晕厥的病因和诊断策略

1、晕厥的病因和诊断策略The Significance of Syncope1 National Disease and Therapeutic Index on Syncope and Collapse, ICD-9-CM 780.2, IMS America, 19972 Blanc J-J, Lher C, Touiza A, et al. Eur Heart J, 2002; 23: 815-820.3 Day SC, et al, AM J of Med 19824 Kapoor W. Evaluation and outcome of patients with syncope. M

2、edicine 1990;69:160-1751 Day SC, et al. Am J of Med 1982;73:15-23.2 Kapoor W. Medicine 1990;69:160-175.3 Silverstein M, Sager D, Mulley A. JAMA. 1982;248:1185-1189.4 Martin G, Adams S, Martin H. Ann Emerg Med. 1984;13:499-504.nSome causes of syncope are potentially fatalnCardiac causes of syncope ha

3、ve the highest mortality ratesThe Significance of Syncope短暂的意识丧失 (TLOC)晕厥 特点n发作前可有不同的先兆。发作前可有不同的先兆。n发作突然，发作突然，多在站立或坐位时发生。多在站立或坐位时发生。n意识丧失为自限性，常伴有肌张力增高。意识丧失为自限性，常伴有肌张力增高。n意识可迅速恢复。意识可迅速恢复。n苏醒无后遗症。苏醒无后遗症。机制：一过性脑灌注减少机制：一过性脑灌注减少.Brignole M, et al. Europace, 2004;6:467-537. 晕厥的原因体位性低血压体位性低血压心律失常心律失常心肺病变心肺

4、病变1 VVS CSS SituationalCoughPost- Micturition2 Drug-Induced ANS FailurePrimarySecondary3 BradySN DysfunctionAV BlockTachyVTSVT Long QT Syndrome4 Acute Myocardial Ischemia Aortic Stenosis HCM Pulmonary Hypertension Aortic Dissection神经介导神经介导 Unexplained Causes = Approximately 1/3DG Benditt, MD. U of M

5、 Cardiac Arrhythmia Center其他病因和类似病症其他病因和类似病症先天性心脏病、主动脉窦瘤破入右心吞咽性晕厥脑部因素：TIA、癫痫、椎基底动脉供血不足、偏头痛、脑部 肿瘤代谢因素：重度贫血、脱水、电解质紊乱、低血糖。内分泌因素：甲状腺、肾上腺病变。呼吸系统因素：窒息、哮喘。精神因素：过渡换气：急性中毒：酒精、药物。Cardiac Rhythms During Unexplained SyncopeSeidl K. Europace. 2000;2(3):256-262.Krahn AD. PACE. 2002;25:37-41.Medtronic ILR Replacem

6、ent Data. FY03, 04. On file. No Recurrence 36%(31-48%)Normal Sinus Rhythm 31%(17-44%)Other 11%Arrhythmia 22%(13-32%)Tachycardia 6%(2-11%)Bradycardia 16%(11-21%)Composite: N=133 to 7109晕 厥 诊 断诊断目的n是否晕厥是否晕厥n有无心脏病有无心脏病 n病因诊断病因诊断 估计预后估计预后制定预防和治疗措施制定预防和治疗措施详细病史n近期发生情况近期发生情况发生前状态、目击证人介绍发生前状态、目击证人介绍发生前和发生时

7、症状发生前和发生时症状后遗症后遗症医生检查和治疗情况医生检查和治疗情况n过去发生情况过去发生情况n伴随疾病伴随疾病 n家族史家族史心脏病心脏病猝死猝死代谢疾病代谢疾病 n过去药物治疗情况过去药物治疗情况神经系统病史神经系统病史晕厥晕厥Brignole M, et al. Europace, 2004;6:467-537.体格检查n生命体征生命体征心率心率不同体位血压不同体位血压n心血管检查心血管检查 n神经系统检查神经系统检查n颈动脉窦按摩颈动脉窦按摩 Brignole M, et al. Europace, 2004;6:467-537.颈动脉窦按摩 (CSM)n方法方法1按摩按摩 5-10

8、s不要使颈动脉闭塞不要使颈动脉闭塞卧位和直立位（倾斜床上卧位和直立位（倾斜床上)n结果结果心脏停博心脏停博3 s和或者收缩压下降和或者收缩压下降 50 mmHg 伴有症状伴有症状 =颈动脉综颈动脉综合症合症n禁忌征禁忌征2颈动脉明显病变颈动脉明显病变 既往有脑卒中既往有脑卒中, 近近3个月有个月有MI n并发症并发症 神经系统表现神经系统表现发病率小于发病率小于 0.2%3通常是短暂的通常是短暂的1Kenny RA. Heart. 2000;83:564.2Linzer M. Ann Intern Med. 1997;126:989.3Munro N, et al. J Am Geriatr

