小儿阵发性室上性心动过速治疗方法选择

阵发性室上性心动过速（PSVT）简称室上速,是一组疾病的诊断,包括多种心律失常,但90%以上为房室结折返性心动过速和房室折返性心动过速[1].主要由折返机制造成,少数为自律性增高或平行心律,其发生率为1/25 000,是小儿时期严重心律失常之一,若不及时治疗易致心力衰竭.     

心律平治疗阵发性室上速46例次临床观察

阵发性室上速(PSVT)是临床常见心律失常之一,常见于无器质性心脏病患者,也可发生于各种心脏疾病,其发生机制多数为激动折返所致,少数为异位兴奋点自律性增高所至,是临床常见急症.     

食管心房调搏不同方法检出室上性心动过速成功率的比较

阵发性室上性心动过速(室上速)是临床常见的心律失常,其发生机制为异位节律点兴奋性增高、折返、触发激动,由折返机制引起的室上速可通过食管心房调搏诱发和终止。为了比较不同方法检出室上速的成功率,我们采用三个不同的刺激方案进行观察对比,现总结如下:     

房室结折返性心动过速(附6例电生理检查)

阵发性室上性心动过速(PSVT)是临床常见的心律失常,其发生机制,绝大多数系“折返激动”,在折返性室上速中,58～69%为房室结内折返,15～30%为房室旁道折返(隐性或显性预激征)。大量临床电生理学研究揭示,房室结折返性心动过速(AVNRT)与房室结内双径路(DAVNP)密切有关,认为这是导致激动折返的病理     

高分辨心电图鉴别室速与预激综合征逆向折返性心动过速

目的 :应用高分辨心电图鉴别室性心动过速 (室速 )与预激综合征逆向折返性心动过速。方法 :对17例室律整齐的室速和12例预激综合征逆向折返性心动过速患者进行心电信号叠加高频滤波分析 ,观测QRS波与P波的关系。结果 :在心电信号叠加高频滤波图上 ,17例室速中16例未见P波 ,12例预激综合征逆向折返性心动过速者全部见到P波 ,两组差异有统计学意义 (P<0.001)。结论 :应用心电信号叠加高频滤波分析显示P波的方法有助于室律整齐的室速与预激综合征逆向折返性心动过速的鉴别诊断     

折返性心动过速的电生理研究

折返是产生心速和异位节律的一个重要机制。折返必须具备:折返环、单向阻滞和传导减慢。它可发生在心肌的任何部位,构成了各种心速或早搏,因此研究不同部位折返是阐明不同心速机制的关键。窦房结区折返窦房结区折返包括了窦房结内、窦房之间和窦房交接区的折返,但临床电生理上不易区别,故统称窦房结区折返。窦房结组织传导缓慢,有效不应期长(300—500ms)因此房早刺激容易诱发窦折返性心速。窦折返性心速的P 波形态、极性、心房激动顺序都与窦性心律相同。     

腺苷对儿茶酚胺依赖性室上速的疗效

腺甙明显减慢房室结传导速度，药理剂量时具有负性变导性效应，可引起一过性完全性房室传导阻滞。因而，外源性腺背能十分有效地终止那些以房室结作为一部分折返环的室上速。但房室结折返性室上速常呈地茶酚胺依赖性，几条酚胺则对腺背的作用在某些方面有拈抗作用。21例室上速，其中房室顺传型反复性心动过速12例、房室结折返性心动过速9例。分为H组：组1（13例），在无外源性儿茶酚胺情况下能诱出室上速；组2（8例），在静脉滴注异丙肾上腺素（每分钟1．6土0．4灿g）时能诱出室上速。组1和2窦性心律时RR间期分别为793土38和561上23毫秒（…     

室性心动过速的电生理研究及程控起搏治疗

本文报告4例PVT电生理检查及程控起搏治疗结果,3例被心室程控刺激中止,提示为折返性室性心动过速。电生理检查表明,其折返途径1例可能为HPS折返,2例心室内折返,1例可能为自律性增加引起。心室程控刺激及电生理检查时均须备有除颤装置。     

