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天津泰达国际心血管病医院

  泰达国际心血管病医院(泰心医院)是由天津经济技术开发区(Tianjin Economic Technological Development Area,缩写TEDA,音译“泰达”)政府投资兴建的三级甲等心血管病专科医院,于2003年9月26日建成。医院总投资7.2亿元,建筑面积7.6万平米,设置病床500张。医院是天津医科大学心血管病临床学院,心脏大血管外科、心血管内科和护理为国家临床重点专科建设项目单位,2009年6月通过美国国际医院标准(JCI)评审,2012年7月通过复审,同时急性心肌梗死和心力衰竭两个诊疗项目通过了JCI临床诊疗规范(CCPC)认证,使医院成为我国内地首家通过心血管领域疾病国际认证的医院,也因此成为唯一获得三块JCI金章的医院。 
  泰达国际心血管病医院心内科为国家临床重点专科建设项目单位、天津医科大学重点学科、天津滨海新区重点学科,设有博士后流动站,具有博硕士研究生学位授予权,现有包括国家级科研项目在内的18项在研课题,科研经费近1000万元。心内科实际开放床位200张,由心内4个科室和CCU组成,共有医生81人,其中副主任医师以上30人,博硕士占78%,博士生导师3人,硕士生导师4人。心血管内科在学科带头人齐向前教授带领下,形成了老、中、青相结合,以中青年骨干为核心,实力雄厚的医疗团队。各亚专业在学科骨干带领下,常规开展冠心病的诊治和介入(包括左主干病变、慢性闭塞病变、分叉病变等)、射频消融、起搏器及ICD、CRT/CRT-D植入、先心病封堵等介入手术以及高血压、心力衰竭、心肌病、心包炎、感染性心内膜炎、高脂血症、糖尿病等疾患的诊治,对于复杂冠脉介入如左主干病变,多支复杂病变,慢行闭塞病变的介入治疗均达到了较高水平,近年开展了冠状动脉内超声检查(IVUS)、FFR(血流储备分数)测定、冠脉旋磨技术、CTO病变逆向导丝技术等。2013年,冠脉造影7543例,PCI 2909例。 
  在仪器设备方面,医院建有5间独立导管间,均配备先进大型数字平板心血管造影机、多参数电生理记录仪、射频消融心脏治疗仪、导管工作站及除颤器、呼吸机、临时起搏器等应急设备,并具备血管内超声波成像诊断仪、非接触心内膜标测系统、主动脉内球囊反搏泵等设备系统。2010年,医院投资兴建了天津市首个杂交手术室,术间配备了新一代数字平板心血管造影机Allura Xper FD20。其它相关配套设施,如64排宝石螺旋CT、PET-CT,心磁图等。 

培训基地负责人简介: 
齐向前,教授,主任医师,博士(后),博士/博士后导师,国务院政府特殊津贴专家,国家重点/滨海新区心血管病重点学科带头人,国家卫生部电生理和冠脉介入培训基地负责人/导师和中华人民共和国特聘外籍心血管病专家。目前在中华心血管病学和中国介入影像和治疗学杂志等学术团体任职。曾先后在北京阜外医院(10年,破格晋升副教授和教授)、多伦多大学附属St. Michael’s医院(7年,博士后研究员)、上海第二医学院附属仁济医院(2年,心内科主任)工作,现任职泰达国际心血管病医院/天津医科大学心血管病临床学院(11年)。 
从事心血管疾病临床、教学和科研工作30多年,具有丰富的临床科研教学和介入工作经验,个人独立完成冠脉或支架、起搏器或ICD、射频消融术和先心病封堵术等万例以上,其中心脏猝死ICD一级预防等工作近年来在国内领先。 
完成卫生部青年基金、加拿大心脏与中风和国家自然科学基金(第一承担人)等课题工作数项,现有科研经费百万以上。中英文杂志外发表论文论著100多篇,其中第一作者在CIRCULATION或J CARDIOVASC PHARMACOL等国际一流杂志发表论著数篇,主编《心脏性猝死防治》等论著2部,参与编写论著6部,先进工作曾在中央电视台、中央广播电台和健康报等媒体广泛宣传,近年来先后数次被评为或授予天津市好医生称号。 
Xiangqian Qi, MD, MSc, PhD
Professor of Cardiology and Supervisor of PhD/Postdoctoral Fellow
Director of Department II /State key of Cardiology at Teda International Cardiovascular Hospital and Tianjin Medical University, Tianjin, China
Current Mailing Add.: 61 the Three Street, TEDA Tianjin 300457, China. Email: qixq@tedaich.com
Dr. Qi is a nationally-renowned academic interventional cardiologist and practicing interventional cardiology for more than 35 years. He has earned a series of clinical, research and academic distinctions, including a Post-Doctoral Research Fellowship at Toronto University St. Michael’s hospital. He has been an author on more than 100 academic publications and presentations on a variety of cardiac topics. Dr. Qi’s personal areas of expertise include angioplasty and stent placement, pacemaker implantation and radiofrequency catheter ablation of arrthymias, and ASD/PFO closure. He is also available for comprehensive inpatient and outpatient consultations. His team takes great pride in providing you with meticulous, expert and compassionate care, that goes well beyond the current standard and into the realm of the best cutting-edge therapies.

