颅血肿清除术、锥颅血肿碎吸术、钻孔抽血注入尿激醇溶解３种术式治疗老年人高血压性脑出血６４例，并与同期手术的４３例非老年患者进行比较。结果经６个月至６年随访，老年组恢复良好者３７例（５７．８％），死亡１４例（２１．９％）；非老年组分别为２８例（６５．１％）及９例（２０．９％），两组差异无显著性（Ｘ２检验，Ｐ值＞０．０５）。老年组术后并发症发生率为３５．９％，远高于非老年组的１３．９％（Ｘ２检验，Ｐ值＜０．００１）。结论年龄不再是决定手术与否的主要条件，加强并发症的防治有助于提高老年患者手术成功率。     

刺激犬心植物神经对心电功率谱的影响

在心电频域分析中，心电功率谱基波的大小约占心电总能量的１／３左右，而且基波所在的频率与心率一致，因而基波的大小是心电信号频域分析中一个重要指标。基波主要与心电图中Ｔ波和ＳＴ段相对应，与Ｐ波和ＱＲＳ关系不大。电刺激犬心迷走神经时，心率由刺激前的１８９±２７次／ｍｉｎ下降到１５５±３２次／ｍｉｎ（Ｐ＜０．０１）；Ⅱ导联基波大小由８５．２±４４．２下降到５２．７±４４．９（ｐ＜０．０１）。电刺激犬心交感神经时，心率由刺激前的１８７±２９次／ｍｉｎ上升到１９８±２７次／ｍｉｎ（Ｐ＜０．０１）；基波由６１．１±４５．８增加到９１．８±５７．５（ｐ＜０．０１）。电刺激犬右侧迷走神经引起基波下降的主要原因是由迷走神经负性变时作用引起的；电刺激犬左侧心交感神经引起基波增加的原因是心电综合向量增大所致。     

MS-551对麻醉犬心肌的电生理作用及血液动力学影响

为研究１，３二甲基－６［２－（Ｎ－２羟乙基－３－４硝苯丙氨基）乙氨基］－２，４（１Ｈ，３Ｈ）－盐酸嘧啶二酮即ＭＳ－５５１（简称ＭＳ）对麻醉犬心肌的电生理作用和血液动力学影响，采用自身前后对照的方法测定用药（５ｍｉｎ内每公斤体重静脉注射ＭＳ０．５ｍｇ，继以每公斤体重静脉滴注０．５ｍｇ持续３０ｍｉｎ）前后麻醉犬（ｎ＝８）有关电生理参数及心输出量、肺毛细血管楔嵌压等变化。结果表明ＭＳ：①使心房有效不应期和心室有效不应期显著延长，分别为２７．１±６．８，２０．７±５．２ｍｓ，Ｐ均＜０．０１。②使自发性窦性周期、窦房结恢复时间和校正的窦房结恢复时间均显著延长，分别为４１．４±８．０，５０．０±９．８，８．６±３．４ｍｓ，前两者Ｐ＜０．０１，后者Ｐ＜０．０５。但对窦房传导时间无明显影响（３．６±１．８ｍｓ，Ｐ＞０．０５）。③对ＡＨ、ＨＶ、ＰＱ间期及ＱＲＳ波群时限无明显影响，显著延长ＱＴ间期，明显降低文氏点（调搏周长延长）。④轻度减低心输出量，但无统计学意义（变化值：－０．５６±０．２３Ｌ／ｍｉｎ，Ｐ＝０．０６１），对肺毛细血管楔嵌压无显著性影响。结论：ＭＳ延长心肌不应期，对心内传导影响不明显，有良好的血液动力学特性，可?     

经食管心房阈下串刺激终止室上性心动过速

经食管心房阈下串刺激终止室上性心动过速江泽龙岑黎明⒇经食管心房调搏终止室上性心动过速（室上速）的各种形式电刺激，均为阈上刺激，即刺激电压大于阈电压（２５．０±５．８Ｖ），由于刺激电压较高，不适感较重，可能引发心房颤动，作者应用经食管心房非程序刺激Ｓ１...     

