房室结慢径区域消融对迷走神经功能及心房颤动易感性的影响

目的心房颤动（房颤）与房室结折返性心动过速有着某种程度的关联性,慢径区域消融可能影响了心房自主神经功能而导致窦性心动过速。但慢径区消融对心房自主神经功能的具体影响目前尚不清楚。本文旨在探讨慢径区消融对心房迷走神经调节功能及房颤易感性的影响。方法11条成年杂种犬,全身麻醉下行颈交感一迷走神经干剥离术。经右颈内静脉穿刺放置冠状静脉窦导管,经左股静脉穿刺放置右心室导管及右心房标测电极导管（Halo导管）,经右股静脉穿刺放置消融导管和希氏束导管。静脉应用美托洛尔阻断交感神经活性。测量慢径区域消融前后基础状态及迷走神经刺激下的窦性周长（SCL）及高位右心房（HRA）、低位右心房（IRA）、冠状静脉窦近端（CSp）和冠状静脉窦远端（CSd）的有效不应期（ERP）及心房易感窗口（VW）。结果（1）SCL的变化：消融前后迷走神经刺激导致的SCL缩短值无明显改变[（107±19）次／min对（108±8）次／min,P〉0．05],提示慢径区域消融没有明显改变迷走神经对窦房结的调节作用。（2）ERP的变化：消融前后迷走神经刺激导致的ERP缩短值在HRA分别为[（69±37）ms对（55±34）ms,P〉0．05],CSd分别为[（55±30）ms对（42±32）ms,P=0．08],IRA分别为[（66±24）ms对（19±21）ms,P〈0．001],CSp分别为[（46±24）ms对（7±18）ms,P〈0．001]。提示慢径区域消融对HRA及窦房结区域的迷走神经调节功能无明显影响,对CSd区域的迷走神经调节功能有一定的影响,而导致了IRA及CSp区域去迷走神经效应。（3）心房VW的变化：消融前后基础状态下各个部位刺激均较难诱发房颤（VW接近0）。消融后,HRA迷走神经刺激诱发房颤的能力较消融前没有明显变化[（63±31）ms对（63±25）ms,P〉0．05],CSd的VW有一定程度的降低[（35±37）ms对（57±28）ms,P     

上腔静脉隔离对迷走神经功能及心房颤动易感性的影响

目的 通过分析迷走神经调节的心房电生理指标(心房有效不应期及心房颤动易感窗口)的变化,间接揭示上腔静脉(SVC)隔离对犬的心房迷走神经功能及心房颤动(房颤)易感性的影响.方法 9条成年杂种犬,全身麻醉下行颈交感-迷走神经干剥离术.经右颈内静脉穿刺放置冠状静脉窦导管,经股静脉穿刺放置右心室导管(行临时右心室起搏)、环状标测导管(Lasso导管)及消融导管.静脉应用美托洛尔阻断交感神经活性.分别于SVC隔离前后在基础状态及迷走神经刺激时测量右心耳(RAA)、冠状静脉窦近端(CSp)和冠状静脉窦远端(CSd)的不应期(ERP)、心房易感窗口(VW)及窦性周长(SCL).结果 (1)窦性周长的变化SVC隔离前迷走神经刺激明显缩短SCL[(65.78±28.49)次/min vs(142.67±15.42)次/min,P《0.001],SVC隔离后基础状态及迷走神经刺激下SCL差异无统计学意义[(134.89±19.19)次/min vs(114.33±31.41)次/min,P》0.05].(2)有效不应期的变化SVC隔离前,迷走神经刺激下测得的心房ERP较基础状态下明显缩短[右心耳(RAA)分别为(51.11±18.33)ms vs(101.11±27.59)ms;CSd分别为(56.67±22.36)ms VS(98.89±14.53)ms;CSp分别为(48.89±25.22)ms vs(101.11±12.69)ms,P《0.001].SVC隔离后,迷走神经刺激所致的心房ERP缩短的能力明显下降(RAA分别为(94.40±16.70)ms vs(94.44±16.67)ms;CSd分别为(89±15)ms vs(96.7±18.0)ms;CSp分别为(93.3±18.7)ms vs(98.9±20.3)ms,P》0.05].(3)心房易感窗口的变化 SVC隔离前后基础状态下测得的VW无变化.SVC隔离后迷走神经刺激时测得的VW较隔离前明显降低[RAA分别为(6.67±11.18)ms vs(21.11±20.88)ms,CSd分别为(8.89±14.52)ms vs(16.66±23.97)ms,CSp分别为(2.22±6.67)ms vs(22.22±18.55)ms,P《0.05].结论 SVC隔离能导致迷走神经介导的窦房结抑制、心房不应期缩短能力及房颤易感窗口增加能力明显下降.提示SVC隔离可导致心房局部去神经反应,抑制迷走神经介导的房颤发生.     