J Cardiovasc Pharmacol 1999 Dec;34(6):898-903

Related Articles, Links

  1. The class III effect of azimilide is not associated with reverse use-dependence in open-chest dogs.
    Qi XQ, Newman D, Dorian P.
    Department of Medicine, St. Michael's Hospital and University of Toronto, Ontario, Canada.
    Certain class III antiarrhythmic agents manifest loss of effect at short cycle lengths (CLs). This effect may limit their efficacy in the presence of tachycardia. We studied the frequency-dependent effect of azimilide (NE-10064), a new class III agent, on the right ventricular monophasic action potential (APD90) in 12 open-chest dogs. The monophasic action-potential duration at different pacing CLs (140-400 ms), during sinus rhythm, and ventricular fibrillation CL (VFCL) from left epicardial electrograms were recorded before and after increasing doses of intravenous azimilide. At pacing CL of 400 ms, APD90 was significantly prolonged after 7, 17, and 30 mg/kg of azimilide by 5.4, 7.7, and 10.7%, respectively. The extent of APD90 prolongation was independent of rate. Azimilide increased the APD90 by similar amounts at CL of 400 ms and at the fastest possible stimulation rate maintaining 1:1 capture (mean, 171 +/- 23 ms): by 2.6 +/- 8.6% and 5.6 +/- 5.9% at 2 mg/kg, 5.4 +/- 4.8% and 4.8 +/- 4.7% at 7 mg/kg, 7.7 +/- 5.6% and 9.9 +/-4.5% at 17 mg/kg, and 10.7 +/- 2.6% and 19.3 +/- 11.9% at 30 mg/kg, respectively. Azimilide caused no changes in arterial blood pressure or heart rate. Azimilide prolongs APD90 even at very short CLs. The absence of reverse use-dependence of effect on APD90 may have clinical importance.
    PMID: 10598136 [PubMed - indexed for MEDLINE]

  2. 2/6

J Interv Card Electrophysiol 1999 Mar;3(1):61-7

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  1. Azimilide decreases defibrillation voltage requirements and increases spatial organization during ventricular fibrillation.
    Qi XQ, Newman D, Dorian P.
    Department of Medicine, St. Michael's Hospital and University of Toronto.
    INTRODUCTION: Drugs with class III antiarrhythmic properties generally decrease defibrillation threshold (DFT). However, the concentration effect relation for this effect and drug effects on ventricular fibrillation (VF) itself are not well understood. The objectives of this study were to determine the effect of azimilide (NE-10064), a new class III agent, on DFT, and on spatial organization during VF. METHODS: Defibrillation patch electrodes were sutured to the right and left ventricular epicardium in 12 open-chest anesthetized dogs. The delayed up-down algorithm was used to measure DFT and to estimate the shock strength (voltage) with a 50% probability of successful defibrillation (V50). The magnitude squared coherence (MSC), which measures the spatial relation in the frequency domain, was measured during VF between two unipolar epicardial electrodes 3 mm apart. The V50, MSC, electrophysiologic parameters, and plasma concentrations were determined before and after four cumulative i.v. doses of azimilide (2, 7, 17, and 30 mg/kg). RESULTS: Azimilide elicited a dose dependent reduction of V50 and increase in MSC. Compared with baseline, azimilide lowered mean V50 by 2 +/- 9%, 10 +/- 18%, 11 +/- 14% and 19 +/- 5%, and increased MSC by 17 +/- 20%, 32 +/- 31%, 20 +/- 44% and 27 +/- 20% (p < 0.05 for dose effect) at 2, 7, 17 and 30 mg/kg, respectively. Mean increases in monophasic action potential duration at 90% repolarization (3-11%), ventricular effective refractory period (6-13%) at 400 msec paced cycle length, and VF cycle length (5-37%) (p < 0.01 for dose effect) were observed with the 4 increasing doses of azimilide, respectively. CONCLUSION: Azimilide significantly decreases DFT and increases coherence in VF in a dose dependent manner.
    PMID: 10354978 [PubMed - indexed for MEDLINE]

