特发性室性心动过速射频消融治疗的临床研究

射频消融３１例特发性室性心动过速（ＩＶＴ）,对其定位、标测方法及复发原因进行探讨。采取激动和（或）起搏标测结合的方法进行标测和消融治疗。结果：右室ＩＶＴ１３例。起源于流出道部位１２例,其Ｉ导联以Ｑ波为主者偏前,ｒ波为主者偏后;Ｖ３导联的Ｒ／Ｓ＞１者在上部,Ｒ／Ｓ＜１者在下部。游离壁１例电轴左偏。起搏标测靶点心电图ＩＶＴ时与１２导联心电图一致,局部电位提前４２．０８±８．９１ｍｓ。１例术后复发。左室ＩＶＴ１８例。起源间隔者１４例,随着起源点从基底部向心尖部移行,电轴更右偏;游离壁４例电轴明显左偏。靶点局部电图均提前３２．１９±８．３６ｍｓ。左室间隔部ＩＶＴ记录到浦肯野纤维电位（ＰＰ）７例、异常电位（ＡＰ）４例;１例未记录到ＰＰ及ＡＰ且起搏标测１０导联心电图一致,术后复发。２例未诱发ＩＶＴ,均以起搏标测消融成功。左室游离壁起搏标测１２导联心电图一致３例,１１导联一致者１例且术后复发。３例４例次复发,１例（左室间隔ＩＶＴ）未再接受消融治疗,２例最终采用温控导管消融成功。结论：体表心电图对ＩＶＴ起源点定位有指导意义;激动标测与起搏标测相结合的方法更好。     

右室流出道特发性室速的射频消融治疗体会

目的 总结不同起源部位特发性右室流出道室性心动过速（ＩＲＶＯＴ）经导管射频消融（ＲＦＣＡ）治疗的方法和结果。方法 对３５例ＩＲＶＯＴ进行ＲＦＣＡ治疗,男性１８例、女性１７例,平均年龄（３９．１±１８．３）岁（８～７２岁）。其中１５例用常规方法消融,２０例用非常规方法消融,非常规方法加用８Ｆ ＳＢ０ Ｓｗａｒｔｚ鞘并在右室流出道放置参考电极。两者均采用起搏与激动标测来确定消融靶点。结果ＲＦＣＡ治疗ＩＲＶＯＴ的总成功率为８８．６％（３３／３５）,常规方法组成功率为８６．７％,复发率为１５．３％,非常规方法组分别为９０．１％和５．６％;常规方法组的导管操作时间为（７１±１２）ｍｉｎ,Ｘ线曝光时间平均为（３２±８）ｍｉｎ,非常规组分别为（４０± ９）ｍｉｎ和（１６ ±５）ｍｉｎ。ＩＲＶＯＴ起自右室流出道近间隔部１３例、游离壁１０ 例及介于两者之间 １２例。成功消融部位激动标测 Ｖ波提前 ＱＲＳ波 １８～３８ｍｓ,起搏标测与心动过速时１２导联心电图（ＥＣＧ）之ＱＲＳ波形态完全相同。结论ＩＲＶＯＴ非常规方法消融可以明显缩短导管操作时间、减少Ｘ线曝光时间及降低复发率;ＩＲＶＯＴ采用ＲＦＣＡ治疗具有较高的成功率和较低的复发率及并发症。     

特发性室性心运过速射频消融治疗的临床研究

射频消融３１例特发性室性心动过速（ＩＶＴ），对其定位、标测方法及复发原因进行探讨。采取激动和（或）起搏标准结合的方法进行标测和消融治疗。结果：右室ＩＶＴ１３例．起源于流出道部位１２例，其Ｉ导联以Ｑ波为主者偏前，ｒ波为主者偏后：Ｖ３导联的Ｒ／Ｓ〉１者在上部，Ｒ／Ｓ〈１者在下部。游离壁１例电轴左房。起搏标测靶点心电图ＩＶＴ时与１２导联心电图一致，局部电位提前４２．０８±８．９１ｍｓ。１例术后复发。左室     

射频消融特发性室性心动过速的标测方法初探（附五例分析）

５例特发性室性心动过速（ＶＴ）经射频电流导管消融（ＲＦＣＡ）而获治愈。本文从成功的ＲＦＣＡ结果着重探讨特发性ＶＴ兴奋灶的标测方法。心内膜激动时间标测，以局部电图较体表导联ＱＲＳ波时间提前≥１０ｍｓ处定为心室最早激动点（ＥＶＡ），５例平均心室最早激动至ＱＲＳ波起始时间为１８±１１．７ｍｓ，在ＥＶＡ处放电消融仅１例成功。采用起搏标测法定位以略低于自发ＶＴ的频率沿ＥＶＡ上下左右逐点标测，寻找起搏电图至少１１个导联的ＱＲＳ波形态、振幅、极性与自发ＶＴ相同的标测点放电消融，４例均获成功。消融成功的局部电图较ＱＲＳ波平均提前２６±１２．８ｍｓ。结果提示联合应用心内膜激动时间标测和起搏标测并侧重于后者，可能是提高ＲＦＣＡ特发性ＶＴ成功率的一种有效方法。     