房室结慢径消融对心房电生理性质的影响

目的 慢径消融降低了心房颤动(房颤)的易感性,但具体机制不明.本文旨在探讨消融后心房电生理性质的改变及其具体机制.方法 32例房室结折返性心动过速患者,测量射频消融前后窦性心率及高位右心房、低位右心房、冠状静脉窦近端和远端各部位的有效不应期和易感窗口,以及房室结快径前传不应期的变化.结果 (1)慢径消融前后下列部位的有效不应期的变化分别为:冠状静脉窦近端(21 8.1±21.8)ms,(235.3±23.6)ms,P＜0.0001;冠状静脉窦远端(230.9±21.0)ms,(244.7±25.1)ms,P＜0.01;低位右心房(198.8±26.7)ms,(219.7±28.7)ms,P＜0.005;高位右心房(214.4±35.1)ms,(213.4±37.3)ms,P=0.6.(2)在消融术后,房颤的诱发比例下降,冠状静脉窦近端的易感窗口显著降低(P=0.03),冠状静脉窦远端和低位右心房的易感窗口有所降低,高位右心房的易感窗口不变,但差异无统计学意义.(3)消融后窦性心率有一定程度的上升(72.1±5.6)次/min对(74±6.8)次/min,但差异无统计学意义(P=0.17).(4)慢径消融使快径前传不应期缩短,消融前后分别为(391±55)ms,(369±78)ms,P＜0.01.结论 慢径消融使心房多部位的电生理性质发生了改变,导致冠状静脉窦近端和远端,以及低位右心房的有效不应期延长,房颤诱发几率降低.该现象的原因可能与消融造成的迷走神经功能改变有关.     