血管紧张肽Ⅱ受体1拮抗药在快速性心律失常预防和治疗中的作用

血管紧张肽Ⅱ可诱发或加重室性或房性快速性心律失常的发生。血管紧张肽Ⅱ可使心肌纤维化,缩短有效不应期,减慢传导速度,有利于折返激动的形成。血管紧张肽Ⅱ可使交感神经张力增高,有利于自律性增高性快速性室性心律失常的发生。研究表明血管紧张肽Ⅱ受体1拮抗药有一定的预防和治疗心律失常的作用。     

心房颤动伴快速性心律失常的临床研究

目的研究分析房颤与其共存的,常见的快速性心律失常的关系与临床意义。方法将742例资料完整的房颤住院患者,伴其他常见的快速性心律失常患者98例,进行回顾性研究。其中伴房扑60例;伴室上性心动过速(室上速)20例(房室折返性心动过速AVRT2例;房室结折返性心动过速AVNT 18例),其中10例行射频消融术(RFCA)。室速16例,室颤2例由室速转化,电转复100次。结果①10例室上速伴房颤在RFCA后无室上速。其中6例(AVRT2例及AVNRT4例)在RFCA后,未诱发房颤及室上速。②文中房颤转化为室速例和室速转化为室颤例,均有急性心肌缺血或急性心肌梗死的背景。房颤的心室率> 120次/分。结论①室上速可能在房颤的发生中起板机作用。②在急性心肌缺血或急性心肌梗死时,控制房颤的心室率,有助防止室速及室颤的发生。     

Development of ventricular tachyarrhythmias in the conscious canine during the recovery phase of experimental ischemic injury: effect of bethanidine administration

The antiarrhythmic and antifibrillatory actions of bethanidine were evaluated in two conscious canine models which are capable of developing ventricular tachyarrhythmias during the recovery phase of myocardial infarction. In the first model, nonsustained (n = 3) or sustained (n = 12) ventricular tachycardia (cycle length, 165 +/- 6 ms; mean +/- SD) was initiated by programmed electrical stimulation, 4-9 days after experimental myocardial infarction. Bethanidine was administered in cumulative doses of 2, 4, 8, and 16 mg/kg and programmed stimulation repeated. Bethanidine, in doses of 4, 8, and 16 mg/kg, slowed the cycle length of the tachycardia and allowed slower rates of ventricular pacing to produce equivalent delays at epicardial sites in the ischemic zone. Despite these changes, induction of sustained ventricular tachycardia was prevented in only two of 13 animals. Bethanidine (8 mg/kg i.v. every 8 h, n = 4; 16 mg/kg i.v. every 8 h, n = 5) failed to prevent the development of premature ventricular beats, ventricular tachycardia, and ventricular fibrillation which developed in response to a transient ischemic episode superimposed on the heart that had a previous acute myocardial infarction. No differences in survival at 24 h were observed between saline- (10%, n = 10) and bethanidine-treated (0%, n = 9) groups. These results suggest that bethanidine acts to increase the refractory period and depresses conduction velocity in ischemically injured tissue, slowing the rate of ventricular tachycardia. However, the drug fails to suppress the development of ventricular arrhythmias and ventricular fibrillation in both canine models.     

心肌梗死时期前逸搏的机制探讨

目的：探讨急性心肌梗死时期前逸搏的发生机制。方法：以开胸结扎犬冠状动脉左前降支（ＬＡＤ）建立心肌梗死的动物模型,观察急性心肌梗死前后犬心室对程序电刺激（ＰＥＳ）的反应。结果梗死后期前逸搏发生率明显增加。结论：期前逸搏机制可能为延迟后除极（ＤＡＤｓ）所致的触发激动。     

Antiarrhythmic effects of MS-551, a new class III antiarrhythmic agent, on canine models of ventricular arrhythmia.