9、Soc. 1994;42:1248-1251.其他检查n心电图：心电图：n心脏成像检查心脏成像检查 心脏彩超、冠脉造影。心脏彩超、冠脉造影。n心电监测心电监测Holter Event recorderIntermittent vs. LoopInsertable Loop Recorder (ILR)Brignole M, et al. Europace, 2004;6:467-537.Heart Monitoring OptionsILREvent Recorders(non-lead and loop)Holter Monitor12-Lead2 Days7-30 DaysUp to 14

10、 Months10 SecondsOPTIONTIME (Months) 01234567891011121314Brignole M, et al. Europace, 2004;6:467-537.n ATP试验：可短暂使血管迷走神经张力增高试验：可短暂使血管迷走神经张力增高n电生理检查电生理检查 (EPS)n倾斜试验倾斜试验n脑电图脑电图, 头颅头颅 CT, 头颅头颅 MRIn可能有助诊断癫痫可能有助诊断癫痫n颈椎颈椎MRI其他检查电生理检查价值n老年人或者有心脏猝死病史意义较大。老年人或者有心脏猝死病史意义较大。n健康人没有心脏猝死病史意义较小。健康人没有心脏猝死病史意义较小。 n阳性

11、发现阳性发现:诱发单形诱发单形 VTSNRT 3000 ms or CSNRT 600 ms诱发诱发 SVT 同时合并低血压同时合并低血压HV 间期间期 100 ms 起搏诱发房室结以下传导阻滞起搏诱发房室结以下传导阻滞Benditt D. In: Topol E, ed. Textbook of Cardiovascular Medicine. Lippencott;2002:1529-1542.Lu F, et al. In: Benditt D, et al. The Evaluation and Treatment of Syncope. Futura. 2003;80-95.Brig

12、nole M, et al. Europace. 2004;6:467-537.电生理检查局限性n很难判断自发晕厥和实验室发现是否相关很难判断自发晕厥和实验室发现是否相关 n阳性率阳性率1无心脏猝死者：无心脏猝死者： 6-17%有心脏猝死者有心脏猝死者: 25-71%n快速心律失常比缓慢心律失常有价值快速心律失常比缓慢心律失常有价值2 nEPS 发现必须与病史相结合发现必须与病史相结合注意假阳性注意假阳性1Linzer M, et al. Ann Int Med. 1997;127:76-86.2Lu F, et al. In: Benditt D, et al. The Evaluation

13、 and Treatment of Syncope. Futura. 2003;80-95. 正常人当体位由平卧正常人当体位由平卧 头高倾斜立位头高倾斜立位 , 静静脉回流减少脉回流减少 ,心室充盈下降心室充盈下降 ,减少了（与脑干迷走减少了（与脑干迷走背核直接相连系的）心室后下壁纤维背核直接相连系的）心室后下壁纤维 的激活的激活 ,反反射性地增加了交感输出射性地增加了交感输出 ,结果心跳加快结果心跳加快 ,周围血管周围血管阻力增高。所以阻力增高。所以 ,体位直立的正常反应是心率增快体位直立的正常反应是心率增快 ,舒张压升高舒张压升高 ,收缩压轻度升高。收缩压轻度升高。倾斜试验（机制）60 -

14、 80 VVS患者当体位由平卧转成头高倾斜患者当体位由平卧转成头高倾斜立位立位 , 静脉回流减少静脉回流减少 ,心室充盈量快速下降心室充盈量快速下降，心室强烈收缩心室强烈收缩，心室排空现象，激活心室，心室排空现象，激活心室后下壁后下壁C纤维，冲动传导纤维，冲动传导 脑干迷走中枢，脑干迷走中枢，迷走活动增强，血压下降心率减慢。迷走活动增强，血压下降心率减慢。倾斜试验（机制）60 - 80v 血压下降标准为收缩压血压下降标准为收缩压 80和和 (或或 )舒张压舒张压 50 ,或平均动脉压下降或平均动脉压下降25%。v 有的患者即使血压未达到此标准有的患者即使血压未达到此标准 ,但已出现晕厥或接近但