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。     

肺静脉隔离对迷走神经对心房电生理特性调节及对心房颤动易感性的影响

目的越来越多的证据表明肺静脉隔离(PVI)不仅去除了心房颤动(房颤)的触发病灶,也可能改变了房颤赖以维持的物质基础,但PVI如何改变了房颤的维持机制的研究较少.研究目的在于PVI对迷走神经对心房电生理特性调节及对房颤易感性的影响.方法11只成年杂种犬,全麻及机械通气下行颈部交感-迷走神经干剥离术,经右颈内静脉穿刺术放置右心室及冠状窦导管,经左股静脉放置右心房导管,经房间膈穿刺途径放置消融及标测导管于左心房.静脉应用普萘洛尔阻断交感神经活性.分别于肺静脉消融前后在基础状态及迷走神经刺激时测量右心耳(RAA)、左心房游离壁(LAFW)、冠状窦近段(CSP)及冠状窦远端(CSD)的不应期(ERP)及心房易感窗口(VW).不应期缩短值为基础状态下的ERP与迷走神经刺激时的ERP的差值,VW定义为引起房性早搏或房颤的最长与最短S1S2间期的差值.结果(1)有效不应期的变化消融术前,迷走神经刺激能明显缩短心脏各部位的ERP.消融术后,左心房内迷走神经刺激所致的ERP缩短值明显降低[LAFW(43.64±21.57)ms与(11.82±9.82)ms,78,P＜0.001;CSP(50.91±26.25)ms与(11.82±14.01)ms,P＜0.001;CSD(50±31.94)ms与(17.27±20.54)ms,P＜0.005]右心房内变化不明显[(58.18±28.22)ms与(50.91±22.12)ms,P=0.245].(2)VW的变化消融术后,基础状态下测得的VW无明显变化[RAA(32.5±37.32)ms与(21.25±27.48)ms LAFW(31.25±28.5)ms与(35±35.46)msCSP(20±23.3)ms与(22.5±26.05)ms;CSD(30±32.95)ms与(27.5±31.51)ms.P=0.21-0.74],而迷走神经刺激时左房内测得的VW明显降低[LAFW(36.25±11.88)ms与(11.25±16.42)msP＜0.001;CSP(52.5±19.82)ms与(13.75±19.96)msP＜0.005;CSD(43.75±19.23)mS与(17.5±19.82)ms,P＜0.05],右心房内无明显变化[(52.5±22.52)ms与(42.5±10.35)ms,P=0.316].结论PVI能导致左心房(包括冠心窦)去迷走神经反应,引起迷走神经刺激时的心房不应期延长及心房易感窗口缩短.提示PVI所致的左心房去迷走神经反应可能为PVI改变房颤赖以维持的物质基础的机制之一.     

犬心脏第3脂肪垫对左心房及左上肺静脉电生理特性的影响

目的研究犬心脏第3脂肪垫（SVC-AO FP）对左心房及左上肺静脉有效不应期（PERP）及心房有效不应期（AERP）离散度的影响。方法10只犬麻醉后,自颈部离断并结扎双侧迷走神经,正中开胸暴露SVC-AO FP,右肺静脉（RPV）及下腔静脉（IVC）脂肪垫。消融RPV和IVC后,分别测定基础状态下、SVC-AO FP刺激后、SVC-AO FP消融后的左AERP、不应期离散度（dAERP）及左上PERP。结果SVC-AO FP刺激后AERP从基础状态下的（135±14）m s缩短至（106±16）m s（P<0.05）,消融后延长至（140±9）m s;dAERP从（15±4）m s,增加至（26±6）m s（P<0.05）,消融后为（11±9）m s;PERP从（131±12）m s缩短至（108±17）m s（P<0.05）,消融后的延长至（136±10）m s。结论刺激犬心脏SVC-AO FP缩短心房和肺静脉的有效不应期,增加心房有效不应期离散度。左心房及左上肺静脉的迷走神经支配部分可能直接来自SVC-AO FP。     

迷走神经干预对犬心房电生理的影响

目的心房电重构可导致心房有效不应期缩短,通过测量心房有效不应期来研究迷走神经对心房电重构的影响。方法 10只成年犬给予酒石酸美托洛尔和阿托品阻断交感神经和迷走神经。分别测量心房电重构前后基础状态及迷走神经刺激下的心房有效不应期（ERP）和房颤易感窗口（VW）。结果①阿托品应用前后基础状态下的ERP无变化。阿托品应用前后迷走神经刺激下的ERP变化明显;②心房电重构后ERP：基础状态及迷走神经刺激下,无论右心房还是冠状静脉窦远端测得的ERP与重构前（阿托品应用后）ERP相比无明显差异（p值均〉0.05）;③VW的变化：阿托品应用前,迷走神经刺激下容易诱发房颤。阿托品应用后,心房电重构前后无论基础状态或迷走神经刺激均不能诱发房颤。结论迷走神经阻滞能减轻心房电重构所导致的心房不应期缩短,从而抑制迷走神经介导的房颤诱发。     

