犬右房不同部位Kv4.3、KchIP2、Cav1.2 mRNA的表达

目的研究犬右房不同部位短暂外向钾电流、L型钙电流亚单位mRNA的表达情况,探讨其在致房性心律失常中的意义。方法应用逆转录-聚合酶链反应半定量分析犬界嵴、梳状肌、右心耳的短暂外向钾电流α亚单位(Kv4.3)、β亚单位(KchIP2)及L型钙电流的α亚单位(Cav1.2)mRNA的表达量(以β-actin为内参照)。结果界嵴和梳状肌Kv4.3、KchIP2 mRNA高于右心耳(P<0.05或0.01);界嵴Cav1.2 mRNA高于梳状肌和右心耳(P均<0.05),而梳状肌和右心耳之间没有差异。结论Kv4.3、KchIP2、Cav1.2 mRNA在右房空间表达上的差异与其相应离子流在右房空间上的差异一致,可能是其离子流差异的分子基础。     

左室特发性室性心动过速折返路径标测和消融点的选择

报道 1 0例 (男 8、女 2 )左室特发性室性心动过速 (简称室速 )折返路径标测结果和选择折返路径的不同部位为消融点的消融效果。电生理检查常规插入右室心尖与冠状静脉窦电极 ,并经左、右股动脉分别插入大头电极和2 8 2mm间距冠状静脉窦 1 0极标测电极至左室 ,后者贴靠在室间隔表面。窦性心律时各电极对可依次记录到His束电位 (HP)、左束支电位 (LBP)和左后分支的蒲氏纤维电位 (PP) ,室速时仍可同时记录到上述各电位 ,但顺序相反 ,PP领先 ,HP最后 ;而各部位的V波激动顺序在窦性心律和室速时是相同的 ,都是远端电极 (PP以远 )的V波最早 ,近端电极 (HP)的V波最晚。大头电极置于PP电极对附近。结果 :1 0例中 9例能记录到折返路径各电位心内电图 ,折返路径记录成功率为 90 % ( 9/1 0 )。第 1例大头电极位于PP电极对略上方处放电 ,消融成功 ,但导致完全性左束支阻滞。第 2 ,3例开始在PP电极对略下方处放电 ,但凡未记录到PP的点 ,虽然V波最早 ,都是放电无效点。最后消融成功的点 ,都记录到最领先的PP。第 4例以后 ,都必须记录到最领先的PP后才放电 ,除 1例 2次放电成功外 ,都是 1次放电成功。 1 0例随访至今 3～ 1 8个月 ,未服任何抗心律失常药均无室速发作。结论 :左室标测法不仅对研究左室特发性室速的折返     

Zearalenone alters the excitability of rat neuronal networks after acute in vitro exposure

Zearalenone (ZEA) is a mycotoxin produced by Fusarium species, detectable in various cereals and processed food products worldwide. ZEA displays a significant estrogenic activity, thus its main health risk is the interference with sexual maturation and reproduction processes. However, in addition to being key hormonal regulators of reproductive function, estrogenic compounds have a widespread role in brain, as neurotrophic and neuroprotective factors, and they may influence the activity of several brain areas not directly linked to reproduction, as well. Therefore, in the present study, acute effects of ZEA were studied on certain neuronal functions in rats.Experiments were performed on rat brain slices or live rats. Slices were incubated in ZEA-containing (10–100 μM) solution for 30 min. Electrically evoked and spontaneous field potentials were studied in the neocortex and in the hippocampus. At higher concentrations, ZEA incubation of the slices altered excitability and the pattern of epileptiform activity in neocortex and inhibited the development of LTP in hippocampus.For the verification of these in vitro results, in vivo electrophysiological and immunohistochemical investigations were also performed. ZEA was administered systemically (5 mg/kg, i.p.) to male rats and somatosensory evoked potentials and neuronal activation studied by c-fos expression were analyzed. No neuronal activation could be demonstrated in the hippocampus within 2 h of the injection. In the somatosensory cortex, ZEA did not change in vivo evoked potential parameters, but the activation of a small neuronal population could be demonstrated with the c-fos technique in this brain area. This result could be associated with the ZEA-induced alteration of epileptiform activity observed in vitro.Altogether, the toxin altered the excitability and plasticity of neuronal networks after direct treatment in slices, but the effects were less prominent on the given brain areas after systemic treatment in vivo. A probable explanation for the partial lack of in vivo effects may be that after a single injection, ZEA did not cross the blood-brain barrier at sufficient rate to allow the build-up of comparable concentrations in the investigated brain areas. However, in case of compromised blood-brain barrier functions or long-term repeated exposure, alterations in cortical and hippocampal functions cannot be ruled out.     