15、已出现晕厥或接近晕厥症状晕厥症状 ,仍应判为阳性。仍应判为阳性。倾斜试验阳性标准（血压）60 - 80倾斜试验阳性标准（心率）v窦性心动过缓窦性心动过缓 ( 50次次 /分分 )、窦性停搏、窦性停搏v交界性逸搏心律交界性逸搏心律v度及以上房室传导阻滞度及以上房室传导阻滞v 3秒以上的心脏停搏。秒以上的心脏停搏。倾斜试验评价 60 70倾斜角度倾斜角度 ,试验的特异性可达试验的特异性可达 9 0% ;60角倾斜角倾斜 45分钟分钟 ,者阳性率约者阳性率约 30% 50% ;加用异丙肾上腺素激发试验加用异丙肾上腺素激发试验 ,可使特异性降低。可使特异性降低。加用异丙肾上腺素加用异丙肾上腺素 ,试验

16、阳性率可达试验阳性率可达 85% 9 0%。 反复发作频繁的患者应给予治疗。反复发作频繁的患者应给予治疗。v 受体阻滞剂受体阻滞剂 ,可阻滞儿茶酚胺的作用可阻滞儿茶酚胺的作用 ,降低纤维的刺降低纤维的刺激激v 丙吡胺也可应用丙吡胺也可应用 ,它通过抗胆碱能和负性肌力作用而达治它通过抗胆碱能和负性肌力作用而达治疗目的。疗目的。v 茶碱类对抗腺苷介导的低血压和心动过缓茶碱类对抗腺苷介导的低血压和心动过缓 ,因此也有治疗因此也有治疗作用。作用。v 氟氢考的松为盐皮质酮氟氢考的松为盐皮质酮 ,具有保钠、扩容作用具有保钠、扩容作用 ,可能减少可能减少发作。发作。v 以心脏抑制型为主以心脏抑制型为主 ,而

17、药物效果不好者而药物效果不好者 ,可考虑置入双腔可考虑置入双腔起搏器。起搏器。的药物治疗的药物治疗诊断评价 (N=3411 to 4332) References Available结果结果 (%)评价指标评价指标 病史病史,体检体检, ECG, 心脏成像心脏成像38-40其他检查其他检查 倾斜试验倾斜试验27 体外心电监测体外心电监测5-13 Insertable Loop Recorder (ILR)43-883-5 电生理检查电生理检查 35%60 PatientsAECG, Tilt,EP StudyDiagnosisILR+ILRConventional Testing(AECG,

18、Tilt, EPS)30 Patients30 PatientsPrimaryStrategyCrossover14618+ISSUEInternational Study of Syncope of Uncertain EtiologynMulticenter, international, prospective studynAnalyzed the diagnostic contribution of an ILR in three predefined groups of patients with syncope of uncertain origin:Isolated syncop

19、e: No SHD, Normal ECG1Negative tiltPositive tiltPatients with heart disease and negative EP test2Patients with bundle branch block and negative EP test31Moya A. Circulation. 2001; 104:1261-1267. 2Menozzi C, et al. Circulation. 2002;105:2741-2745.3Brignole M, et al. Circulation. 2001;104:2045-2050.IS

20、SUEPatients with Isolated Syncope and Tilt-Positive Syncope Moya A. Circulation. 2001;104:1261-1267. Follow-Up to Recurrent Spontaneous Episode111 Patients with Syncope No SHD, Normal ECG29: Tilt-Positive 82: Tilt-Negative “Isolated Syncope”Tilt Test Followed byInsertable Loop RecorderISSUE Patients

21、 with Heart Disease and a Negative EP TestMenozzi C, et al. Circulation. 2002;105:2741-2745.35 Pts with Heart Diseaseand Insertable Loop RecorderSyncope: 6 Pts (17%)ECG-Documented: 6 Pts (17%)Pre-Syncope: 13 Pts (37%)ECG-Documented: 8 Pts (23%)AV block + asystole: 1A.Fib + asystole: 1Sinus arrest: 1

22、Sinus tachycardia: 1Rapid A.Fib: 2Sustained VT: 1Parox. A.Fib/AT: 1Post tachycardia pause: 1No rhythm variations: 4Sinus tachycardia: 1ISSUEPatients with Heart Disease and a Negative EP TestConclusionsnPatients with unexplained syncope, overt heart disease, and negative EP study had a favorable medi

23、um-term outcomenMechanism of syncope was heterogeneousnVentricular tachyarrhythmia was unlikelyn“ILR-guided strategy seems reasonable, with specific therapy safely delayed until a definite diagnosis is made.”Menozzi C, et al. Circulation. 2002;105:2741-2745.ISSUEPatients with Bundle Branch Block and

