经冠状动脉化学消蚀法心肌病理改变及其发生机理

本实验观察22条犬经冠状动脉注射96％乙醇后心肌病理改变及其发生机理,结果实验犬经冠状动脉注射乙醇后均出现不同程度的心肌坏死及冠状动脉内血栓形成.提示心肌损伤可能由乙醇对心肌组织的直接作用和乙醇使冠状动脉内皮损伤,进而使血栓形成,心肌缺血两方面原因所致,急性期内心肌坏死可能以前者为主,晚期则以后者为主。     

Transcoronary ethanol ablation of experimental ventricular tachycardia after epicardial ice mapping and localizing.

Thirty-seven reproducible ventricular tachycardias (VTs) were induced in 19 dogs after the onset of myocardial infarction. The site of origin of VT was localized in 19 (59%) of 32 VTs by ice epicardial mapping. After 0.3-1.2 ml of 95% ethanol was injected into a small coronary artery supplying the arrhythmogenic area, VT was no longer inducible in 10 of 14 dogs. Intramyocardial ethanol (1-3 ml) was injected into the site of origin of VT in 9 dogs including 4 with VTs reinduced after intracoronary ethanol. Six of these VTs were not reinduced. Thus, the total efficacy rate was 84%. In 7 dogs, after injection of 0.4-1.2 ml (mean 0.5 ml) of 95% ethanol into a small normal coronary artery, the extent of the changes in ECG, CK-MB and pathology was found to be related to the size of myocardial damage and to the dose of ethanol. The smaller the dose of ethanol was given and the more distal the branch of coronary artery into which the ethanol was injected, the smaller the myocardial damage was. The data demonstrated that intracoronary or intramyocardial injection of ethanol may ablate the experimental VT induced by programmed heart stimulation in dogs after myocardial infarction, indicating that this approach may be useful and meaningful in some selected instances. However, it is necessary to limit the myocardial damage as far as possible.

     

碱性成纤维生长因子对急性心肌梗死血管生成和碱性成纤维生长因子及血管内皮生长因子表达的作用

目的探讨心肌内注射碱性成纤维生长因子(bFGF)对急性心肌梗死(MI)血管生成和bFGF、血管内皮生长因子(VEGF)表达的作用。方法24只犬建立急性MI模型后随机分成对照组(MI区注射生理盐水15ml)和实验组(MI区注射50mg bFGF与生理盐水的混合液15ml)。每组观察4个不同的时间点(术后第1天、第3天、第10天、第17天)。各组分别在处死前应用敏感编码技术行磁共振电影成像。免疫组织化学方法检测各组心肌细胞中bFGF和VEGF的表达及微血管数量。结果实验组左心室射血分数自第10天明显增加;除第1天外各个时间点的微血管数量实验组比对照组明显增多;心肌缺血区对照组bFGF和VEGF的表达增多。结论局部心肌内注射bFGF有促进MI区域毛细血管形成及提高左心室功能的作用。     

ω-3鱼油脂肪乳对乌头碱诱发大鼠心律失常的影响

目的探讨ω-3鱼油脂肪乳对乌头碱诱发大鼠心律失常的影响及相关机制。方法 50只雄性大鼠随机分为ω-3鱼油脂肪乳组和对照组,每组25只。实验前15 d,ω-3鱼油脂肪乳组大鼠隔日经尾静脉注射ω-3鱼油脂肪乳2 mL.kg-1;对照组注射等量的生理盐水。应用乌头碱诱发心律失常大鼠模型,观察记录2组大鼠室性期前收缩、室性心动过速出现的时间及心律失常评分,Western blot检测大鼠心肌组织缝隙连接蛋白43(CX43)的表达。结果ω-3鱼油脂肪乳组大鼠室性期前收缩和室性心动过速出现时间均显著长于对照组(P<0.05)。静脉注射乌头碱后1 min,2组大鼠心律失常评分比较差异无统计学意义(P>0.05);静脉注射乌头碱后3、5、7 min,ω-3鱼油脂肪乳组大鼠心律失常评分均低于对照组(P<0.05)。ω-3鱼油脂肪乳组大鼠心肌组织中CX43蛋白的表达高于对照组(P<0.05),但2组大鼠心肌组织中去磷酸化CX43蛋白表达比较差异无统计学意义(P>0.05)。结论ω-3鱼油脂肪乳可能通过促进CX43的磷酸化改善乌头碱诱导的大鼠心律失常。     