卡托普利治疗对急性心肌梗塞二级预防的作用

８２２例首次急性心肌梗塞症状后７２小时内入院且无心源性休克患者中，４７８例自入院后开始并于随访期持续接受常规及卡托普利治疗（甲组），３４４例单纯接受常规治疗（乙组）。住院期间中，甲组病死率（６．９％）明显低于乙组（１８％）（Ｐ＝０．００１），且心肌梗塞前壁或（和）下壁具相似作用（前壁：６．８％和１８．３％，Ｐ＜０．００１；下壁：６．４％和１３．５％，Ｐ＜０．０５；前壁＋下壁：１０．７％和３９．２％，Ｐ＜０．０３）。随访期（平均２０个月）中，尽管两组再梗塞和严重心律失常发生率相似，但甲组的病死率（２．３％和１６．２％，Ｐ＝０．０３２４）和总心脏性事件发生率（１０．３％和３７．４％，Ｐ＝０．０５５）显著低于乙组。因此，急性心肌梗塞后早期并持续应用血管紧张素转换酶抑制剂－卡托普利治疗对患者的预后具有益作用。     

普罗帕酮、维拉帕米对豚鼠乳头肌延迟后除极和触发电活动的影响

应用标准玻璃微电极技术，研究哇巴因诱发豚鼠心室乳头肌的延迟后除极（ＤＡＤ）和触发电活动（ＴＡ）的变化规律及特点；探讨普罗帕酮和维拉帕米对ＤＡＤ和ＴＡ的影响。结果表明：①心室肌细胞在高浓度Ｃａ２＋条件下加哇巴因灌流时可以出现ＤＡＤ及ＴＡ，ＴＡ的诱发率为７７．８％（７／９）。②心室肌细胞诱发的ＤＡＤ幅度（ＤＡＤ－Ａｍｐ）、ＤＡＤ偶联间期（ＤＡＤ－Ｃ）和ＤＡＤ升支上升速率（ＤＡＤ－ｄｖ／ｄｔ）呈明显的频率依赖性，即刺激频率愈快，ＤＡＤ－Ａｍｐ愈高、ＤＡＤ－ｄｖ／ｄｔ愈快，ＤＡＤ－Ｃ则愈短。③上述两种抗心律失常药物均通过降低ＤＡＤ－Ａｍｐ、减慢ＤＡＤ－ｄｖ／ｄｔ和延长ＤＡＤ－Ｃ而发挥其抗触发性心律失常作用；两者对哇巴因诱发的ＤＡＤ和ＴＡ的抑制作用无显著性差异，在普罗帕酮或维拉帕米的作用下，哇巴因对ＴＡ的诱发率分别为３３．３％（３／９）和２２．２％（２／９），与哇巴因的诱发率（高钙条件下，７７．８％）比较Ｐ＜０．０１。     

Ultrarapid subthreshold stimulation for termination of atrioventricular node reentrant tachycardia.

OBJECTIVES. We investigated the efficacy and safety of ultrarapid subthreshold electrical stimuli in terminating sustained atrioventricular (AV) node reentrant tachycardia. BACKGROUND. Subthreshold stimuli, singly and in trains, have been reported to prolong the effective refractory period, inhibit the response to subsequent suprathreshold extrastimuli and to terminate ventricular tachycardia and reciprocating tachycardia. METHODS. Seventeen consecutive patients with inducible sustained slow-fast AV node reentrant tachycardia (mean tachycardia cycle length 358 +/- 61 ms) were studied. Trains of subthreshold stimuli were tested at various right atrial sites. RESULTS. Trains of subthreshold stimuli reproducibly terminated AV node reentrant tachycardia in 15 patients without administration of adjunctive pharmacologic agents. Effective subthreshold current strength ranged from 0.5 to 1.5 mA (mean 0.9 +/- 0.3). The cycle length of effective subthreshold stimuli trains ranged from 30 to 80 ms (mean 57 +/- 17), and the number of stimuli in the train ranged from 4 to 16 (mean 8 +/- 4). The site of successful termination was the proximal coronary sinus in 6 patients and the right low atrial septum in 12. During successful subthreshold termination, no atrial capture could be detected. Neither atrial fibrillation nor flutter nor tachycardia acceleration occurred. CONCLUSIONS. Low current, high frequency trains of stimuli, when applied at a site presumed to be close to the reentrant circuit, provided a safe and effective method of terminating the common type of AV node reentrant tachycardia. This technique could be used to identify critical parts of the reentrant circuit suitable for ablation and further investigations with this method are warranted.     