起源点邻近二尖瓣环的频发室性早搏体表心电图特征及射频消融治疗

目的评估起源点邻近二尖瓣环的频发室性早搏(简称室早)体表心电图特点及射频消融治疗效果。方法10例频发室早患者接受常规电生理检查及射频消融治疗,对所有病例12导联体表心电图进行分析。结果10例室早均消融成功,并证实起源点邻近二尖瓣环的不同部位,根据成功消融靶点将本组病例分为3组,二尖瓣环前侧壁组(4例)、二尖瓣环后侧壁组(3例)、二尖瓣环后间隔组(3例)。所有病例胸前导联R波移行区位于V1～V2导联,绝大部分病例V6导联可见s波。对各组二尖瓣环室早心电图做进一步比较,可概括出系列心电图判断指标用以估计消融靶点的部位。结论射频消融治疗起源点邻近二尖瓣环的频发室早可取得良好效果,掌握其体表心电图特点有助于判定室早的起源部位。     

冷冻消融慢径治疗房室结折返性心动过速的初步临床应用

为探讨冷冻消融治疗房室结折返性心动过速(AVNRT)的疗效、安全性及其方法。对13例AVNRT行冷冻消融慢径,用-30℃冷冻粘附后行冷冻标测,确定有效靶点且无快径损伤后,立即进行-75℃冷冻消融,消融240～300s,消融过程中密切观察房室结传导功能,一旦发现有房室结损伤,立即终止消融,改换靶点。结果:13例,均获成功,随访1～9个月,无复发;在-30℃冷冻标测时,冷冻消融导管头端与靶点冷冻粘附,无位移现象;冷冻消融过程中无结性早搏或结性心律出现;1例在冷冻标测,另1例在冷冻消融过程中出现一过性房室阻滞,立即停止冷冻后复温,即刻传导恢复。无其它并发症发生。结论:冷冻消融是治疗AVNRT的有效方法,并能降低永久性房室阻滞的风险。     

Slow pathway catheter ablation of atrioventricular nodal re-entrant tachycardia guided by electroanatomical mapping: a randomized comparison to the conventional approach.

BACKGROUND: Electroanatomical mapping may be expected to improve safety, efficiency and efficacy of selective slow pathway ablation for atrioventricular nodal re-entrant tachycardia (AVNRT). The goal of this prospective randomized study was to compare the efficiency of conventional fluoroscopic and electroanatomical mapping in guiding catheter ablation of AVNRT. METHODS AND RESULTS: Following induction of typical AVNRT, 20 consecutive patients were randomized to either conventional fluoroscopic or electroanatomical (CARTO) mapping to guide slow pathway ablation using a 4mm electrode. Endpoints for ablation were non-inducibility and no more than a single AV nodal echo on aggressive retesting. Acute procedural success was 100% in both groups, with no complications. Although there were no differences in time taken for pre- and post-ablation electrophysiological evaluations, in the electroanatomical group the ablation portion of the procedure showed a substantial reduction in duration (12.6+/-6.8 vs 35.9+/-18.3 min; P< 0.001) and fluoroscopic exposure (0.7+/-0.5 vs 9.6+/-5.0 min; P< 0.001) compared with the fluoroscopic group, reflected in reduced total procedure time (83.6+/-23.6 vs 114+/-19.3 min; P=0.008) and total fluoroscopic exposure (4.2+/-1.4 vs 15.9+/-6.4 min; P< 0.001). Electroanatomical mapping was associated with a lower number (2.7+/-1.6 vs 5+/-2.8; P=0.018), duration (165.3+/-181.6 vs 341+/-177.7s; P=0.013), and total energy delivery (24.3+/-3.1 vs 28.7+/-4.5 watts; P=0.042) of RF applications. There were no acute or long-term (8.9+/-2.2 month) complications or arrhythmia recurrence in either group. CONCLUSIONS: While both conventional and non-fluoroscopic electroanatomical mapping are associated with excellent results in guiding ablation of typical AVNRT, the latter offers significantly shorter procedure and fluoroscopy times, improving the efficiency of the procedure and reducing X-ray exposure.     