Electrophysiologic studies: recent experience at the Charleston Area Medical Center

Electrophysiologic studies (EPS) were performed in 122 patients for evaluation of supraventricular tachycardia (16 patients), syncope (30 patients), ventricular tachycardia (48 patients), sudden cardiac death (7 patients), and other reasons (21 patients). Sixty patients had an induced sustained supraventricular and/or ventricular arrhythmia. Therapy was rendered to all 60 patients based on the results of the EPS. The evaluation and treatment of supraventricular and ventricular arrhythmias is assisted by EPS. The capability of inducing the clinical arrhythmia, determination of the arrhythmia mechanism, and evaluation of the response to various pharmacologic agents improves therapeutic choices. Patient morbidity from cardiac arrhythmias is thereby reduced.     

急性心肌梗死患者急性期体表心电图T波峰末间期与恶性室性心律失常的关系研究

目的探讨急性心肌梗死患者体表心电图T波峰末间期(TpTe)与急性期室性心律失常的关系。方法102例接受直接PCI(pPCI)治疗的急性心肌梗死患者中,共有46例出现室性心动过速(VT)和心室纤颤(VF),作为病例组。其余56例未出现室性心律失常,作为对照组。测量并比较两组pPCI前后12导联心电图的QT、TpTe、QT离散度(QTd)及经心率校正的QT间期(QTc间期)、TpTe(TpTec)。研究室性心律失常与QTc和TpTec各时段上限值的相关性并比较不同梗死部位的QT及TpTe值。结果 pPCI治疗前两组对象的QT间期、QTd间差异无统计学意义(P>0.05),但QTc和TpTec间差异有统计学意义(P<0.05)。经pPCI治疗后第3天,两组间QT和QTd间差异仍无统计学意义,而QTc、TpTe和TpTec间差异有统计学意义(P<0.05)。pPCI治疗后1周TpTe、QTc和TpTec间差异仍有统计学意义(P<0.05)。两组pPCI治疗前后的RR间期无差异(P>0.05)。QTc间期各时段上限值与VT+VF的发生率无相关性(r=0.376,P>0.05)。TpTe及TpTec间期各时段上限值与VT+VF的发生率呈正相关(r=0.677,P<0.05;r=0.698,P<0.05)。结论在急性期出现VT和VF的急性心肌梗死患者与不出现室性心律失常的患者相比,TpTe和TpTec明显延长,但QT和QTd则无明显差异。TpTe可能预示着心肌梗死急性期恶性心律失常。     

复方刺五加注射液对药物诱发实验性心律失常的影响

目的: 观察复方刺五加注射液（CASI）对药物诱发实验性心律失常的影响。方法：制备氯化钡(BaCl₂)、哇巴因及乌头碱诱导的大鼠及豚鼠实验性心律失常模型,CASI按25、50、100 mg•kg^-1分为3个剂量组,舌下静脉给药1次,不给CASI作为对照组,记录大鼠给BaCl₂后心律失常的发生率、出现时间、持续时间及动物的死亡率;观察豚鼠及大鼠出现室性早搏（VP）、室性心动过速（VT）、心室颤动（VF）及心脏停搏（CA）时哇巴因及乌头碱的用量。结果：与对照组比较,CASI 25 、50、100 mg•kg^-1组大鼠BaCl₂性心律失常的发生率降低（P<0.05）,出现时间推迟（P<0.01）,持续时间缩短（P<0.05）,死亡率减少（P<0.01）;CASI 50、100 mg•kg^-1组豚鼠对哇巴因中毒诱发VP、VT、VF及CA的耐受剂量高于对照组（ P<0.05或P<0.01）;CASI 100 mg•kg^-1组大鼠对乌头碱诱发VP、VT及VF的 耐受剂量高于对照组（P<0.05）,并且明显优于阳性药维拉帕米注射液。结论：CASI对多种药物诱发的实验性心律失常均具有明显保护作用,其对抗Ca2+性心律失常的作用明显优于Na+性心律失常,提示CASI可能为钙通道阻滞剂。     