The antiarrhythmic effects of MS-551, which prolongs cardiac action potential duration without affecting the maximum upstroke velocity of the action potential, were assessed in three different canine ventricular arrhythmia models: 1) ventricular tachycardia (VT) induced by electrical stimuli 3-5 days after myocardial infarction, 2) spontaneous ventricular tachyarrhythmias 24-48 hr after two-stage coronary ligation and 3) ventricular tachyarrhythmias induced by digitalis. Intravenous administration of MS-551 (0.1-1 mg/kg) decreased the susceptibility in 10 dogs out of 13 to VT or ventricular fibrillation evoked by programmed electrical stimulation (PES) delivered to the ventricular septum 3-5 days after myocardial infarction. Oral administration of MS-551 (3 mg/kg) also decreased the susceptibility to VT evoked by PES in 7 out of 10 conscious postinfarction dogs. Concurrently, intravenous (0.1-1 mg/kg) or oral (3 mg/kg) administration of MS-551 produced increases in the ventricular effective refractory periods (ERP) by 7 +/- 1% - 17 +/- 3% or 13 +/- 2%, respectively. Similarly, d-sotalol (0.3-3 mg/kg, i.v. and 10 mg/kg, p.o.) decreased the susceptibility to VT with increased ERP. However, MS-551 (1 and 10 mg/kg, i.v.) failed to inhibit both canine two-stage coronary ligation arrhythmia and digitalis arrhythmia. These results suggest that MS-551 is a pure class III antiarrhythmic drug which may be effective in the treatment of life-threatening reentrant tachyarrhythmias, but not in automaticity arrhythmias.     

Failure of thromboxane synthetase inhibition to protect the postinfarcted heart against the induction of ventricular tachycardia and ventricular fibrillation in a conscious canine model of sudden coronary death

The role of thromboxane as a contributor to the genesis of ventricular tachycardia and fibrillation was examined in conscious dogs which had been subjected to myocardial infarction. CGS 12970, a thromboxane synthetase inhibitor was administered in a dose of 10 mg/kg (i.v.) every 12 h. Ex vivo thrombin-activated thromboxane synthesis, as determined by assay for thromboxane B2, was reduced to 15% of baseline 2 h after administration of CGS 12970. Drug administration was found to inhibit ex vivo platelet aggregation significantly in response to arachidonic acid, while aggregation to ADP and collagen was unaffected. CGS 12970 did not protect against the induction of ventricular tachycardia by programmed electrical stimulation of the postinfarcted heart. During provocative electrical stimulation, 9 of 11 (82%) animals continued to respond in the post-treatment period with the development of VT. Pretreatment with CGS 12970 failed to prevent the spontaneous development of ventricular fibrillation which occurred in 7 of 10 (70%) animals when a secondary ischemic event was superimposed in the region of the noninfarct-related circumflex coronary artery. The results suggest that the thromboxane synthetase inhibitor, CGS 12970, when administered in the subacute phase of recovery from myocardial infarction, does not protect against the induction of ventricular tachycardia by programmed electrical stimulation or the spontaneous development of ventricular fibrillation in the postinfarcted canine heart. The findings suggest that thromboxane may not serve a critical role in the genesis of ventricular tachyarrhythmias and ventricular fibrillation in the postinfarcted canine heart.     

Effects of pimobendan (UD-CG 115 BS), a new positive inotropic agent, on ventricular tachycardia and ischemic ventricular fibrillation in a conscious canine model of recent myocardial infarction

Pimobendan (UD-CG 115 BS; 4,5-dihydro-6-[2-(4-methoxyphenyl)-1H-benzimidazol-5-yl]-5-methyl- 3(2H)- pyridazinone) is a newly developed, structurally novel compound with positive inotropic as well as coronary and peripheral vasodilator activities. In vitro, pimobendan has been reported to prolong the duration of the cardiac action potential of ventricular myocardial tissue, suggesting the potential for this agent to increase myocardial refractoriness and possibly exert antiarrhythmic activity in vivo. In the present study, the effects of pimobendan upon cardiac electrophysiologic parameters, the induction of ventricular tachycardia by programmed ventricular stimulation, and upon the development of ischemic ventricular fibrillation were assessed in 16 conscious dogs 3 to 5 days after experimental anterior myocardial infarction. The intravenous administration of 0.3 mg/kg pimobendan to postinfarction dogs significantly reduced the rate-corrected QTc and paced QT intervals, and reduced the relative and effective refractory periods in normal noninjured ventricular myocardium. Electrophysiologic parameters in infarcted ventricular myocardium were not altered by pimobendan. Ventricular tachycardia remained inducible early after anterior myocardial infarction in eight of eight pimobendan-treated postinfarction dogs tested. Six of the eight pimobendan-treated animals that had nonsustained tachyarrhythmias elicited as initial responses to baseline programmed stimulation testing had sustained tachycardias induced at postdrug testing, with a reduction in the number of programmed extrastimuli required to induce the postpimobendan tachyarrhythmias occurring in three animals.(ABSTRACT TRUNCATED AT 250 WORDS)     