Inhibition of premature ventricular extrastimuli by subthreshold conditioning stimuli

The purpose of this study was to determine whether trains of subthreshold high frequency conditioning stimuli (333 Hz, 1 ms duration, 2 ms interval) delivered to the canine ventricle inhibited the response to a premature stimulus (S2) more effectively than did a single subthreshold conditioning stimulus. It was found that trains of conditioning stimuli (mean 1.21 mA) inhibited the response to S2 152 ms beyond expiration of the ventricular effective refractory period, whereas a single conditioning stimulus inhibited S2 only 20 ms or less beyond the ventricular effective refractory period. In late diastole, trains of conditioning stimuli failed to inhibit S2 when the train of stimuli caused ventricular depolarization or the latter occurred in response to the next sinus impulse. Trains of conditioning stimuli did not induce ventricular arrhythmias. Lidocaine or autonomic blockade did not alter the response to trains of conditioning stimuli. Trains of conditioning stimuli or a single conditioning stimulus inhibited the response to S2 only when they were delivered at the same electrode site. By lengthening the ventricular effective refractory period, trains of conditioning stimuli could prevent or terminate tachycardias, but this possibility is constrained, at present, by the spatial limitations of the technique.     

Quantitative study of the supernormal phase of ventricular excitability in man.

The supernormal phase of excitability of the human heart was studied by means of fixed rate endocardial pacing in 11 patients with acute and chronic bradyarrhythmias. Ten of the eleven patients manifested a supernormal phase. The duration of the phase increased with increasing intensity of subthreshold stimuli and ranged from 91 to 148 percent of the Q-T interval. Subthreshold stimuli of a wide range of intensity could elicit a full response. Two types of supernormal phase, early and late in relation to the cardiac cycle, were observed. The latter was attributed to the summation of subthreshold stimuli with either spontaneous phase 4 depolarization of a ventricular ectopic pacemaker or atrial depolarization potentials. Its possible connection with Wedensky facillitation was suggested. The ventricle was less excitable after an ectopic beat than after a normally conducted beat.     

Pacing-induced angina pectoris and induction of ventricular arrhythmias in coronary artery disease

Ischemia caused by rapid pacing during electrophysiologic study could facilitate induction of ventricular arrhythmias. The results of extrastimulation were retrospectively analyzed in 32 patients with coronary artery disease (CAD) without a history of symptomatic arrhythmia. These patients were studied at cardiac catheterization for angina pectoris refractory to medical therapy. Eleven patients (group I) had typical angina during trains of rapid right ventricular pacing (repeated trains of 8 stimuli [mean cycle length (CL) 473 +/- 47 ms]) but were asymptomatic during slower trains (CL 800 +/- 100 ms). Twenty-one patients (group II) had no symptoms with either rapid (CL 448 +/- 51 ms) or slow (CL 688 +/- 105 ms) trains, despite comparable left ventricular function, CAD severity and medication. Effective refractory periods (S1S2) after rapid drive were shorter in group I than in group II patients (225 +/- 9 vs 240 +/- 14 ms, p less than 0.002), but refractory periods during slow pacing were similar (251 +/- 12 vs 253 +/- 17 ms, difference not significant). No patient in either group had sustained arrhythmia (more than 15 beats) induced by single and double ventricular extrastimuli, decrementally applied at the right ventricular apex. The number of extra beats provoked in group I when rapid trains caused angina (4.3 +/- 3.6) was similar to that induced by extra-stimulation after slower pacing without angina (4.4 +/- 3.5) and to that obtained with rapid or slow pacing in group II (3.1 +/- 3.3 and 2.8 +/- 2.2).(ABSTRACT TRUNCATED AT 250 WORDS)     

Recent advances in the treatment of ectopic tachycardias by electrical pacing

Cardiac pacing may be useful both prophytactically and therapeutically in the management of ectopic tachycardias. Ectopic tachycardias may be prevented by atrial or ventricular pacing for a sustained period at a rate faster than the spontaneous rate but slower than the rate of the tachycardia being suppressed.

