山东省立医院Cox迷宫手术解决术后房颤难题

日前,患有风湿性心脏病长达16年的唐凤喜女士,因长期患病后导致风心病二尖瓣狭窄合并房颤,在心脏病严重威胁生命的情况下,经山东省立医院心外科专家为其实施Cox迷宫Ⅲ型手术,彻底解决了折磨唐女士多年的风心病,并应用新术式解决了传统术式术后出现房颤的棘手问题。     

采用射频消融改良迷宫术治疗心脏房颤手术成功实施

“没想到不到一小时,医生居然为我的心脏换了瓣膜又消除了房颤,一台手术解决两个心脏疾病,效率真是高啊。”不再感到胸闷、恶心、乏力,手术后的关先生十分开心。39岁的关先生患风湿性心脏病6年了。3月23日,心脏外科为他做了二尖瓣置换、射频消融改良迷宫手术。术后关先生恢复了健康。     

窦房结功能测定与病态窦房结综合征的分型研究

随着无创性窦房结功能检查的广泛开展,使对病态窦房结综合征(SSS)的认识进一步提高,有人通过电生理检查提出,SSS可分为窦房结自身自律性降低型、窦房传导功能障碍型、及迷走神经张力过高型。有人还认为,SSS可分为器质性病变和功能障碍两种,前者为内源性,后者为外源性改变,并认为迷走神经张力过高,属功能性改变。本文通过食管心房调搏测定窦房结功能,试就SSS的电生理测定标准、分型、及临床意义进行初步探讨。1 资料与方法1.1 研究对象:本文共127例,其中男性90例,女性37例。分两组,窦性心动过缓(下     

干式双极射频消融手术治疗器质性心房颤动

目的 探讨在心脏直视手术同期采用干式双极射频消融技术治疗心房颤动的方法及其早、中期疗效.方法 2005年3月至2009年8月,共有208例心房颤动患者接受了干式双极射频消融手术治疗.其中阵发性心房颤动40例,持续性/永久性心房颤动168例.消融径线包括3种：标准Cox-Maze Ⅲ手术;改良Cox Mini-Maze手术;单纯左心房迷宫手术.结果 平均射频消融时间（7.1±3.2）min,没有与消融有关的并发症出现;9例围术期死亡;3例患者因病态窦房结综合征而于术后安置永久起搏器;1例发生脑中风及下肢栓塞,总体中风率0.5%.随访5～58个月,与同期施行的单极射频消融组相比,双极射频消融组在术后6个月、12及12个月以上的成功率均高于后者.以末次随访时间分析,阵发性心房颤动组的非心房颤动心律为92.5%,持续性/永久性心房颤动组为72.1%;3种射频消融路径组间的成功率差异无统计学意义.在末次随访中,60例患者进行了相关血流动力学检测,结果示左心房收缩功能恢复率为95.0%.结论 干式双极射频消融技术实施简便、安全,耗时短,无论是实施Cox-Maze Ⅲ手术径线,还是改良的消融术式,其近期及远期疗效满意.     

不同房颤持续时间患者之间窦房结及房室结功能的差异研究

目的 探讨不同房颤持续时间患者之间窦房结及房室结功能的差异。方法 选择2019年2月至2021年5月梅州市人民医院动态心电图房颤合并长RR间期（≥1.5 s）患者50例作为对象,根据房颤持续时间是否>48 h分为两组。≤48 h组患者行体外同步直流电复律或药物复律,>48 h组患者先进行3周抗凝后再进行复律,转为窦性心律后停用洋地黄药物及抗心律失常药物,两组均完成食管心脏电生理检测,比较两组窦房结功能、房室结前传不应期及文氏点、2∶1阻滞点。结果 ≤48 h组成功率为84.00%,高于>48 h组的64.00%(P <0.05);≤48 h组SNRT、SACT、房室结前传不应期及文氏点均短于>48 h组（P <0.05）;≤48 h组复律后房室结2∶1阻滞点<150次/min患者1例,>48 h组房室结2∶1阻滞点<150次/min患者1例,两组比较差异无统计意义（P> 0.05）;≤48 h组复律后长RR间期时间及次数短（少）于>48 h组（P <0.05）。结论 经食管心脏电生理检查用于阵发性房颤合并长RR间期...     