24、 Negative EP TestBrignole M., ET AL.,Circulation. 2001;104:2045-2050. * 5 of these also had 1 presyncope* Drop-out before primary-end point52 Pts with BBBand Insertable Loop RecorderSyncope: 22 Pts (42%)*ILR-Detected: 19AVB: 12 (63%)SA: 4 (21%)Asystole-undefined: 1 (5%)NSR: 1 (5%)Sinus tachy: 1 (5%)

25、Not Detected: 3Stable AVB: 3 Pts (6%)ILR-DetectedPre-Syncope:2 Pts (4%)*Death: 1 Pt (2%)AVB: 2 (4%)ISSUEPatients with Bundle Branch Block and Negative EP TestConclusion: nIn patients with BBB and negative EP study, most syncopal recurrences have a homogeneous mechanism that is characterized by prolo

26、nged asystolic pauses mainly attributable to sudden-onset paroxysmal AV blockBrignole M. Circulation. 2001;104:2045-2050. Section III:Specific Conditions and TreatmentSpecific ConditionsnCardiac arrhythmiaBrady/TachyLong QT syndromeTorsade de pointesBrugadaDrug-inducednStructural cardio-pulmonarynNe

27、urally-mediatedVasovagal Syncope (VVS)Carotid Sinus Syndrome (CSS)nOrthostaticCardiac SyncopenIncludes cardiac arrhythmias and SHDnOften life-threateningnMay be warning of critical CV diseaseTachy and brady arrhythmiasMyocardial ischemia, aortic stenosis, pulmonary hypertension, aortic dissectionnAs

28、sess culprit arrhythmia or structural abnormality aggressivelynInitiate treatment promptly Brignole M, et al. Europace. 2004;6:467-537.“cardiac syncope can be a harbinger of sudden death.”nSurvival with and without syncopen6-month mortality rate of greater than 10%nCardiac syncope doubled the risk o

29、f deathnIncludes cardiac arrhythmias and SHDNo SyncopeVasovagal andOther CausesCardiac Cause051015Follow-Up (yr)Probability of Survival1.00.20.0Soteriades ES, et al. N Engl J Med. 2002;347:878.Syncope Due to Structural Cardiovascular Disease: Principle MechanismsnAcute MI/Ischemia2 neural r

30、eflex bradycardia Vasodilatation, arrhythmias, low output (rare)nHypertrophic cardiomyopathyLimited output during exertion (increased obstruction, greater demand), arrhythmias, neural reflexnAcute aortic dissectionNeural reflex mechanism, pericardial tamponadenPulmonary embolus/pulmonary hypertensio

31、nNeural reflex, inadequate flow with exertionnValvular abnormalitiesAortic stenosis Limited output, neural reflex dilation in peripheryMitral stenosis, atrial myxoma Obstruction to adequate flowBrignole M, et al. Europace. 2004;6:467-537.Syncope Due to Cardiac ArrhythmiasnBradyarrhythmiasSinus arres

32、t, exit blockHigh grade or acute complete AV blockCan be accompanied by vasodilatation (VVS, CSS)nTachyarrhythmiasAtrial fibrillation/flutter with rapid ventricular rate (eg, pre-excitation syndrome)Paroxysmal SVT or VTTorsade de pointesBrignole M, et al. Europace. 2004;6:467-537.ILR RecordingsCASE:

33、 28 year-old man presents to ER multiple times after falls resulting in trauma. VT: Ablated and medicated.CASE: 83 year-old woman with syncope due to bradycardia: Pacemaker implanted.Reveal ILR recordings; Medtronic data on file.Long QT SyndromesnMechanismAbnormalities of sodium and/or potassium cha

34、nnelsSusceptibility to polymorphic VT (Torsade de pointes)nPrevalenceDrug-induced forms CommonGenetic forms Relatively rare, but increasingly being recognized“Concealed” forms: May be commonProvide basis for drug-induced torsadeSchwartz P, Priori S. In: Zipes D and Jalife J, eds. Cardiac Electrophys

35、iology. Saunders;2004:651-659.Syncope: Torsade de PointesFrom the files of DG Benditt, MD. U of M Cardiac Arrhythmia CenterLong QT Syndromes: 12-Lead ECGFrom the files of DG Benditt, MD. U of M Cardiac Arrhythmia CenterDrug-Induced QT Prolongation(List is continuously being updated)nAntiarrhythmicsC