两种不同机制心动过速并存的射频消融治疗

目的：观察两种不同机制心动过速并存的心内电生理特点射频消融的疗效。方法：８例患经全面的心内电生理检查,确定存在两种不同机制的心动过速,常规消融一种心动过速后,重复电生理检查,诱发第２种心动过速;,再次消融治疗。结果：房室结折性心动过速;＋房室折返性心动过速３例,ＡＶＮＲＴ＋房内折返性心动过速３例,ＡＶＮＲＴ＋室性心动过速１例,ＡＶＲＴ＋ＩＡＲＴ１例。     

A Study on Protective Action of Astragalus Injection(黄芪注射液)in Ouabain-Induced Cardiac Toxicity of Guinea Pigs

ＡｓｔｒａｇａｌｕｓＩｎｊｅｃｔｉｏｎ（ＡＩ）ｈａｓｂｅｅｎｗｉｄｅｌｙｕｓｅｄｔｏｔｒｅａｔｃｈｒｏｎｉｃｃｏｎｇｅｓｔｉｖｅｈｅａｒｔｆａｉｌｕｒｅ（ＣＨＦ）．Ｒｅｃｅｎｔｌｙ,ＹＡＮＧｅｔａｌ．ｈａｖｅｒｅｐｏｒｔ ｅｄｔｈａｔＡＩｗａｓｃｌｉｎｉｃａｌｌｙｅｆｆｅｃｔｉｖｅｉｎｄｅｃｒｅａｓｉｎｇｔｈｅｉｎｃｉｄｅｎｃｅｏｆｄｉｇｉｔａｌｉｓｍ（1）．ＡｌｔｈｏｕｇｈＡＩｈａｓｂｅｅｎｃｌａｉｍｅｄｔｏｉｎｈｉｂｉｔｄｉｇｉｔａｌｉｓｍ,ｉｔｓｍｅｃｈａ ｎｉｓｍｏｆａｎｔｉ ｄｉｇｉｔａｌ…     

甲状腺素诱发房性和室性心律失常的实验研究

目的:应用单相动作电位技术,通过比较甲亢状态下心房肌和心室的电生理特性的改变来探讨发生房性心律失常的可能机制。方法:24只日本大耳白兔随机分为对照组(12只)和甲状腺素组(12只)。甲状腺素组腹腔注射左旋甲状腺素(L-T4)1 mg/(kg.d)复制甲状腺机能亢进模型。对照组给予等体积的生理盐水腹腔注射。两组动物各自随机分为心房组和心室组进入实验(每组6只)。采用单相动作电位记录技术记录四组心房肌和心室肌电生理指标的变化,同时程序刺激诱发房性和室性心律失常。结果:心房肌和心室肌单相动作电位时程(MAP90)、有效不应期(ERP)和ERP/MAP90比值均较对照组明显缩短,具有显著性差异;但是在给予程序性电刺激时,甲状腺素组的房性心律失常的发生率明显高于对照组;而两组间室性心律失常的发生率差异无显著性。结论:甲亢状态下房性心律失常比室性心律失常易于诱发,可能与心房肌单相动作时程和有效不应期非同步性缩短的电异质性,以及和心房解剖结构存在的各向异性密切相关。     

A Study on Protective Action of Astragalus Injection（黄芪注射液）in

Objective: To study the protective action of Astragalus Injection (AI) on ouabain-induced cardiac toxicity. Methods: Forty guinea-pigs were randomly divided into the AI group and the control group, AI injected intravenously in the AI group and 0.9% normal saline injected in the control group, ouabain was injected in contralateral of both groups intravenously 8 mins later. The time of cardiac ventricular tachycardia (VT) and cardiac ventricular fibrillation (VF), and the dose of ouabain were documented.Results: Compared with the control group AI could markedly prolong the time of VT and VF, and increase the dose of ouabain induces VT and VF (P<0.01). Conclusion: AI decreases the incidence of digitalism.     