The antiarrhythmic actions of intravenous and oral UM424 in postinfarction canine myocardium

The electrophysiologic and antiarrhythmic effects of oral and intravenous UM424 were studied in canine models of acute and chronic myocardial injury. In the first phase of this study, reentrant ventricular tachyarrhythmias and/or ventricular fibrillation were initiated by programmed electrical stimulation techniques in seven dogs 48-120 h after myocardial infarction. The cycle length of these reentrant ventricular beats was 176 +/- 16 ms, and they were accompanied by fractionated asynchronous epicardial electrical activity in the injured region that bridged the diastolic interval, i.e., 143 +/- 37 ms. When this prolonged, diastolic electrical activity ceased, the ventricular tachyarrhythmias ceased. UM424 5 mg/kg i.v. increased the effective refractory period of the normal myocardium by 21 ms (p less than 0.05), depressed cardiac conduction in the injured, infarcted myocardium and suppressed these reentrant tachyarrhythmias. Ventricular fibrillation could not be initiated after UM424. In the second phase of this study, a canine model of coronary artery thrombosis was used to produce spontaneous ventricular arrhythmias. UM424 60 mg/kg p.o. converted these ventricular arrhythmias to normal sinus rhythm. This pharmacologic action was not associated with deleterious hemodynamic side effects and lasted for 3 h, the duration of each experiment. These results demonstrate that after oral or intravenous administration, UM424 possess antiarrhythmic and antifibrillatory actions in canine models of acute and chronic myocardial injury.     

评价抗快速室性心律失常药物的心电生理-电药理学方法

用冠状动脉Harris二期结扎并部分再灌注及吻合支缝扎法造成犬急性心肌梗塞，5－8天后，辅以心脏程控制激技术（PES）进行心电生理检查及复制快速室性心律失常，研制成犬在体心脏心电生理－电药理学实验模型，并观察了普鲁卡因胺（PA）对该实验模型的电生理影响。结果表明。PA能显著延长QTc间期，RERP，NERP及IERP，缩小IDR和VDR，抑制心室PES诱发的室速和室颤，并能有效地预防犬心肌梗塞后再次急性缺血所导致的自发性室颤，表明PA有抗缺血性快速室性心律失常的心电生理－电药理作用。结果同时表明，该心电生理－电药理学实验的犬模型具有很高的可靠性，重复性及临床相关性，是一种有价值的评价抗快速室性心律失常药物的心电生理一电药理学方法。     

Effects of combined thromboxane synthetase inhibition/thromboxane receptor antagonism in two models of sudden cardiac death in the canine: limited role for thromboxane.