36、lass IA .Quinidine, Procainamide, DisopyramideClass IIISotalol, Ibutilide, Dofetilide, Amiodarone, NAPA*nAntianginal AgentsBepridil*nPsychoactive AgentsPhenothiazines, Amitriptyline, Imipramine, ZiprasidonenAntibioticsErythromycin, Pentamidine, Fluconazole, Ciprofloxacin and its relativesnNonsedatin

37、g antihistaminesTerfenadine*, AstemizolenOthersCisapride*, Droperidol, Haloperidol*Removed from U.S. MarketBrignole M, et al. Europace, 2004;6:467-537.Treatment of Long QTnSuspicion and recognition are criticalnEmergency treatmentIntravenous magnesiumPacing to overcome bradycardia or pausesIsoproter

38、enol to increase heart rate and shorten repolarizationICD if prior SCA or strong family historyIf drug induced: Reverse bradycardiaWithdraw drugAvoid ALL long-QT provoking agentsIf genetic:Avoid ALL long-QT provoking agentsnFor more information visit Schwartz P, Priori S. In: Zipes D a

39、nd Jalife J, eds. Cardiac Electrophysiology. Saunders;2004:651-659.Treatment of Syncope Due to BradyarrhythmianClass I indication for pacing using dual chamber system wherever possiblenVentricular pacing in atrial fibrillation with slow ventricular responseACC/AHA/NASPE 2002 Guideline Update. Circ.

40、2002;106:2145-2161.nV-0.2-0.4:45:44:43:42:41:40:39:38:37:37:36:35:34:33:32:31:30:29:29:28:27:26:25:24:23:22:2108:23:218:23:2908:23:3-0.2-0.0-0.2-0.4Treatment of Syncope Due to TachyarrhythmianAtrial tachyarrhythmiasAVRT due to accessory pathway Ablate pathwayAVNRT Ablate

41、AV nodal slow pathwayAtrial fib Pacing, linear/focal ablation for paroxysmal AFAtrial flutter Ablate the IVC-TV isthmus of the re-entrant circuit for typical flutter nVentricular tachyarrhythmiasVentricular tachycardia ICD or ablation where appropriateTorsade de pointes Withdraw offending drug or im

42、plant ICD (long QT/Brugada/short QT)nDrug therapy may be an alternative in many casesBrignole M, et al. Europace. 2004;6:467-537.Neurally-Mediated Reflex SyncopenVasovagal Syncope (VVS)nCarotid Sinus Syndrome (CSS)nSituational syncopePost-micturitionCoughSwallow DefecationBlood drawing, etc.Brignole

43、 M, et al. Europace, 2004;6:467-537.PathophysiologyAutonomic Nervous SystemBenditt D, et al. Neurally mediated syncope: Pathophysiology, investigations and treatment. Blanc JJ, et al. eds. Futura. 1996.VVSClinical PathophysiologynNeurally-mediated physiologic reflex mechanism with two components:1.

44、Cardioinhibitory ( HR) 2. Vasodepressor ( BP) despite heart beats, no significant BP generatednBoth components are usually presentWieling W, et al. In: Benditt D, et al. The Evaluation and Treatment of Syncope. Futura. 2003;11-22.12VVSIncidencenMost common form of syncope8% to 37% (mean 18%) of sync

45、ope casesnDepends on population sampledYoung without SHD, incidenceOlder with SHD, incidenceLinzer M, et al. Ann Intern Med. 1997;126:989.VVS vs. CSSnIn general:VVS patients younger than CSS patientsAges range from adolescence to older adults (median 43 years)Linzer M, et al. Ann Intern Med. 1997;12

46、6:989.VVS Recurrences1Savage D, et al. STROKE. 1985;16:626-29. 2Sheldon R, et al. Circulation. 1996;93:973-81.n35% of patients report syncope recurrence during follow-up 3 years1nPositive HUT with 6 lifetime syncope episodes: recurrence risk 50% over 2 years210008005010025842112362484480Months Since

47、 Symptoms BeganTwo Year RiskTotal Number of Syncopal Episodes 75%50-75%25-50% 2 hoursECG and continuous blood pressure, supine, and uprightTilt to 70, 20 minutesIsoproterenol/Nitroglycerin if necessaryEnd point Loss of consciousness60 - 80Benditt D, et al. JACC. 1996;28:263-275.Brignole M, et al. Eu

48、ropace, 2004;6:467-537.VVS General Treatment Measures nOptimal treatment strategies for VVS are a source of debatenTreatment goalsAcute interventionPhysical maneuvers, eg, crossing legs or tugging armsLowering headLying downnLong-term preventionTilt trainingEducationDiet, fluids, salt Support hoseDr