胺碘酮治疗急性心肌梗死后室性心律失常临床观察

目的探讨胺碘酮（Amiodarone,AM）静脉注射治疗急性心肌梗死危及生命的室性心律失常的疗效与安全性。方法21例急性心肌梗死（AMI）后反复发作持续室性心动过速（VT）／心室颤动（VF）患者,男17例,女4例,年龄56—79（53．5±11．7）岁,对常规抗心律失常药物无效,静脉注射AM首剂150—300mg,10min内静脉注入,继以1．0～1．5mr,／min静注维持,以后根据病情加减,静脉给药同时口服胺碘酮600mg/24h,若第一次负荷量后,心律失常控制不满意,可每隔30min再加注75—150mg,直至VT、VF消失为有效。结果第1个24hAM静脉用量（1482．6±304．5）mg,心律失常控制率62％（13／21）,72h全部控制。1例大面积心肌梗死15d后再发VT、VF,加用AM后获得控制。2例死于心源性休克。结论静脉注射（AM）治疗AMI后心律失常,安全有效。     

硫化氢对压力负荷性心力衰竭大鼠心脏功能的保护

目的观察腹主动脉缩窄大鼠心衰形成过程中硫氢化钠（NaHS）／硫化氢（H2S）对心脏功能的影响。方法成年雄性SD大鼠63只,随机平分为3组：对照组、心衰组、NaHS组。术后3周NaHS组腹腔注射NaHS 56μmol／kg／日,对照组与心衰组每日同法给予等量生理盐水。各组均在第4、8、12周时取7只行血流动力学及心脏功能检测,后处死取血及心脏行H2S含量、硫化氢合酶活性检测。结果NaHS组各期尾动脉压、平均动脉压、左室收缩压、左室舒张末压均有降低,±LVdp／dtmax在12周时升高。结论外源性给予H2S供体NaHS能改善系统和心脏血流动力学异常及心脏收缩和舒张功能。     

静脉注射胺碘酮治疗急性心肌梗死合并室性心动过速的临床研究

目的观察静脉注射胺碘酮治疗急性心肌梗死合并室性心动过速的临床疗效及其安全性。方法选择急性心肌梗死合并室性心动过速患者29例,静脉注射胺碘酮后观察室性心动过速的控制情况,同时密切观察用药前后血压、心率、P-R间期、QRS波时限、QTc间期变化情况及药物的不良反应。结果静脉注射胺碘酮能终止急性心肌梗死合并室性心动过速,治疗后的总有效率为93.1%;用药前后患者血压、P-R间期、QRS波时限比较差异均无显著性(P>0.05),但心率和QTc间期比较有显著性差异(P<0.01或<0.05)。结论静脉注射胺碘酮治疗急性心肌梗死合并室性心动过速患者安全、有效。     

烟浪丁的抗心律失常作用

静脉注射18mg/kg烟浪丁可预防BaCl_2所致的大鼠心律失常,使乌头碱诱发室性早搏,室性心动过速和心室颤动时所需的剂量增加。豚鼠静脉注射9mg/kg可使哇巴因产生室性早搏和心脏停搏时剂量增加,家兔静脉注射4mg/kg可预防肾上腺素及氯仿一肾上腺素所致的心律失常,但不提高兔电室颤阈值。     

重症室性心律失常的探讨

本文对１１４例重症室性心律失常患者的病因及心电图演变规律进行了分析。结果表明：室早频率、提前指数、易激指数等指标对重症室性心律失常的诊断和预测具有重要意义；抗心律失常药可加重心律失常。     

