1、暈厥的病因和診斷策略陳慶華 ppt課件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 s

2、yncope. Medicine 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 s

3、yncope have the highest mortality ratesThe Significance of Syncope短暫的意識喪失 (TLOC)暈厥 特點n發作前可有不同的先兆。發作前可有不同的先兆。n發作突然，發作突然，多在站立或坐位時發生。多在站立或坐位時發生。n意識喪失為自限性，常伴有肌張力增高。意識喪失為自限性，常伴有肌張力增高。n意識可迅速恢復。意識可迅速恢復。n蘇醒無后遺癥。蘇醒無后遺癥。機制：一過性腦灌注減少機制：一過性腦灌注減少.Brignole M, et al. Europace, 2004;6:467-537. 暈厥的原因體位性低血壓體位性低血壓心律失常心

4、律失常心肺病變心肺病變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神經介導神經介導 Unexplained Causes = Approximately 1/3DG Benditt, M

5、D. U of M Cardiac Arrhythmia Center其他病因和類似病癥其他病因和類似病癥先天性心臟病、主動脈竇瘤破入右心吞咽性暈厥腦部因素：TIA、癲癇、椎基底動脈供血不足、偏頭痛、腦部 腫瘤代謝因素：重度貧血、脫水、電解質紊亂、低血糖。內分泌因素：甲狀腺、腎上腺病變。呼吸系統因素：窒息、哮喘。精神因素：過渡換氣：急性中毒：酒精、藥物。Cardiac Rhythms During Unexplained SyncopeSeidl K. Europace. 2000;2(3):256-262.Krahn AD. PACE. 2002;25:37-41.Medtronic ILR

6、 Replacement 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暈 厥 診 斷診斷目的n是否暈厥是否暈厥n有無心臟病有無心臟病 n病因診斷病因診斷 估計預后估計預后制定預防和治療措施制定預防和治療措施詳細病史n近期發生情況近期發生情況發生前狀態、目擊證人介紹發生前狀態、目擊證人

7、介紹發生前和發生時癥狀發生前和發生時癥狀后遺癥后遺癥醫生檢查和治療情況醫生檢查和治療情況n過去發生情況過去發生情況n伴隨疾病伴隨疾病 n家族史家族史心臟病心臟病猝死猝死代謝疾病代謝疾病 n過去藥物治療情況過去藥物治療情況神經系統病史神經系統病史暈厥暈厥Brignole M, et al. Europace, 2004;6:467-537.體格檢查n生命體征生命體征心率心率不同體位血壓不同體位血壓n心血管檢查心血管檢查 n神經系統檢查神經系統檢查n頸動脈竇按摩頸動脈竇按摩 Brignole M, et al. Europace, 2004;6:467-537.頸動脈竇按摩 (CSM)n方法方法1

8、按摩按摩 5-10s不要使頸動脈閉塞不要使頸動脈閉塞臥位和直立位（傾斜床上臥位和直立位（傾斜床上)n結果結果心臟停博心臟停博3 s和或者收縮壓下降和或者收縮壓下降 50 mmHg 伴有癥狀伴有癥狀 =頸動脈綜頸動脈綜合癥合癥n禁忌征禁忌征2頸動脈明顯病變頸動脈明顯病變 既往有腦卒中既往有腦卒中, 近近3個月有個月有MI n并發癥并發癥 神經系統表現神經系統表現發病率小于發病率小于 0.2%3通常是短暫的通常是短暫的1Kenny RA. Heart. 2000;83:564.2Linzer M. Ann Intern Med. 1997;126:989.3Munro N, et al. J Am

9、 Geriatr Soc. 1994;42:1248-1251.其他檢查n心電圖：心電圖：n心臟成像檢查心臟成像檢查 心臟彩超、冠脈造影。心臟彩超、冠脈造影。n心電監測心電監測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 Day

10、sUp to 14 Months10 SecondsOPTIONTIME (Months) 01234567891011121314Brignole M, et al. Europace, 2004;6:467-537.n ATP試驗：可短暫使血管迷走神經張力增高試驗：可短暫使血管迷走神經張力增高n電生理檢查電生理檢查 (EPS)n傾斜試驗傾斜試驗n腦電圖腦電圖, 頭顱頭顱 CT, 頭顱頭顱 MRIn可能有助診斷癲癇可能有助診斷癲癇n頸椎頸椎MRI其他檢查電生理檢查價值n老年人或者有心臟猝死病史意義較大。老年人或者有心臟猝死病史意義較大。n健康人沒有心臟猝死病史意義較小。健康人沒有心臟猝死病史

11、意義較小。 n陽性發現陽性發現:誘發單形誘發單形 VTSNRT 3000 ms or CSNRT 600 ms誘發誘發 SVT 同時合并低血壓同時合并低血壓HV 間期間期 100 ms 起搏誘發房室結以下傳導阻滯起搏誘發房室結以下傳導阻滯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;8

12、0-95.Brignole M, et al. Europace. 2004;6:467-537.電生理檢查局限性n很難判斷自發暈厥和實驗室發現是否相關很難判斷自發暈厥和實驗室發現是否相關 n陽性率陽性率1無心臟猝死者：無心臟猝死者： 6-17%有心臟猝死者有心臟猝死者: 25-71%n快速心律失常比緩慢心律失常有價值快速心律失常比緩慢心律失常有價值2 nEPS 發現必須與病史相結合發現必須與病史相結合注意假陽性注意假陽性1Linzer M, et al. Ann Int Med. 1997;127:76-86.2Lu F, et al. In: Benditt D, et al. The E