一种能反映窦房结功能变化的心律失常模型

<正> 现有心律失常模型多采用在体动物模型,离体心脏模型较少,主要采用工作心脏或者Langendorff心脏模型。然而,一种能直接反映窦房结起搏细胞功能变化的心律失常模型未见报道,通过摸索,我们在家兔离体心肌标本上,成功地建立了这种模型。     

心房程序刺激测定窦房结功能的临床研究

心房调搏是心脏电生理研究和诊治各种心律失常及心脏疾患的重要方法。尤其是心脏程序刺激更能提供精确的测量数据。经典的心内膜刺激法,需穿刺及切开静脉将电报导管送到右心,此为有创性方法,又需在X光下定位,故临床应用受到限制。而食道调搏法为无创性不需X光设备,无危险,操作方便,经和心内法相比较,有良好的相关性,     

动态心电图评价窦房结功能的价值探讨

动态心电图评价窦房结功能的价值探讨赵恍＊刘中梅＊刘蓉＊张瑞云＊陈兆銮＊病态窦房结综合征（病窦）是由于窦房结功能低下而使窦性心率减慢致临床上机体各主要脏器表现出供血不足的一组综合征。本文通过临床表现拟诊而行食道心房调搏术检查窦房结功能确诊为病窦的４４例...     

迷宫手术及其改良方法治疗慢性房颤的现状

心房颤动 (简称房颤 )是一种最常见的心律失常 ,约占６５岁以上的病人中３ %～５ %患有房颤 ,在接受二尖瓣手术的病人中约５０%患有房颤［１］。有研究表明 ,房颤是中风的主要原因 ,也是充血性心力衰竭的一个促进因素 ［２，３］。近２０年来 ,通过外科手术治愈房颤取得了进展 ,以迷宫手术效果最好 ,但手术比较复杂 ,在临床上推广较慢。目前 ,希望在维持迷宫手术疗效的前提下简化手术的改良方法 ,已取得了显著进展。１外科手术治疗房颤的尝试房颤治愈标准［４］:①消除房颤恢复窦性心律 ;②保持房室协调同步功能 ;③恢复心房正常血流状态且…     

Electrophysiologic effects of dextro- and levo-verapamil on sinus node and AV node function in humans

The electrophysiologic effects of dextro (d)- and levo (l)-verapamil on sinoatrial (SA) and atrioventricular (AV) node function were studied in ten patients undergoing electrophysiologic evaluation of their supraventricular tachyarrhythmias. Both isomers elicited a significant prolongation of sinus node recovery time (SNRT) and AH interval. No difference between d- and l-verapamil regarding the magnitude of the effects were observed. However, 50 mg d-verapamil was required to elicit the same electrophysiologic effects as 5 mg l-verapamil. The d- and l-verapamil plasma concentrations associated with the maximum effect on AH interval and SNRT showed a more than 20-fold difference (d: 380 ng/ml; l: 19 ng/ml). These data demonstrate that both verapamil isomers possess qualitatively similar slow channel blocking effects on the SA and AV node in humans, but the l isomer is 20 times more potent than the d isomer.     

动态心电图对窦房结功能的评估研究

目的评价动态心电图对窦房结功能的诊断价值。方法将60例窦性心动过缓患者根据阿托品试验结果分为病态窦房结综合征（病窦组）28例和单纯窦性心动过缓（单纯窦缓组）32例，比较两组动态心电图（DCG）、心率和心律失常情况；对病窦组行食管心房调搏术，分析电生理结果与DCG结果的相关性；对单纯窦缓组进行随访和复查。结果病窦组24hDCG总心率[（77460．4±2612．3）次]和平均心率[（53．8±3．2）次／min]低于单纯窦缓组[分别为（79159．5±3245．2）次、（56．1±3．7）次／min]（P〈0．05）．最高心率和最低，心率显著低于单纯窦缓组（P〈0．01）；严重窦性心动过缓、窦性停搏、窦房阻滞、交界性逸搏发生率高于单纯窦缓组（P〈0．05）；DCG间歇时间与窦房结恢复时间（SNRT）间存在明显的正相关（r=0．56，P〈0．05）。单纯窦缓组有8例DCG符合病窦，随访3～6年后，均诊断病窦。结论DCG检测窦房结功能敏感性高，有助于诊断慢快综合征和双结病变，对DCG窦房结功能异常者，宜作长期随访。     