射频导管消融术阻滞经冠状静脉窦传导通路的实验研究

目的　探讨利用射频导管消融术阻滞经冠状静脉窦的电传导通路的方法及可行性。方法　冠状静脉窦口内 5～ 10mm处射频导管消融 ,低位右心房起搏下 ,观察最早激动部位、冠状静脉窦激动顺序和时间、房间隔激动时间、心房激动时间。结果　 (1)冠状静脉窦口或近端射频导管消融可造成经冠状静脉窦电传导通路的完全或部分阻滞。表现在消融前 ,低位右心房起搏时 ,窦口处的电激动明显早于Bachmann束。消融后 ,窦口处的电激动迟于Bachmann束或两者基本一致 ;(2 )消融前后 ,心房激动时间由 (6 1 14± 8 36 )ms延长至 (88 4 3± 19 2 2 )ms,说明低位心房起搏时冠状静脉窦是优势传导通路 ;(3)消融前后的房间隔激动时间及冠状静脉窦激动时间分别为 (2 6 4 3± 8 87)ms对(15 2 8± 10 13)ms和 (39 4 3± 9 78)ms对 (38 0 0± 5 86 )ms。结论　冠状静脉窦近端射频导管消融术阻断经冠状静脉窦的电传导通路的方法是可行的     

肺静脉隔离对迷走神经功能及心房颤动易感性的影响

目的研究肺静脉隔离(PVI)对犬的心房迷走神经功能及心房颤动(简称房颤)易感性的影响。方法9条成年杂种犬,全麻下行颈交感-迷走神经干剥离术。静脉应用美托洛尔阻断交感神经活性。分别于肺静脉消融前后在基础状态及迷走神经刺激时测量窦性周长(SCL)、右心耳(RAA)、左心耳(LAA)、冠状静脉窦近端(CSp)和冠状静脉窦远端(CSd)的不应期(ERP)及心房易感窗口(VW)。结果①PVI前迷走神经刺激能明显降低SCL(P<0.001),PVI后迷走神经刺激对SCL影响较小(P>0.05)。②PVI前,迷走神经刺激能明显缩短心房各部位ERP(P均<0.05)。PVI后,迷走神经刺激对心房ERP的影响较小(P均>0.05)。③PVI前后基础状态下测得的VW无变化。PVI后迷走神经介导的房颤诱发率明显下降(P均<0.05)。结论PVI能导致迷走神经介导的窦房结抑制、心房不应期缩短能力及房颤易感窗口增加能力明显下降。     

Koch三角下位与中位线性消融对治疗常规消融方法困难的房室结折返性心动过速的比较

目的: 比较常规消融方法困难的房室结折返性心动过速(AVNRT)Koch三角下位与中位线性消融两种方法的有效性和安全性。方法: 回顾性分析比较常规消融方法困难的房室结折返性心动过速Koch三角下位线性消融（三尖瓣环至冠状窦口中部）和中位线性消融（三尖瓣环至希氏束与冠状窦口连线的中下1/3交界水平）的手术成功率、慢径消除率、放电时间和操作时间。结果: 下位和中位线性消融均具有较高的成功率（94.4%、100%）。在放电时间上,下位法消融组显著高于中位法线性消融［（578±177）ms vs ( 481±185)ms,P<0.01］,而整个手术操作时间,下位法组要明显低于中位法［（153±51）ms vs (199±56)ms,P<0.01）］。在消融过程中,中位法出现1例一过性Ⅰ度房室传导阻滞,两组无任何程度的持续房室传导阻滞发生。结论: 对常规方法消融后复发的AVNRT,Koch三角下位线性消融与中位线性消融方法均较为安全,但下位法可能操作更简洁。     

Effect of autonomic nervous system modulation on retrograde atrioventricular nodal conduction in the human heart