49、ug therapyPacingBrignole M, et al. Europace, 2004;6:467-537.VVS Tilt Training ProtocolnObjectivesEnhance orthostatic toleranceDiminish excessive autonomic reflex activityReduce syncope susceptibility/recurrences nTechnique Prescribed periods of upright posture against a wallStart with 3-5 min BIDInc

50、rease by 5 min each week until a duration of 30 min is achievedReybrouck T, et al. PACE. 2000;23(4 Pt. 1):493-498.VVS Tilt Training: Clinical OutcomesnTreatment of recurrent VVS nReybrouck, et al.*: Long-term study38 patients performed home tilt trainingAfter a period of regular tilt training, 82% r

51、emained free of syncope during the follow-up periodHowever, at the 43-month follow-up, 29 patients had abandoned the therapy Conclusion: The abnormal autonomic reflex activity of VVS can be remedied. Compliance may be an issue. *Reybrouck T, et al. PACE. 2000;23:493-498.VVS Tilt Training: Clinical O

52、utcomesnFoglia-Manzillo, et al.*: Short-term study68 patients35 tilt training33 no treatment (control)Tilt table test conducted after 3 weeks19 (59%) of tilt trained and 18 (60%) of controls had a positive testTilt training was not effective in reducing tilt testing positivity ratePoor compliance in

53、 the majority of patients with recurrent VVS*Foglio-Manzillo G, et al. Europace. 2004;6:199-204.VVS Pharmacologic TreatmentnFludrocortisone nBeta-adrenergic blockersPreponderance of clinical evidence suggests minimal benefit1nSSRI (Selective Serotonin Re-Uptake Inhibitor)1 small controlled trial2nVa

54、soconstrictors1 negative controlled trial (etilefrine)32 positive controlled trials (midodrine)4,51Brignole M, et al. Europace, 2004;6:467-537.2Di Girolamo E, et al. JACC. 1999;33:1227-1230.3Raviele A, et al. Circ. 1999;99:1452-1457.4Ward C, et al. Heart. 1998;79:45-49.5Perez-Lugones A, et al. J Car

55、diovasc Electrophysiol. 2001;12(8):935-938.Midodrine for VVS Perez-Lugones A, Schweikert R, Pavia S, et al. J Cardiovasc Electrophysiol. 2001;12(8):935-938. Monthsp 0.001Symptom-Free Interval180160140120100806040200100806040200FluidMidodrineThe Role of Pacing as Therapy for SyncopenVVS with +HUT and

56、 cardioinhibitory response:Class IIb indication for pacingnThree randomized, prospective trials reported benefits of pacing in select VVS patients:VPS I1VASIS2SYDIT3nSubsequent study results less clearVPS II4Synpace5INVASY61Connolly SJ. J Am Coll Cardiol. 1999;33:16-20.2Sutton R. Circulation. 2000;1

57、02:294-299.3Ammirati F. Circ. 2001;104:52-57.4Connolly S. JAMA. 2003;289:2224-2229.5Giada F. PACE . 2003;26:1016 (abstract).6Occhetta E, et al. Europace. 2004;6:538-547.VPS I (North American Vasovagal Pacemaker Study)nObjective: To evaluate pacemaker therapy for severe recurrent vasovagal syncopenRa

58、ndomized, prospective, single centernN=54 patients27: DDD pacemaker with rate drop response 27: No pacemakernInclusion: Vasodepressor responsenPrimary outcome: First recurrence of syncopeConnolly SJ. J Am Coll Cardiol. 1999;33:16-20. 100908070605040302010003691215Time in MonthsNo Pacemaker (PM)2P=0.

59、000022PacemakerCumulative Risk (%)Connolly SJ. J Am Coll Cardiol. 1999;33:16-20. Results:n6 (22%) with PM had recurrence vs. 19 (70%) without PMn84% RRR (2p=0.000022)VPS I (North American Vasovagal Pacemaker Study)VASIS (VAsovagal Syncope International Study)nObjective: To evaluate pacemaker therapy

60、 for severe cardioinhibitory tilt-positive neurally mediated syncopenRandomized, prospective, multi-centernN=42 patients19: DDI pacemaker (80 bpm) with rate hysteresis (45 bpm)23: No pacemakernInclusion: Positive cardioinhibitory responsenPrimary outcome: First recurrence of syncopeSutton R. Circula