Electrophysiological effects of intravenous clonidine on sinus node function and conduction in man

We studied the electrophysiological effects of clonidine in 10 patients (mean age, 69 years) without sinus dysfunction or atrioventricular block. An endocavitary study was performed with two multipolar catheters, one to record and stimulate the right atrium, the other to record the His bundle potential. The stimulations were delivered by an orthorhythmic stimulator. Clonidine, 150 micrograms, was injected intravenously over 10 min. The usual electrophysiological parameters for studying atrioventricular conduction and sinus function were measured under basal conditions, between the 10th and 25th min, and between the 25th and 40th min following the onset of the injection of clonidine. Sinus cycle length, maximum corrected sinus node recovery time, estimated atrio-sinoatrial conduction time, and premature atrial stimulation-response curve were not influenced by clonidine. There were also no changes in conduction interval, anterograde conduction point, effective refractory period of the atrioventricular node, and intraventricular conduction time. We conclude that intravenous clonidine does not change the electrophysiological parameters in man.     

Effects of intravenous diltiazem on sinus node function and atrioventricular conduction in patients

We studied the electrophysiologic effects of injectable diltiazem (dosage: bolus of 0.15 mg/kg, maintenance infusion of 0.3 mg/kg/h for 20 min) on sinus node function and atrioventricular function in 33 patients (22 men and 11 women, mean age 63.6 +/- 15.8 years). Seventeen patients had an electrophysiological exploration considered as normal, eight had sinus node dysfunction (corrected sinus recovery time greater than 525 ms), and eight had AV nodal block (PH greater than 160 ms and/or a Wenckebach point less than 125/min). Effects of the drug were assessed 20 min after the beginning of the infusion, which was continued until the end of examination. In normal subjects diltiazem lengthened corrected sinus node recovery time (305 +/- 115 ms leads to 451 +/- 283 ms) and slightly depressed AV nodal conduction (Wenckebach point: 163 +/- 23 leads to 147 +/- 25). In patients with sinus node dysfunction diltiazem provoked a bradycardia without significant changes in corrected sinus node recovery time or in estimated atrio-sino-atrial conduction time. In patients with AV nodal block diltiazem provoked a lowering of the Wenckebach point (137 +/- 47 leads to 122 +/- 38). There was no effect on hissian or infrahissian conduction, even when this was abnormal in the basal state. These data suggest that diltiazem must be utilized with caution in patients with sinus node dysfunction and AV nodal block.     

Electrophysiologic effects of intravenous nicardipine on sinus node function and conduction in humans.

We conducted an intracardiac study of the electrophysiologic effects and kinetics of intravenous nicardipine (N) in 16 patients with or without impaired cardiac conduction, using a randomized, double-blind, crossover design versus placebo (P). N or P were infused intravenously over 5 min: the dose of N was 9.46 +/- 3.85 mg. Standard electrophysiologic parameters of atrioventricular (AV) conduction and sinus function were measured under basal conditions, between 10 and 25 min, and at 65 min, after beginning the first infusion of N or P, and between 10 and 25 min after beginning the second infusion of N or P. Treatment with N significantly reduced systolic (S) and diastolic (D) blood pressure (BP) at 10 min (35 +/- 19 and 25 +/- 17 mm Hg, respectively). N significantly shortened sinus cycle length (SCL), corrected sinus recovery time (CSNRT), AH interval, AV node (AVN) Wenckebach cycle length, and anterograde and retrograde effective (ERPs) and functional refractory periods (FRPs) of the AVN. Infranodal parameters were unaffected. Mean plasma N concentrations at 10 min were 18.5 +/- 7.7 ng/ml/kg and 5.3 +/- 3 ng/ml/kg at 60 min. Two patients experienced slight adverse effects (anginal pain and nausea); another with sick sinus syndrome developed a sinus pause. We conclude that intravenous N affects nodal, but not His conduction, and that it should be administered with care in the presence of SSS.     