Although the influence of the autonomic nervous system on anterograde atrioventricular nodal conduction is well established, its effect on retrograde atrioventricular nodal conduction has not been examined systematically. Since retrograde atrioventricular nodal conduction in subjects with normal anterograde conduction may vary from intact retrograde conduction to complete retrograde block when assessed during ventricular pacing, in this study patients with (a) intact retrograde atrioventricular nodal conduction (group 1) were studied during parasympathetic (vagal) stimulation by carotid sinus pressure and during sympathetic inhibition (propranolol 0.2 mg.kg-1 intravenously) and (b) retrograde atrioventricular nodal block (group 2) were studied during vagal blockade (atropine 0.04 mg.kg-1 intravenously) and during sympathetic stimulation (isoproterenol 1-4 micrograms.min-1 infusion). In both groups changes in sinus cycle length and anterograde atrioventricular nodal conduction were measured. In group 1 vagal stimulation by carotid sinus pressure in 20 patients caused the cycle length at which retrograde atrioventricular nodal block was induced to be significantly lengthened from a mean(SD) of 375(59) to 451(51) ms in six patients; caused complete retrograde block in 10 patients; and had no effect in four patients. Sympathetic inhibition by propranolol in another 15 patients delayed the onset of pacing induced retrograde atrioventricular nodal block from a mean(SD) of 340(60) to 418(80) ms in 11 patients; caused complete retrograde atrioventricular nodal block in three patients; and had no effect in one patient. In group 2 vagal blockade by atropine caused a 1:1 retrograde response during ventricular pacing up to a mean(SD) cycle length of 470(135) ms in six out of eight patients. The infusion of isoproterenol caused the retrograde atrioventricular nodal block to be abolished and 1:1 conduction to be resumed up to a ventricular pacing mean(SD) cycle length of 364(57) ms in six out of eight patients. It is concluded that (a) the autonomic nervous system modulates retrograde atrioventricular nodal conduction in a similar manner to its anterograde counterpart and (b) that since retrograde atrioventricular nodal conduction was reversible after the administration of either atropine or isoproterenol retrograde atrioventricular nodal block may be dynamic (physiological) rather than fixed (anatomical) in nature.     

Change in delay of atrioventricular conduction after radiofrequency catheter ablation for atrioventricular nodal re-entry tachycardia.

OBJECTIVE--To monitor atrioventricular conduction after radiofrequency ablation for atrioventricular nodal re-entry tachycardia. DESIGN--Measurement of PR interval from 12 lead surface electrocardiograms before; at 0, 24, 48, 72, and 96 hours; and at 1 and 6 months after radiofrequency ablation. PATIENTS--40 consecutive patients with atrioventricular nodal re-entry tachycardia. The anterior approach was used in 23 patients, the posterior approach in 17. RESULTS--With the anterior approach the PR interval increased significantly and progressively until 48 hours after ablation (maximum 282 (SD 62.2) ms, before ablation 142 (29.5) ms; P < 0.0001). Up to 96 hours no further change was observed, but one month after ablation the PR interval had decreased to a value not significantly different from that 24 hours after the procedure (231 (51.2) ms). In one patient total atrioventricular block developed 24 hours after an uncomplicated procedure and a permanent pacemaker was implanted. With the posterior approach the PR interval increased slightly in the first 24 hours (156 (22.7) ms, before ablation 144 (21.2) ms P = 0.004), but it had returned to preablation values at 1 month. One patient developed second degree atrioventricular block during the first 24 hours after ablation, despite delivery of all radiofrequency pulses posterior to Koch's triangle at sites without His bundle deflection. PR intervals at 6 months did not differ significantly from the values at 1 month. CONCLUSION--After the anterior approach the progressive delay in atrioventricular conduction up to 48 hours after radiofrequency ablation for atrioventricular nodal re-entry tachycardia warrants continuous in hospital monitoring of patients for at least two days after the procedure.     