  2. 3/6

Can J Physiol Pharmacol 2002 Jan;80(1):22-30

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  1. Combination IK1 and IKr channel blockade: no additive lowering of the defibrillation threshold.
    Varma P, Qi X, Newman D, Dorian P.
    Department of Pharmacology, University of Toronto, ON, Canada.
    Selective blockade of the inward rectifier potassium channel I(K1) by barium, or of the rapidly activating delayed rectifier potassium channel I(Kr) by D,L-sotalol, prolongs repolarization and reduces the defibrillation threshold (DFT). This study hypothesized that combination I(K1) and I(Kr) channel block would produce concentration-dependent additive effects on DFT and ventricular refractoriness. A range of barium and D,L-sotalol concentrations, alone and in combination, were examined with respect to DFT, ventricular effective refractory period (VERP), and ventricular fibrillation cycle length (VFCL) in 133 Langendorff-perfused rabbit hearts. Barium produced a concentration-dependent reduction of DFT (-49+/-4%), with concentration-dependent increases in VERP (26+/-6%) and VFCL (42+/-18%). D,L-Sotalol produced a concentration-dependent lowering of DFT (-53+/-6%) with a concentration-dependent increase in VFCL (34+/-8%) but not VERP. Low (1.6 microM), intermediate (3.1 microM), and high (12.5 microM) barium concentrations combined with varying D,L-sotalol concentrations produced equal or smaller decreases in DFT compared with corresponding doses of barium or D,L-sotalol alone. Except at the lowest concentrations of barium (1.6 and 3.1 microM) (p < 0.05), there was no significant additive interaction between barium and D,L-sotalol on VERP or VFCL. Combination I(K1) and I(Kr) channel block by barium and D,L-sotalol does not produce additive reduction of DFT.
    PMID: 11911222 [PubMed - indexed for MEDLINE]

  2. 4/6

J Cardiovasc Pharmacol 2002 Feb;39(2):242-50

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  1. Terikalant and barium decrease the area of vulnerability to ventricular fibrillation induction by T-wave shocks.
    Qi X, Varma P, Newman D, Mamalias N, Dorian P.
    Division of Cardiology, Department of Medicine, St. Michael's Hospital and University of Toronto, Toronto, Ontario, Canada.
    The area of vulnerability (AOV) to ventricular fibrillation (VF) induction by high-voltage shocks has been proposed as a measure of vulnerability to VF. Biphasic shocks spanning the T wave and ranging between 50 V and the upper limit of vulnerability (ULV) to VF were delivered before and after terikalant (1 mg/kg) and barium (1.1 mg/kg load followed by 0.05-0.10 mg/kg/min maintenance) or vehicle in dogs. The AOV decreased by 34% and 28% (p < 0.01) after terikalant and barium (n = 8 dogs each), respectively. Mean ULV, defibrillation threshold (DFT), and ventricular vulnerability period (VVP) decreased by 16%, 23%, and 31% (p < 0.01), respectively, after terikalant, and by 25%, 17% (p < 0.01), and 13% (p = 0.08), respectively, after barium. Vehicle (n = 14) did not significantly alter any of these variables. The ULV was correlated with the DFT before and after terikalant (r = 0.78, p < 0.01) and barium (r = 0.83, p < 0.01). Potassium channel blockers of the current reduce the ability to induce VF; this effect may be related to the anti-fibrillatory action of class III anti-arrhythmic drugs and their ability to decrease DFT.
    PMID: 11791010 [PubMed - indexed for MEDLINE]

  2. 5/6

Chin Med J (Engl) 1999 Dec;112(12):1147-52

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  1. Antiarrhythmic drugs and ventricular defibrillation energy requirements.
    Qi X, Dorian P.
    Division of Cardiology, Department of Medicine, St Michael's Hospital, University of Toronto, Canada. Xiangqian.qi@utoronto.ca
    PURPOSE: To understand the potential interaction between antiarrhythmic therapy and the implantable cardioverter-defibrillator (ICD) in patients who receive pharmacologic therapy as an adjunct to ICD therapy. DATA SOURCES: MEDLINE searching was employed and the information was indexed from approximately 3600 journals published world-wide from 1966 to 1998. STUDY SELECTION AND DATA EXTRACTION: Data were collected from 66 of approximately 455 originally identified articles and abstracts using explicit methodological criteria. RESULTS: The ICD therapy has been widely used for therapy of life-threatening ventricular arrhythmias (VT/VF) and prevention of recurrence of sudden cardiac death. Studies reported that 40%-70% or 10%-40% of ICD patients required concomitant antiarrhythmic medication to reduce the frequency of sustained arrhythmic episodes and to minimize the frequency of device discharges. Most studies on antiarrhythmic drug-ICD interactions have been performed in experimental animals. Antiarrhythmic drugs can influence the effectiveness of ICD to terminate arrhythmias through their effects on defibrillation threshold (DFT). Studies have demonstrated a rise in DFTs with class Ib agent lidocaine and class Ic agents encainide and flecainide. Class Ia agents, as well as amiodarone, bretylium and propafenone may have more variable effects on DFT probably because of the difference between acute and chronic drug dosing, dose-related changes, active metabolites, and reproducibility in determining DFT. Class III agents, with the exception of amiodarone, consistently decrease DFT. These drugs can be used as front-line agents in ICD patients. CONCLUSIONS: Antiarrhythmic drugs can increase, decrease, or have no effect on DFT. Class III agents except amiodarone can be safely administered in conjunction with ICD patients as long as the interaction between these therapeutic modalities is appreciated.
    PMID: 11721458 [PubMed - indexed for MEDLINE]