Supraventricular tachycardias, except atrial fibrillation, may be terminated by atrial or ventricular pacing for a brief period in one of three ways: (1) delivery of a single stimulus or two serial stimuli in quick succession; (2) repetitive stimulation at a rate slower than the tachycardia; or (3) repetitive stimulation (atrial only) at a rate faster than the tachycardia.

Atrial pacing may slow the ventricular rate of supraventricular tachycardia resistant to all forms of therapy by (1) actually increasing the atrial rate which produces functional atrioventricular block and reduces the number of transmitted impulses to the ventricle, or (2) inducing stable atrial fibrillation with a slower average rate more easily controllable by digitalis.

Aside from its relative simplicity, pacing offers certain advantages over standard d-c cardioversion for the termination of tachyarrhythmias, particularly when the latter is contraindicated as in digitalis toxicity.     

Subthreshold atrial pacing in patients with a left-sided accessory pathway: an effective new method for terminating reciprocating tachycardia

This study investigated the possibility of terminating reciprocating atrioventricular (AV) tachycardia using subthreshold atrial pacing. Ten patients with a left-sided accessory pathway and sustained AV tachycardia underwent subthreshold atrial pacing from the coronary sinus site closest to insertion of the accessory pathway. In seven of these patients, the tachycardia could be reliably terminated with subthreshold atrial overdrive pacing. When pacing at a cycle length of 80 +/- 23% of the tachycardia cycle length, the minimal subthreshold current that was effective in tachycardia termination was 64 +/- 14% of threshold current and the maximal ineffective current was 49 +/- 17% of threshold (p less than 0.05). In all cases, the tachycardia was terminated by one or two instances of atrial capture that resulted in a premature atrial impulse (20 +/- 4% advancement of the atrial cycle) that blocked the AV node limb of the tachycardia. Anterograde conduction over the accessory pathway never occurred, either during the tachycardia or during subthreshold pacing after a return to normal sinus rhythm. No instances of atrial fibrillation were provoked by subthreshold pacing. Possible explanations for the intermittent atrial capture with critically placed subthreshold impulses include supernormal atrial conduction or summation of impulses at the atrial insertion site of the accessory pathway. It is concluded that subthreshold pacing is effective in selected patients with AV tachycardia due to an accessory pathway. Furthermore, because neither atrial fibrillation nor anterograde conduction over the accessory pathway is seen with subthreshold pacing, this modality may hold significant promise for permanent antitachycardia pacing in these patients.     

Supraventricular Tachycardia Due to Multiple Atrial Ectopic Foci: A Relatively Common Problem

Multiple Atrial Ectopic Foci. Atrial ectopic focus is a common mechanism for chronic incessant supraventricular tachycardia in children. The majority of patients require treatment because of symptoms or tachycardia-induced cardiomyopathy. Management with traditional drugs fails to restore sinus rhythm and surgery has heen thought to be curative. We have had 54 patients with atrial ectopic focus tachycardia; 40 right atrial (36 with normal P waves simulating sinus tachycardia), and 14 left atrial. Surgical treatment of tachycardia was performed in 28 patients; all 28 had a single abnormal P wave axis before surgery, had mapping in the electrophysiology lab, and were thought to have a single focus. However, in 14/28 (50%) after surgical removal of this focus, additional foci became apparent. In 11/14, the next focus appeared during surgery; between 3–15 additional foci were identifled and surgically treated. This resulted in cure in 9/11, but 2/11 despite almost total atrial disconnection, continued to have atrial ectopic focus tachycardia. The other three patients with multiple foci had atrial ectopic focus tachycardia recur with a diflPerent P wave axis from 1 week to 2 months postoperatively. Since the overall initial success rate for multiple foci was different from single foci, patients with multiple foci and single foci were compared to try to predict multiple foci. Patients with multiple foci had: (1) the same incidence of cardiomyopathy (78%); (2) faster maximum atrial rate on Holter (89% of multiple foci had a rate faster than 160/min vs 43% of single foci, (P < 0.05); (3) faster minimum atrial rate on Holter (89% of multiple foci had a minimum rate faster than 70/min vs 0% single foci, (P < 0.05); and (4) different preoperative electrocardiogram (0% multiple foci had left atrial P waves vs 44% of single foci, (P < 0.025). In conclusion: (1) approximately half the patients with atrial ectopic tachycardia had multiple foci; (2) surgical treatment of multiple foci was less successful than single foci, although with improvement in surgical techniques, even multiple foci were successfully eliminated by surgery, and surgery was successful in 100% of the last 10 cases; (3) multiple foci were unlikely with left atrial P waves and slower atrial rates. We speculate that atrial ectopic focus tachycardia may have different etiologies: multiple foci may be due to extensive atrial disease such as that found in primary cardiomyopathy or after myocarditis, whereas single foci may be a developmental aberration. (J Cardiovasc Electrophysiol, Vol. J, pp. 132–138, April 1990)     