Surgery for Wolff-Parkinson-White syndrome interrupts efferent vagal innervation to the left ventricle and to the atrioventricular node in the canine heart

The hypothesis that cardiac surgery to interrupt accessory pathways also interrupts autonomic nerves to the canine ventricle and to the atrioventricular node was tested in four groups of dogs. Group 1 (n = 6) underwent dissection of the atrioventricular fat tissue and cryolesion created by application of a cryoprobe at -60 degrees C for 2 min along the lateral left atrioventricular groove, the same surgical procedure as carried out in patients with Wolff-Parkinson-White syndrome with accessory pathways located in the left ventricular free wall. Group 2 (n = 6) underwent dissection of the atrioventricular fat pad alone and group 3 (n = 6) dissection and cryolesion along the posterior left atrioventricular groove as performed in patients with Wolff-Parkinson-White syndrome with accessory pathways located in the posterior paraseptal area. Group 4 consisted of 11 non-operated control dogs. Four to 13 days after surgery the ventricular effective refractory period (ERP) was determined during bilateral ansae subclaviae stimulation (4 ms pulses, 2-3 Hz, and 2-3 mA), noradrenaline infusion (0.5 micrograms.kg-1.min-1), and bilateral vagal stimulation (4 ms pulses, 20 Hz, and current strength to induce asystole or complete atrioventricular block). Atrioventricular nodal conduction (AH interval) and spontaneous sinus cycle length were also determined in group 3 dogs. Ansae subclaviae stimulation and noradrenaline infusion shortened effective refractory period significantly at each left ventricular test site. The amount of effective refractory period shortening induced by ansae subclaviae stimulation did not differ among the test sites except for the posterior left ventricle in group 1 dogs.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of sympathetic tone on vagally induced phasic changes in heart rate and atrioventricular node conduction in the anesthetized dog

We examined the effects of stellate ganglia stimulation on the phase-dependent chronotropic and dromotropic responses to brief vagal bursts in open-chest anesthetized dogs. Stellate stimulation affected the phasic vagal effects on heart rate by shortening the latent period, shifting the phase at which maximum decrease in heart rate occurred to earlier phases, and reducing the maximum decrease in heart rate. These effects were due primarily to an increase in the basic heart rate. No significant sympathetic-parasympathetic interaction occurred for heart rate, indicating that accentuated antagonism did not occur with brief vagal bursts. Stellate stimulation primarily decreased the amplitude of the phasic vagal effects on atrioventricular nodal conduction, regardless of the underlying heart rate, and a significant sympathetic-parasympathetic interaction was associated with this effect. The peak of the phase-dependent vagal effects on heart rate and atrioventricular nodal conduction were phase-shifted with one another. From these findings, we postulate the small changes in sympathetic tone might shift the predominant phase-dependent vagal effect from one on heart rate to one on atrioventricular nodal conduction. Furthermore, our results suggest that dynamic vagal control of heart rate and atrioventricular node conduction involves both phase-dependent and phase-independent factors. Sympathetic activity appears to affect only the phase-independent factor(s) in the control of heart rate, whereas it affects both phase-dependent and phase-independent factors in the control of atrioventricular node conduction.     

Influence of the site of stimulation on atrioventricular nodal refractory periods and the effect of verapamil

The refractory periods of the atrioventricular (AV) node appear dependent on the pattern of AV nodal input. In 21 superfused AV rabbit heart preparations stimulated from each of the 2 principal input regions, crista terminalis or atrial septum, the effect of changing the site of stimulation of the AV nodal refractoriness and the relative effect of verapamil on AV nodal refractoriness was determined. In 6 of 21 preparations the functional AV refractory curve became discontinuous only when stimulation was applied at the atrial septum and suggested dual AV nodal pathways (dual pathways group). In the 15 other preparations no interruption of the curve occurred with either crista terminalis or atrial septal stimulation (normal conduction group). In the normal conduction group, the difference in the effective refractory period of the AV node obtained by crista terminalis vs atrial septal stimulation was not significant (154 +/- 25 vs 150 +/- 28 ms). However, the functional refractory period was significantly longer with crista terminalis vs atrial septal stimulation (232 +/- 19 vs 239 +/- 19 ms, p less than 0.001). After verapamil administration, the effective and functional refractory periods during crista terminalis vs atrial septal stimulation were prolonged to 270 +/- 49 vs 285 +/- 55 ms (p less than 0.01) and 335 +/- 43 vs 351 +/- 41 ms (p less than 0.001), respectively. Thus, the difference in refractory periods associated with changing the stimulation site was exaggerated with verapamil.(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes in atrial and ventricular refractoriness and in atrioventricular nodal conduction produced by combinations of vagal and sympathetic stimulation that result in a constant spontaneous sinus cycle length