射频消融房室结改良消融前后心脏电生理变化的探讨

目的比较房室结双径路伴房室结内折返性心动过速(AVNRT)患者,射频消融(RFCA)慢径路改良术,消融前、后心脏各部分腔内电生理改变。方法在相同条件下,于消融前、后分别进行腔内电生理检查。记录消融前、后:希氏束电图(HIS),心房有效不应期(A—ERP),功能不应期(A—FRP),心室有效不应期(V—ERP),功能不应期(V—FRP),房室结前传有效不应期(AVN—ERP),前传文氏点(AVN—WKB),房室结逆传有效不应期(VAN—ERP),逆传文氏点(VAN—WKB),将消融前、后心脏各部分电生理参数进行配对,经SPSS统计分析软件进行T检验分析。结果消融前、后:HIS电图,A—ERP,A—FRP,V—ERP,V—FRP,AVN—ERP,及VAN—WKB均无显著差异(P>0.05)。AVN—WKB,VAN—ERP有显著差异(P<0.05)。讨论射频消融房结改良对房室结双径路AVNRT疗效肯定。在消融前、后(急性期)房室结前、逆传电生理均有一定改变。这与消融改变了房室结的部分结构,如大部分病列慢径路消失有关。不同消融部位对房室结传导电理改变产生不同的结果。没有证据表明消融后,45岁以上年龄组房室结传导改变大于45岁以下年龄组。男女不同性别组之间亦无差异。     

伊布利特对人体心房与心室电生理特性的影响

探讨伊布利特对人体右房、左房及右室有效不应期(RA-ERP、LA-ERP及RV-ERP)与房间、室间传导时间的影响。测定25例射频消融术后患者于静脉推注伊布利特(0.0167mg/kg)前后在基础起搏周长为600ms时的RA-ERP、LA-ERP及RV-ERP,同时测量起搏与窦性心律时的心房、心室传导时间。其中通过起搏冠状静脉窦远端间接起搏左房。结果:①伊布利特明显延长RA-ERP、LA-ERP及RV-ERP(P均<0.001)。②使用伊布利特后,对窦性心律时的P波宽度、PR间期、QRS时限、AH及HV均无明显影响(P>0.05),对房间及室间传导时间无明显影响(P>0.05),亦对急性期的起搏阈值无明显影响(P>0.05)。③使用伊布利特后2例出现右束支阻滞。结论:伊布利特可明显延长RA-ERP、LA-ERP及RV-ERP,但不影响房间、室间传导时间。     

Supraventricular arrhythmias limit effective cardiac resynchronization therapy: Diagnosis using intracardiac electrograms and device based pacing maneuvers

Cardiac resynchronization therapy is an effective tool for the treatment of drug-refractory heart failure in patients with left ventricular dysfunction and inter/intra ventricular conduction delay. Supraventricular tachycardias may prevent effect delivery of this therapy. We report three cases in which effective therapy was limited by asymptomatic supraventricular tachycardia. Diagnostic pacing maneuvers were performed via the implanted device to determine the underlying arrhythmia mechanism. These cases highlight the importance of (1) treating supraventricular tachycardias before and after implantation of cardiac devices and (2) using device based programmed stimulation to diagnose the mechanism of supraventricular tachycardias. Dr. Gerstenfeld is supported by a Scientist Development Grant from the American Heart Association.