The effects of combined thromboxane synthetase inhibition and thromboxane receptor antagonism (TSI/TRA) were studied in conscious and in anesthetized canine models of sudden cardiac death. Administration of the TSI/TRA, R68070 10 mg/kg intravenously (i.v.), decreased thrombin-stimulated thromboxane synthesis and significantly antagonized platelet aggregation in response to the thromboxane-mimetic U46,619. In the conscious canine model, R68070 did not change ventricular refractoriness, did not prevent induction of ventricular arrhythmias by programmed electrical stimulation, and failed to prevent development of spontaneous ventricular fibrillation (VF) in response to ischemia produced at a site remote from the area of previous myocardial infarction (R68070 mortality = 70%, vehicle = 100%, p = NS). In the anesthetized canine model, R68070 prevented development of ischemia in 7 of 11 animals and reduced mortality significantly (R68070 27% and vehicle 73%; p = 0.038). R68070 inhibited thrombus formation in both models (R68070 conscious 7.0 +/- 2.6 mg and vehicle conscious 15 +/- 7.6 mg, p = NS; R68070 anesthetized 5.9 +/- 1.9 mg and vehicle anesthetized 17.7 +/- 4.3 mg; p less than 0.05). The results suggest that inhibition of thromboxane-dependent activity during acute recovery from infarction was able to protect the myocardium from developing ischemia in response to current-mediated intimal damage in a noninfarct-related artery. In the subacute phase of recovery from infarction, when the underlying myocardial substrate is susceptible to electrical derangement induced by transient ischemia, thromboxane inhibition in itself was unable to prevent ischemia-induced sudden cardiac death. Although R68070 may delay onset of ischemia due to thrombotic occlusion of the coronary artery, there does not appear to be an antiarrhythmic/antifibrillatory action to be derived from interfering with the synthesis or receptor-mediated action of thromboxane. Furthermore, R68070 does not alter the electrophysiologic properties of the heart which would result in an antiarrhythmic or antifibrillatory action.     

N-[(omega-amino-1-hydroxyalkyl)phenyl]methanesulfonamide derivatives with class III antiarrhythmic activity

N-[4-[4-(Ethylheptylamino)-1-hydroxybutyl]phenyl]methanesulfonamid e, (E)-2-butenedioate (2:1) salt (ibutilide fumarate, 2E), has been found to have Class III antiarrhythmic activity. In an in vitro rabbit heart tissue preparation designed to evaluate the cardiac electrophysiology of potential antiarrhythmic agents, it selectively prolongs the effective refractory period of papillary muscle. In vivo it increases the ventricular refractory period of the canine heart and prevents the ventricular arrhythmias induced by programmed electrical stimulation 3-9 days after a myocardial infarction. This paper describes the synthesis of 2E and a series of related compounds. The in vitro evaluation of the cardiac electrophysiology of these compounds has allowed us to determine the structural requirements for Class III antiarrhythmic activity in this series. Evaluation of the antiarrhythmic activity of 2E and one of the more potent analogues on the late postinfarction ventricular arrhythmias induced by programmed electrical stimulation of the canine myocardium is also described. This activity is compared with that of the Class III antiarrhythmic agent sotalol. Compound 2E appears to be as effective and 10-30 times more potent than sotalol in this model.     

Effects of angiotensin II and captopril on inducible sustained ventricular tachycardia two weeks after myocardial infarction in the pig

The effects of angiotensin II (AII) and captopril (C) on the inducibility of ventricular tachyarrhythmias were investigated 14 days after infarction in pigs. In 27 pigs, ischemia was induced by 60-min occlusion of the left coronary artery. Four pigs died of ventricular fibrillation during ischemia, and six others died within 24 h due to pump failure. Of the 17 survivors, eight pigs developed a sustained (greater than 30 s) monomorphic ventricular tachycardia (sVT) after programmed electrical stimulation. In nine noninducible pigs, an AII infusion (0.6 microgram/kg/min) caused inducible sVT in three animals and nonsustained VT in two animals (greater than 10 reentrant beats). In two of the remaining four animals, spontaneous premature ventricular beats appeared during the infusion. In a group of five healthy pigs, the electrophysiological effects of AII were evaluated. Infusion of AII caused a rapid and sustained increase in arterial blood pressure to 161 +/- 6.4% (p less than 0.001). The sinus cycle length decreased to 74 +/- 5.2% (p less than 0.02). The effective refractory period of the right ventricle decreased significantly to 82 +/- 5.5% (p less than 0.05). These results show that modulation of the renin-angiotensin system after myocardial infarction influences the inducibility of malignant ventricular tachyarrhythmias, as shown by the increased inducibility of sustained ventricular tachycardia. This may be related to a decreased ventricular refractoriness. Therefore, it is suggested that C can reduce malignant ventricular tachycardia late after myocardial infarction by preventing the deleterious arrhythmogenic effects of AII.