The vagal nerves modulate adrenergic effects on sinus cycle length, atrioventricular (AV) nodal conduction, and refractoriness of atria and ventricles. We tested whether varying levels of vagal-sympathetic input could yield the same spontaneous sinus cycle length but also alter effective refractory periods of the right atrium, right ventricle, and left ventricle and AV nodal conduction times. Dogs anesthetized by alpha-chloralose were studied in the open-chest, neurally decentralized state. In 10 dogs, sinus cycle length was maintained constant during 3 levels of bilateral ansae subclaviae stimulation (4 msec, 3 mA at 1, 2, and 4 Hz) by titrating simultaneous bilateral vagal stimulation (varying pulse width and frequency). Each combination of ansae subclaviae-vagal stimulation yielded the same sinus cycle length as the control value, but refractory periods of right atrium and right and left ventricles shortened progressively as the frequency of ansae subclaviae stimulation increased. Atrioventricular nodal conduction time (AH interval) shortened in 2 dogs and lengthened in 3 dogs. His-Purkinje conduction time (HV interval) was unchanged. In 9 dogs, the effect of simultaneous unilateral ansae subclaviae stimulation at 2 Hz and ipsilateral vagal stimulation that yielded the same sinus cycle length were determined. Right-sided ansae subclaviae-vagal stimulation shortened refractoriness of right atrium and anterior left ventricle significantly. The AH interval lengthened in 1 dog. Left ansae subclaviae-vagal stimulation shortened the refractory periods of anterior and posterior left ventricle significantly and reduced the AH interval in 3 dogs. In 8 dogs, the effects of bilateral ansae subclaviae stimulation alone at 2 Hz, vagal stimulation alone at an intensity required to keep the sinus cycle length constant during ansae subclaviae stimulation, and simultaneous bilateral ansae subclaviae and vagal stimulation were tested. The right atrial refractory period was shortened significantly by ansae subclaviae stimulation alone and by vagal stimulation alone and was shortened further by simultaneous stimulation of both autonomic limbs. The right and left ventricular refractory periods were shortened by ansae subclaviae stimulation alone and by simultaneous stimulation of both limbs but tended to be prolonged by vagal stimulation alone and when added to ansae subclaviae stimulation. In 7 dogs, the effects of simultaneous stimulation of bilateral ansae subclaviae at 2 Hz and vagi at intensities that maintained the AH interval constant at an atrial pacing cycle length of 300 msec were determined.(ABSTRACT TRUNCATED AT 400 WORDS)     