  2. 6/6

Circulation 2001 Sep 25;104(13):1544-9

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  1. Gap junction blockers decrease defibrillation thresholds without changes in ventricular refractoriness in isolated rabbit hearts.
    Qi X, Varma P, Newman D, Dorian P.
    Department of Medicine, St Michael's Hospital, University of Toronto, Toronto, Ont, Canada.
    BACKGROUND: The maintenance and termination of reentry arrhythmias are determined by tissue properties such as refractoriness and conduction velocity. Although the effects of Na(+) and K(+) channel block on electrophysiological properties and defibrillation threshold (DFT) have been studied, little is known about the effect of gap junction blockers on defibrillation and tissue electrophysiological properties. METHODS AND RESULTS: Triplicate DFTs (volts) were obtained before and 15 minutes after 4 micromol/L 16-doxyl-stearic acid (16-DSA, n=8), 1 mmol/L 1-heptanol (n=12) (both gap junction blockers), 3 microg/mL lidocaine (a sodium channel blocker) (n=8), and respective controls (n=27) in isolated perfused rabbit hearts. DFT decreased after 16-DSA (23+/-14%, P<0.01) and 1-heptanol (21+/-16%, P<0.01) but increased after lidocaine (26+/-28%, P<0.05). Ventricular fibrillation cycle length (VFCL) and QRS duration increased after all 3 agents, by 36+/-19% and 44+/-16% (16-DSA), 87+/-42% and 49+/-15% (heptanol), and 57+/-20% and 43+/-26% (lidocaine), respectively (all P<0.01). Spatially averaged temporal VFCL dispersion decreased significantly after all 3 agents, by 47+/-42% (16-DSA, P<0.05), 74+/-19% (1-heptanol, P<0.01), and 82+/-13% (lidocaine, P<0.01), respectively. Ventricular effective refractory period and monophasic action potential duration at 90% repolarization were unchanged after 16-DSA and 1-heptanol (P=NS) but increased after lidocaine (16+/-13%, P<0.01, and 6+/-5%, P=NS, respectively). There were no significant changes in DFT or any other electrophysiological variable in control hearts. CONCLUSIONS: Electrical uncoupling by 16-DSA and 1-heptanol significantly lowers DFT and dispersion of VFCL without altering refractoriness; lidocaine, at doses resulting in similar slowing of conduction, increases DFT.
    PMID: 11571250 [PubMed - indexed for MEDLINE]

 

培训基地导师介绍: 
林文华,医学硕士,主任医师,硕士研究生导师。祖籍广东省揭阳市,现任泰达国际心血管病医院心内一科主任。任重庆时时官方为啥停售心血管内科医师分会委员,重庆时时官方为啥停售心律学专业委员会委员,中国生物医学工程学会组织工作委员会委员,全国重庆时时官方为啥停开导师,天津市心脏学会理事;天津市心脏学会心律学专业委员会副主任委员;天津市生物医学工程学会心血管重症医学工程专业委员会副主任委员;天津市医学会心血管分会常委,天津市医学会心电生理与起搏学分会常委,天津市生物医学工程学会介入专业委员会委员,《中国心脏起搏与心电生理杂志》编委。 
1988年毕业于东南大学医学院医疗系,获学士学位。1997年8月至2000年6月就读于北京大学医学部,获临床医学硕士学位。2006年赴日本研修心脏介入治疗。长期从事冠心病、高血压病、心律失常、心力衰竭等临床研究。擅长复杂冠状动脉病变的介入治疗。目前个人每年完成射频消融术约150例,永久性心脏起搏器安置术约120例,ICD及CRT-P/D安置术约20例,经皮冠状动脉腔内成形术、支架置入术400例。近4年以第一作者及通讯作者发表论文55篇,2012年8月以第一作者撰写专著一部《心脏起搏与除颤》20万字,由人民卫生出版社出版,并获天津市自然科学学术专著资助出版。参加编写著作两部。《埋藏式心脏复律除颤器的临床应用》(第二完成人)被评为2005年度天津市卫生系统引进应用新技术填补空白项目。 
林文华所带领的科室2013年获开发区颁发的“金牌团队”称号,2014年获天津市及滨海新区颁发的“工人先锋号”优秀集体称号。林文华获2014年天津市五一劳动奖章称号。

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