心脏瓣膜置换术中同期射频消融迷宫手术治疗心房纤颤的效果

目的：探讨心脏瓣膜置换术中同期进行射频消融迷宫术治疗心房纤颤（房颤）的临床效果。方法38例合并房颤的风湿性心脏瓣膜病患者行瓣膜置换时,采用Atricure双极射频消融系统,按照迷宫手术线路进行射频消融术。其操作包括肺静脉隔离、左心耳切除、M arshall韧带切断和右房消融。结果38例患者均顺利完成射频消融,操作时间（33.2±6.8） min ,增加主动脉阻断时间（16.1±3.0） min。33例（86.8％）患者术中恢复窦性心律。术后随访3‐18个月,30例（78.9％）患者仍维持窦性心律。结论心脏瓣膜置换术中同期进行射频消融迷宫术治疗房颤安全、有效。     

胰腺癌淋巴结转移的特性及手术治疗

淋巴结转移是胰腺癌转移的主要方式,也是影响预后的重要因素。本文回顾胰头癌淋巴结转移发生的可能途径和转移特性,着重讨论胰头癌淋巴结手术清扫的范围和利弊,目前有关淋巴结清扫的争议、详尽的淋巴结获取分析和准确度肿瘤分期以及更积极的多学科肿瘤治疗是将来胰腺外科努力的发展方向。     

Effect of histamine in sinus node arrested with reserpine

Summary Histamine restored spontaneous activity in the isolated rabbit sinus node arrested with reserpine. This fact suggests that catecholamines are not the unique activators of adenylate cyclase required for cardiac pacemaking, and may be replaced by histamine.     

The sinus node inhibitor UL-FS 49 lacks significant inotropic effect.

UL-FS 49 is a sinus node inhibitor that has been reported to reduce heart rate and may be useful in improving myocardial oxygen supply vs. demand. However, previous studies performed in a variety of preparations have produced mixed results regarding the independent inotropic effect of UL-FS 49. To determine whether UL-FS 49 has an inotropic effect, we measured both steady-state hemodynamic responses and transient hemodynamic responses to random preload and afterload changes, both with and without UL-FS 49. We found that under steady-state conditions, the effect of UL-FS 49 is so small that it would be of doubtful physiologic significance: a 3% increase in stroke volume (p = 0.007) and 7% increase in peak positive dP/dt (p = 0.051), in the presence of no statistically significant differences in end-diastolic pressure, end-diastolic volume, peak systolic pressure, end-systolic pressure, or heart rate. The more powerful multiple linear regression modeling of hemodynamic transient sequences resulting from random preload and afterload changes showed that UL-FS 49 is without a statistically significant direct effect on left ventricular function. We conclude that UL-FS 49 has no physiologically important direct effect on left ventricular pump function.     

Bradycardic and proarrhythmic properties of sinus node inhibitors

Sinus node inhibitors reduce the heart rate presumably by blocking the pacemaker current If in the cardiac conduction system. This pacemaker current is carried by four hyperpolarization-activated, cyclic nucleotide-gated cation (HCN) channels. We tested the potential subtype-specificity of the sinus node inhibitors cilobradine, ivabradine, and zatebradine using cloned HCN channels. All three substances blocked the slow inward current through human HCN1, HCN2, HCN3, and HCN4 channels. There was no subtype-specificity for the steady-state block, with mean IC50 values of 0.99, 2.25, and 1.96 microM for cilobradine, ivabradine, and zatebradine, respectively. Native If, recorded from mouse sinoatrial node cells, was slightly more efficiently blocked by cilobradine (IC50 value of 0.62 microM) than were the HCN currents. The block of I(f) in sinoatrial node cells resulted in slower and dysrhythmic spontaneous action potentials. The in vivo action of these blockers was analyzed using telemetric ECG recordings in mice. Each compound reduced the heart rate dose-dependently from 600 to 200 bpm with ED50 values of 1.2, 4.7, and 1.8 mg/kg for cilobradine, ivabradine, and zatebradine, respectively. beta-Adrenergic stimulation or forced physical activity only partly reversed this bradycardia. In addition to bradycardia, all three drugs induced increasing arrhythmia at concentrations greater than 5 mg/kg for cilobradine, greater than 10 mg/kg for zatebradine, or greater than 15 mg/kg for ivabradine. This dysrhythmic heart rate is characterized by periodic fluctuations of the duration between the T and P wave, resembling a form of sick sinus syndrome in humans. Hence, all available sinus node inhibitors possess an as-yet-unrecognized proarrhythmic potential.