冠心病患者QT间期离散度与程序刺激诱发的室性心动过速相关性研究

目的 :探讨体表心电图QT间期离散度与冠心病患者程序刺激诱发的室性心动过速的关系。方法 :选择 4 0例接受心脏导管手术的患者 ,其中陈旧性心肌梗死患者 2 0例 ,阵发性室上性心动过速患者 2 0例。术前测定患者体表心电图QT间期离散度 ,术中在右心室起搏刺激以诱发持续室性心动过速 ,探讨QT间期离散度与室性心律失常之间的关系。结果 :2 0例陈旧性心肌梗死患者共有 6例诱发出持续室性心动过速 ,2 0例阵发性室上性心动过速患者中无 1例诱发出持续室性心动过速。冠心病患者体表心电图QT间期离散度较阵发性室上速患者明显增大 (85 .7± 2 4 .6msvs 34.8± 11.3ms,P <0 .0 1) ;冠心病患者中诱发出持续室性心动过速者 ,其QT间期离散度较未诱发出持续室性心动过速者亦明显增大 (98.7± 5 6 .2msvs 70 .4± 2 8.5ms,P <0 .0 5 )。取QT间期离散度≥ 110ms,对室性心律失常的预测有一定价值。结论 :体表心电图QT间期离散度与冠心病患者室性心律失常具有相关性 ,取QTd≥ 110ms对室性心律失常有一定的预测价值。     

腹腔神经节（丛）酒精阻滞治疗癌性腹痛的临床和实验动物组织学的初步观察

目的：腹腔神经节（丛）酒精破坏性阻滞是上腹部内脏癌性疼痛止痛常用的方法,本文为了探讨腹腔神经节（丛）阻滞时,酒精浓度、阻滞后时间与止痛效果之间的关系;方法：４３例中晚期上腹部癌性疼痛病人随机用５０％酒精（１４例）,７５％酒精（１８例）１００％酒精（１１例）２０ｍｌ分别注射到病人腹腔神经节（丛）周围,另将活兔腹腔神经节（丛）浸于５０％、７５％、１００％及０．９％生理盐水溶液里１ｄ、３ｄ、一周的经节（     

频域法检测心室晚电位临床应用初探

本文利用计算机信号平均技术及频谱估计方法对110人从体表检测心室晚电位。59个正常人中仅1例发现晚电位,阳性率为1.7％,心肌梗塞未并发室性心律失常患者24例中20.8％(5/24)有晚电位;心肌梗塞并发室性心律失常5例病人中80％(4/5)有晚电位。下壁梗塞者晚电位阳性率47.06％,高于其它部位梗塞者(8.33％)。室性早搏组及非持续性室速患者晚电位阳性率分别为30％(3/10)和38.46(5/13),而持续性室速患者阳性率高达100％(4/4)。研究结果表明:(1)心室晚电位与室性心律失常,特别是持续性室速有密切关系;(2)频阈法体表检测晚电位可能成为辨识心肌梗塞后有严重室性心律失常倾向病人的一种无创方法。     

Clinical and familial study of arrhythmogenic right ventricular cardiomyopathy

Objective　To explore the characteristics of arrhythmogenic right ventricular cardiomyopathy (ARVC). Methods　Seven patients with arrhythmogenic right ventricular cardiomyopathy and 34 members of three families were studied. All patients and family members underwent history collection, clinical examination, electrocardiogram (ECG), two-dimensional echocardiography (2-DE) and a signal averaging electrocardiogram. Programmed ventricular stimulation was performed in five patients. Results　All patients and family members had normal morphologic characteristics and normal function of the left ventricular by 2-DE. Fourteen persons had abnormal findings indicating ARVC. Five had enlargement of the right ventricular with diffused hypocontractility, eight had thin and systolic bulging in the focal anterior wall with hypokinesia and one had bulging of the inferior wall. Twenty-five persons (seven patients and 18 family members) had abnormal findings in ECG. Positive ventricular late potential was recorded in 13 persons (six patients). Two to three monomorphic ventricular tachycardia (VT) with left bundle branch block (LBBB) configurations were induced in five patients. Ventricular fibrillation was induced in two patients during the electrophysiologic study (EPS). Five patients had very high pacing threshold and/or ineffective pacing in one or many regions of the right ventricle. Two members of one family died suddenly. One member was a dwarf with ARVC. Spontaneous VT with a left bundle branch block (LBBB) configuration was recorded in five patients, polymorphic VT with extremely short coupling interval in one, and premature ventricular complexes with LBBB configuration in 12 (six patients). Conclusion　Our familial study strongly suggests that ARVC may be a hereditary disease and it is helpful in the diagnosis and detection of ARVC. The most common manifestations were abnormal structure and function of the right ventricle and abnormal ECG of repolarization and ventricular arrhythmia which originates from the right ventricle.