射频消融术治疗特发性室性心动过速的临床分析

总结射频消融术治疗特发性室性心动过速（简称室速）２７例。左室特发性室速１７例均消融成功，其中１６例采用标测Ｖ波前最早Ｐ电位（浦肯野纤维电位）的方法；１例采用起搏标测的方法，成功靶点处均在左室间隔部。１例复发，再次消融成功。对１０例右室特发性室速采用起搏标测和激动标测的方法，其中８例消融成功，成功靶点７例在右室流出道、１例在流入道部位。成功８例中２例复发或再发，１例复发后电生理检查不能诱发室速，无法消融；１例再发左室室速，再次消融成功。２７例中１例出现静脉炎并发症。以上结果表明射频消融术是治疗特发性室速的安全有效方法。     

射频消融治疗特发性室性心动过速

１２例特发性室性心动过速（室速）病人，７例为左室室速，５例为右室空速，采用激动标测和起搏标测方法，左室室速在室间隔中下部，右室室速在右室流出道寻找消融靶点。结果７例左室室速成功６例，局部激动Ｖ波较体表。Ｃ电图ＱＲＳ波提前２５～５０ｍｓ。右室室速５例全部消融成功，Ｖ波提前２０～４０ｍｓ。消融术程１～４小时，Ｘ线曝光时间３０±２４分钟。无１例出现并发症。     

射频消融治疗儿童特发性室性心动过速

本文报道应用射频消融术治疗6例儿童特发性室性心动过速（IVT）男1例，女5例，平均年龄8.5岁（4－14.5岁）。临床检查排除器质性心脏病.VT起源于左室间隔部4例．起源于右室流出道2例；选用温控消融导管，4例采用起搏标测结合激动顺序标测，于VT发作时放电，2例采用起搏标测，于窦性心律时放电；6例消融均成功。平均随访12．8个月（1－22个月），1例术后第4周复发，第5周于同一部位再次消融成功。无并发症发生。结果表明射频消融治疗儿童IVT是有效、安全的。     

主动脉右冠窦起源室性心律失常患者的电生理特征及射频消融效果

目的探讨主动脉右冠窦(RCC)起源的室性心律失常(VAs)患者的心电生理特征和射频消融疗效。方法入选2008年1月~2016年8月经电生理检查及射频消融证实起源于RCC的27例患者,分别在右室流出道(RVOT)、主动脉根部和左室流出道行激动顺序标测和起搏标测,分析其体表心电图特征,右室流出道标测电生理特点,成功消融靶点处电位特征及射频消融的疗效。结果Ⅰ导联R波振幅较高(0.52±0.35 m V)提示VAs起源于RCC可能。RCC起源VAs在右室流出道标测最早激动点(EAS)位于中后间隔,74.1%(20/27)的患者RVOT EAS处及周围表现为双电位或复合电位,RVOT激动自中间隔向上、下传导,Carto系统测量右室流出道EAS距离希氏束(26.3±4.4)mm。75.0%(6/9)的患者在RVOT最早点处放电消融一过性有效,最终24例(88.9%)成功消融靶点位于RCC前上缘,3例(11.1%)成功靶点位于右窦瓣下。结论 RCC起源VAs在RVOT和RCC标测时具有特征性电位,RVOT EAS处放电可一过性有效,大部分在RCC前上缘消融成功,少数需在瓣下消融始能成功。     

房性心动过束电生理机制,标测和射频消融方法的临床研究

目的 探讨房性心动过速（房速）的电生理学机制、靶点标测和射频消融治疗结果，方法 ４４例房速患者行心内电生理检查和射频消融术，房速靶点标测采用激动标测方法，４例用非Ｘ线心脏磁电解剖学标测系统（ＣＡＲＴＯ系统）标测和指导消融。右心房用两根大头消融导管交替移植标测寻找靶点，采用预设６０～６５℃温控放电消融。结果 经电生理检查证实４４例房速中１１例为自律性房速，３３例为非自律性房速。４０例（９１％）射频消     

导管射频消蚀术治疗特发性室性心动过速（附五例报告）

导管射频消蚀术（ＲＦＣＡ）治疗特发性室性心动过速（ＩＶＴ）５例。其中ＩＶＴ起源于左室间隔区３例，右室流出道２例。４例在ＩＶＴ发作中于室内标测到较体表ＱＲＳ波提早３０～５０ｍｓ的局部电位，在此点给予射频电流，ＩＶＴ即刻终止；１例ＩＶＴ行起搏标测，在左室中间隔区标测到与ＩＶＴ时１２导联相同的ＱＲＳ波群，在该部位给予射频电流。全部病例术后停用各种抗心律失常药物，随访１～４个月，无ＩＶＴ复发，无并发症，表明ＲＦＣＡ是根治ＩＶＴ安全有效的方法。     

Erythropoiesis Inhibiting Factor(s) (EIF)

The specificity and toxicity of the urinary erythropoiesis inhibiting factor (EIF) has been tested both in vivo and in vitro. When EIF was given to ESF stimulated erythropoietically suppressed polycythaemic mice and to mice at maximal endogenous erythropoietic stimulation, a reduction of the erythroid bone marrow cells, the erythropoietic ³H-TdR L.I. and the total number of bone marrow cells were observed. No effect was seen on the myelopoietic bone marrow cells. An unspecific toxic effect was unlikely, since addition of EIF did not alter the proliferation of lymphoblastic cells nor change the glucose utilization of bone marrow cells in vitro. Neither did the amount of dead bone marrow cells increase after being incubated with EIF for 72 h. The results indicate that the urinary EIF is a non-toxic, cell specific inhibitor on erythropoiesis.     