阈下条件电刺激对患者心脏不应期和起搏节律的影响

目的研究阈下条件电刺激对心脏不应期的影响。方法通过右心电极导管法,在24例心律失常患者中,观察阈下条件单个刺激（Ss）和串刺激（St）对心房或心室不应期和心房或心室起搏节律的影响。结果在SlS2间期中加发St,可使人心房及心室相对不应期和有效不应期延长;且随St强度的增加,不应期延长量增加。在SlS2间期中加发Ss,只有6/18例,心房相对不应期延长;另6/18例,心室相对及有效不应期延长。另外,St和Ss可抑制心房及心室起搏节律。结论阈下条件电刺激具有抑制心肌兴奋性的作用。     

Initiation and termination of ventricular tachycardia by supraventricular stimuli: Incidence and electrophysiologic determinants as observed during programmed stimulation of the heart

In 7 of 43 patients in whom a sustained ventricular tachycardia could be induced during programmed electrical stimulation by a single ventricular premature stimulus, an identical tachycardia could also be initiated by a single atrial premature stimulus. This phenomenon was observed only in those patients in whom the ventricular tachycardia could be induced by a single ventricular extrastimulus having a prematurity index (ratio between the longest ventricular premature stimulus interval resulting in tachycardia and the duration of the basic cycle length of the paced ventricular rhythm) above 54 percent. No single instance of initiation of ventricular tachycardia by atrial premature stimuli was observed in patients with a ventricular prematurity index below 54 percent or requiring more than one consecutive ventricular extrastimulus to have tachycardia initiated. Other features of patients showing initiation of ventricular tachycardia by atrial premature stimuli were a right bundle branch block configuration of the QRS complex during tachycardia in all seven patients and a relatively slow rate during tachycardia. In one patient ventricular tachycardia was terminated by a conducted atrial premature stimulus.     

Continuous rapid atrial pacing to control recurrent or sustained supraventricular tachycardias following open heart surgery.

A technique is described to control recurrent or sustained supraventricular tachycardia associated with rapid ventricular rates following open heart surgery. The technique utilizes a pair of temporarily implanted atrial epicardial wire electrodes to pace the heart. In one group of patients with recurrent atrial flutter and 2:1 A-V conduction, continuous rapid atrial pacing at 450 beats/min produced and sustained atrial fibrillation. The ventricular response rate immediately slowed when compared to that during atrial flutter, and if further slowing was required, it was easily accomplished by the administration of digitalis. Another group of patients with different arrhythmias (recurrent paroxysmal atrial tachycardia, sustained ectopic atrial tachycardia, or sinus rhythm with premature atrial beats which precipitated runs of atrial fibrillation) was treated with continuous rapid atrial pacing to produce 2:1 A-V block. In all instances, the continuous rapid atrial pacing suppressed the supraventricular tachycardia and maintained the ventricular response rate in a therapeutically desirable range. It was demonstrated that the technique is safe, effective, and reliable.