13、valuation and Treatment of Syncope. Futura. 2003;80-95. 正常人當體位由平臥正常人當體位由平臥 頭高傾斜立位頭高傾斜立位 , 靜靜脈回流減少脈回流減少 ,心室充盈下降心室充盈下降 ,減少了（與腦干迷走減少了（與腦干迷走背核直接相連系的）心室后下壁纖維背核直接相連系的）心室后下壁纖維 的激活的激活 ,反反射性地增加了交感輸出射性地增加了交感輸出 ,結果心跳加快結果心跳加快 ,周圍血管周圍血管阻力增高。所以阻力增高。所以 ,體位直立的正常反應是心率增快體位直立的正常反應是心率增快 ,舒張壓升高舒張壓升高 ,收縮壓輕度升高。收縮壓輕度升高。傾斜試

14、驗（機制）60 - 80 VVS患者當體位由平臥轉成頭高傾斜患者當體位由平臥轉成頭高傾斜立位立位 , 靜脈回流減少靜脈回流減少 ,心室充盈量快速下降心室充盈量快速下降，心室強烈收縮心室強烈收縮，心室排空現象，激活心室，心室排空現象，激活心室后下壁后下壁C纖維，沖動傳導纖維，沖動傳導 腦干迷走中樞，腦干迷走中樞，迷走活動增強，血壓下降心率減慢。迷走活動增強，血壓下降心率減慢。傾斜試驗（機制）60 - 80v 血壓下降標準為收縮壓血壓下降標準為收縮壓 80和和 (或或 )舒張壓舒張壓 50 ,或平均動脈壓下降或平均動脈壓下降25%。v 有的患者即使血壓未達到此標準有的患者即使血壓未達到此標準 ,但

15、已出現暈厥或接近但已出現暈厥或接近暈厥癥狀暈厥癥狀 ,仍應判為陽性。仍應判為陽性。傾斜試驗陽性標準（血壓）60 - 80傾斜試驗陽性標準（心率）v竇性心動過緩竇性心動過緩 ( 50次次 /分分 )、竇性停搏、竇性停搏v交界性逸搏心律交界性逸搏心律v度及以上房室傳導阻滯度及以上房室傳導阻滯v 3秒以上的心臟停搏。秒以上的心臟停搏。傾斜試驗評價 60 70傾斜角度傾斜角度 ,試驗的特異性可達試驗的特異性可達 9 0% ;60角傾斜角傾斜 45分鐘分鐘 ,者陽性率約者陽性率約 30% 50% ;加用異丙腎上腺素激發試驗加用異丙腎上腺素激發試驗 ,可使特異性降低。可使特異性降低。加用異丙腎上腺素加用異

16、丙腎上腺素 ,試驗陽性率可達試驗陽性率可達 85% 9 0%。 反復發作頻繁的患者應給予治療。反復發作頻繁的患者應給予治療。v 受體阻滯劑受體阻滯劑 ,可阻滯兒茶酚胺的作用可阻滯兒茶酚胺的作用 ,降低纖維的刺降低纖維的刺激激v 丙吡胺也可應用丙吡胺也可應用 ,它通過抗膽堿能和負性肌力作用而達治它通過抗膽堿能和負性肌力作用而達治療目的。療目的。v 茶堿類對抗腺苷介導的低血壓和心動過緩茶堿類對抗腺苷介導的低血壓和心動過緩 ,因此也有治療因此也有治療作用。作用。v 氟氫考的松為鹽皮質酮氟氫考的松為鹽皮質酮 ,具有保鈉、擴容作用具有保鈉、擴容作用 ,可能減少可能減少發作。發作。v 以心臟抑制型為主以心

17、臟抑制型為主 ,而藥物效果不好者而藥物效果不好者 ,可考慮置入雙腔可考慮置入雙腔起搏器。起搏器。的藥物治療的藥物治療診斷評價 (N=3411 to 4332) References Available結果結果 (%)評價指標評價指標 病史病史,體檢體檢, ECG, 心臟成像心臟成像38-40其他檢查其他檢查 傾斜試驗傾斜試驗27 體外心電監測體外心電監測5-13 Insertable Loop Recorder (ILR)43-883-5 電生理檢查電生理檢查 35%60 PatientsAECG, Tilt,EP StudyDiagnosisILR+ILRConventional Testi

18、ng(AECG, 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:Isolat

19、ed syncope: 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;104:204

20、5-2050.ISSUEPatients 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

21、 Patients 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

22、arrest: 1Sinus 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 favor

23、able medium-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

24、Block and 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 tach

25、y: 1 (5%)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

26、 by prolonged 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-pul

27、monarynNeurally-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 diss

28、ectionnAssess 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 t

29、he risk of 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

30、 neural reflex 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 hy

31、pertensionNeural 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 ArrhythmiasnBradyarrhythmiasSi

32、nus arrest, 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 Record

33、ingsCASE: 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 pota

34、ssium channelsSusceptibility 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 El

35、ectrophysiology. 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)nAntiarr

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

37、onsedating 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 pauses

38、Isoproterenol 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:

39、Zipes D and 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 Updat

40、e. Circ. 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 pathwayAVNR

41、T Ablate 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 d

42、rug or implant 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

43、.Brignole 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 compo

44、nents:1. 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%

45、) of syncope 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

46、. 1997;126:989.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 years210008005010025842112362484480Mon

47、ths Since 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,

48、et al. Europace, 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 Suppo

49、rt hoseDrug 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 m

50、in BIDIncrease 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 traini

51、ng, 82% remained 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: C

52、linical OutcomesnFoglia-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 comp

53、liance in 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

54、trial2nVasoconstrictors1 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

55、al. J Cardiovasc 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

56、 +HUT and 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. Circulatio

57、n. 2000;102:294-299.3Ammirati 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 s

58、yncopenRandomized, 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

59、(PM)2P=0.000022PacemakerCumulative 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 pacemake

60、r therapy 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