脂蛋白（a）和载脂蛋白（a）多态性与女性冠心病的相关性研究

冠心病（ＣＨＤ）在病因、发病年龄等诸多方面存在性别差异。载脂蛋白（ａ）［ａｐｏ（ａ）］多态性与脂蛋白（ａ）［Ｌｐ（ａ）］血浆水平对女性ＣＨＤ影响的资料甚少。我们通过检测３５例女性ＣＨＤ患者和４５例女性正常对照者的ａｐｏ（ａ）多态表型及Ｌｐ（ａ）水平，并与相应的男性组对比分析，发现含有等位基因Ｓ１、Ｓ２、Ｂ的ａｐｏ（ａ）低分子量表型的ＣＨＤ患者，女性占３７．１４％，显著高于对照组，而男性仅占２５．７１％，与对照组比较差异无显著性。在女性中低分子量表型发生ＣＨＤ危险度为对照组的４．７倍，在男性中仅为１．４倍。提示：低分子量表型对女性ＣＨＤ的影响大于男性。Ｌｐ（ａ）水平在两性ＣＨＤ组均明显高于对照组，而两性之间则差异无显著性。     

Compound heterozygosity of Hb D(Iran) (beta(22) Glu-->Gln) and beta(0)-thalassemia (619 bp-deletion) in India

The present report describes the hematologic and molecular study of the second case of Hb D(Iran) associated with beta(0)-thalassemia (619 bp-deletion) found in India and the first case in which the mutations have been identified at molecular level. The patient showed hypochromic, microcytic red cell picture with reduced red cell indices. The characterization of the hemoglobinopathy was made by electrophoretic and chromatographic techniques and confirmed by sequencing of the beta-globin gene. Both the propositus and her father were found to be carriers of the gene for beta(0)-thalassemia owing to the 619 bp-deletion mutation as seen by the polymerase chain reaction (PCR). Single base substitution GAA > CAA (indicative of Hb D(Iran)) in the heterozygous form was seen in the propositus as well as the mother by sequencing.     

Fibrodysplasia (myositis) ossificans progressiva (FOP)

Clinical Rheumatology -     

Platelet HDL(3) binding sites are not related to integrin alpha(IIb)beta(3) (GPIIb-IIIa)

Early studies considered that fibrinogen receptor (glycoprotein [GP] IIb-IIIa or platelet integrin alpha(IIb)beta(3)) is the binding site for low-density lipoprotein (LDL) and high-density lipoprotein type 3 (HDL(3)). Recent data, however, do not support the hypothesis that the binding of LDL to human intact resting platelets is related to integrin alpha(IIb)beta(3). In this study we present evidence that platelet integrin alpha(IIb)beta(3) is also not involved in the interaction of HDL(3) and human intact resting platelets. Firstly, specific ligands for platelet integrin alpha(IIb)beta(3), such as fibrinogen, vitronectin, von Willebrand factor and fibronectin, were unable to inhibit the binding of HDL(3) to intact resting platelets. Secondly, the HDL(3) binding characteristics (K(d) and B(max) values), the activation of protein kinase C (PKC) and the inhibition of thrombin-induced inositoltriphosphate (IP(3)) formation and calcium (Ca(2+)) mobilization mediated by HDL(3) particles were similar in platelets from control subjects and patients with type I and type II Glanzmann's thrombasthenia, which are characterized by total and partial lack of GPIIb-IIIa and fibrinogen, respectively. In contrast, nitrosylation of tyrosine residues of HDL(3) by tetranitromethane fully abolished both the ability of particles to interact with its specific binding sites and the functional effects. Thirdly, polyclonal antibodies against the GPIIb-IIIa complex (edu-3 and 5B12), human antiserums against platelet alloantigens (anti-Bak(a/B) and anti-PL(A1/2)), anti-integrin subunits (anti-alpha(V) and anti-beta(3)), and a wide panel of monoclonal antibodies (mAbs) against well-known epitopes of GPIIb (M3, M4, M5, M6, M8 and M95-2b) and GPIIIa (P23-7, P33, P37, P40, and P97) did not affect the binding of HDL(3) particles to human intact resting platelets. Overall results show that neither the GPIIb-IIIa complex nor GPIIb or GPIIIa individually are the membrane binding proteins for HDL(3)on intact resting platelets.