房室结折返性心动过速患者房室结功能曲线连续性的电生理分析

分析房室结折返性心动过速 (AVNRT)中房室结功能曲线呈连续性者的电生理特点。将AVNRT分为房室结功能曲线连续组 (Ⅰ组 )及房室结功能曲线不连续组 (Ⅱ组 ) ,行慢径消融 ,进行消融前后和组间的电生理比较 ,分析房室结功能曲线呈连续性者的特点。结果 :I组心房程序刺激对AVNRT的诱发率仅 42 % (5 / 12 ) ,低于Ⅱ组的 6 6 %(2 3/ 35 )。Ⅰ组房室结前传有效不应期 (ERP AVN)消融前后无显著变化 (2 18.2± 2 9.3msvs 2 5 3.3± 80 .3ms,P >0 .0 5 ) ;心房程序刺激最长A2 H2 间期 (AHmax)消融前后无显著变化 (2 2 5 .8± 71.8msvs 175 .4± 41.9ms,P >0 .0 5 )。Ⅱ组ERP AVN消融后显著延长 (2 78.9± 5 8.9msvs 2 35 .8± 39.6ms,P <0 .0 5 ) ;AHmax消融后显著缩短 (172 .0± 6 7.1msvs 331.6± 86 .6ms ,P <0 .0 5 ) ;消融后房室结快径前传有效不应期 (ERP FP)显著缩短 (2 78.9± 5 8.9msvs 330 .0±5 5 .3ms,P <0 .0 5 )。消融前Ⅰ组AHmax短于Ⅱ组 (P <0 .0 5 ) ,Ⅰ组心动过速时A2 H2 间期 (AHSVT)与消融前AHmax比较差异无显著性 (P >0 .0 5 ) ;Ⅱ组AHSVT短于消融前AHmax(P <0 .0 5 )。结论 :房室结功能曲线连续性者较难经常规心房程序刺激诱发心动过速 ;慢径消融后曲线“尾巴”消失可作为消融终点的一项指     

房室结折返性心动过速冷冻消融术中快径有效不应期的改变

目的对冷冻消融治疗房室结折返性心动过速(AVNRT)术中快径有效不应期(FPERP)改变的生理现象进行探讨。方法对26例冷冻消融治疗AVNRT患者行术前、有效靶点冷冻消融术中及术后电生理检查,记录FPERP及AH间期的改变。结果 26例AVNRT患者冷冻消融均成功阻断慢径。共35处有效靶点消融术中可见FPERP较术前暂时性延长(386.29±67.65msvs330.29±71.80ms,P0.05),术后立即恢复(301.14±73.24msvs330.29±71.80ms,P0.05),同时AH间期术后较术前无改变(83.80±12.24msvs77.77±12.52ms,P0.2)。结论 AVNRT冷冻消融慢径术中FPERP暂时性延长,停止消融即刻恢复。     

射频消融房室交界区慢、快经区域对犬和人心房颤动时心室率的影响

本文观察经导管射频消融房室交界区慢、快径区域对大和人心房颤动时心室率的影响.方法 杂种犬4条,体重11±1.2kg.房室结折返性心动过速患者7例,年龄29～65岁.阵发性房颤患者4例,年龄62～70岁,其中2例为短P-R间期综合征.均先采用“下位法”消融慢径区域后,若房室结有效不应期或房颤时平均R-R间期无明显变化,则加行“快径”区域消融.房颤诱发采用猝发脉冲电刺激(人)或静滴氯化乙酰胆碱后猝发脉冲电刺激(犬).结果 7例房室结折返性心动过速患者中5例经下位法射频消融阻断慢径,房室结前传有效不应期及诱发房颤时平均R-R间期明显延长(222±33ms vs 285±42ms和539±44ms vs 656±53ms P<0.01),无并发症.4条大及4例阵发性房颤患者经心内电生理检查证实均无房室结双径路表现,选择性消融“慢径区域”后,房室结有效不应期和房颤时平均R—R间期无明显变化,加行“快径区域”消融后,房室结有效不应期和房颤时平均R—R间期明显延长(犬145±16ms vs 185±22ms和305±13ms vs 403±17ms P<0.01,人220ms vs 490ms和367ms vs 690msP<0.01),1例房颤患者术后3天出现Ⅲ°AVB,2周后恢复为Ⅰ°AVB.本文还在动物实验中观察到消融快径区域时,房侧靶点(A/V>1)较室侧靶点(A/V<1)更易于造成Ⅲ°AVB.结论 选择性射频消融慢径区域对减?