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Syncope A Diagnostic and Treatment Strategy Developed by: David G. Benditt, M.D. Richard Sutton, DScMed University of Minnesota Medical Center Royal Brompton.

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Presentation on theme: "Syncope A Diagnostic and Treatment Strategy Developed by: David G. Benditt, M.D. Richard Sutton, DScMed University of Minnesota Medical Center Royal Brompton."— Presentation transcript:

1 Syncope A Diagnostic and Treatment Strategy Developed by: David G. Benditt, M.D. Richard Sutton, DScMed University of Minnesota Medical Center Royal Brompton Hospital, London, UK

2 Presentation Overview I.Prevalence & Impact II.Etiology III.Diagnosis & Evaluation Options IV.Specific Conditions V.Treatment Options VI.Insights into more efficient and effective diagnosis and treatment of patients with syncope

3 Section I: Prevalence and Impact

4 The Significance of Syncope The only difference between syncope and sudden death is that in one you wake up. 1 1 Engel GL. Psychologic stress, vasodepressor syncope, and sudden death. Ann Intern Med 1978; 89:

5 The Significance of Syncope 1 National Disease and Therapeutic Index on Syncope and Collapse, ICD-9-CM 780.2, IMS America, Blanc J-J, L’her C, Touiza A, et al. Eur Heart J, 2002; 23: Day SC, et al, AM J of Med Kapoor W. Evaluation and outcome of patients with syncope. Medicine 1990;69:

6  Individuals <18 yrs  Military Population yrs  Individuals yrs*  Individuals >70 yrs* 15% 20-25% 16-19% 23% Syncope Reported Frequency *during a 10-year period Brignole M, Alboni P, Benditt DG, et al. Eur Heart J, 2001; 22:

7 The Significance of Syncope  500,000 new syncope patients each year 5  170,000 have recurrent syncope 6  70,000 have recurrent, infrequent, unexplained syncope 1-4 explained: 53% to 62% infrequent, unexplained: 38% to 47% Kapoor W, Med. 1990;69: Silverstein M, et al. JAMA. 1982;248: Martin G, et al. Ann Emerg. Med. 1984;12: Kapoor W, et al. N Eng J Med. 1983;309: National Disease and Therapeutic Index, IMS America, Syncope and Collapse #780.2; Jan 1997-Dec Kapoor W, et al. Am J Med. 1987;83:

8 1 Day SC, et al. Am J of Med 1982;73: Kapoor W. Medicine 1990;69: Silverstein M, Sager D, Mulley A. JAMA. 1982;248: Martin G, Adams S, Martin H. Ann Emerg Med. 1984;13:  Some causes of syncope are potentially fatal  Cardiac causes of syncope have the highest mortality rates The Significance of Syncope

9 Impact of Syncope 1 Linzer, J Clin Epidemiol, Linzer, J Gen Int Med, Anxiety/ Depression Alter Daily Activities Restricted Driving Change Employment 73% 1 71% 2 60% 2 37% 2 Proportion of Patients

10 Section II: Etiology

11 Syncope: A Symptom…Not a Diagnosis  Self-limited loss of consciousness and postural tone  Relatively rapid onset  Variable warning symptoms  Spontaneous complete recovery

12 Cause Prevalence (Mean) % Prevalence (Range) % Reflex-mediated:  Vasovagal  Situational51-8 Carotid Sinus10-4 Orthostatic hypotension84-10 Medications31-7 Psychiatric21-7 Neurological Organic Heart Disease41-8 Cardiac Arrhythmias Unknown Causes of Syncope 1 1 Kapoor W. In Grubb B, Olshansky B (eds) Syncope: Mechanisms and Management. Armonk NY; Futura Publishing Co, Inc: 1998; 1-13.

13 Syncope: Etiology Orthostatic Cardiac Arrhythmia Structural Cardio- Pulmonary * 1 Vasovagal Carotid Sinus Situational  Cough  Post- micturition 2 Drug Induced ANS Failure  Primary  Secondary 3 Brady  Sick sinus  AV block Tachy  VT  SVT Long QT Syndrome 4 Aortic Stenosis HOCM Pulmonary Hypertension 5 Psychogenic Metabolic e.g. hyper- ventilation Neurological Non- Cardio- vascular Neurally- Mediated Unknown Cause = 34% 24%11%14%4%12% DG Benditt, UM Cardiac Arrhythmia Center

14 Causes of Syncope-like States  Migraine*  Acute hypoxemia*  Hyperventilation*  Somatization disorder (psychogenic syncope)  Acute Intoxication (e.g., alcohol)  Seizures  Hypoglycemia  Sleep disorders * may cause ‘true’ syncope

15 Section III: Diagnosis and Evaluation Options

16 Syncope Diagnostic Objectives  Distinguish ‘True’ Syncope from other ‘Loss of Consciousness’ spells:  Seizures  Psychiatric disturbances  Establish the cause of syncope with sufficient certainty to:  Assess prognosis confidently  Initiate effective preventive treatment

17 Initial Evaluation (Clinic/Emergency Dept.)  Detailed history  Physical examination  12-lead ECG  Echocardiogram (as available)

18 Syncope Basic Diagnostic Steps  Detailed History & Physical  Document details of events  Assess frequency, severity  Obtain careful family history  Heart disease present?  Physical exam  ECG: long QT, WPW, conduction system disease  Echo: LV function, valve status, HOCM  Follow a diagnostic plan...

19 Conventional Diagnostic Methods/Yield Test/ProcedureYield (based on mean time to diagnosis of 5.1 months 7 History and Physical (including carotid sinus massage) 49-85% 1, 2 ECG2-11% 2 Electrophysiology Study without SHD*11% 3 Electrophysiology Study with SHD49% 3 Tilt Table Test (without SHD)11-87% 4, 5 Ambulatory ECG Monitors:  Holter2% 7  External Loop Recorder (2-3 weeks duration) 20% 7  Insertable Loop Recorder (up to 14 months duration) 65-88% 6, 7 Neurological † (Head CT Scan, Carotid Doppler) 0-4% 4,5,8,9,10 *Structural Heart Disease † MRI not studied 1 Kapoor, et al N Eng J Med, Kapoor, Am J Med, Linzer, et al. Ann Int. Med, Kapoor, Medicine, Kapoor, JAMA, Krahn, Circulation, Krahn, Cardiology Clinics, Eagle K,, et al. The Yale J Biol and Medicine. 1983; 56: Day S, et al. Am J Med. 1982; 73: Stetson P, et al. PACE. 1999; 22 (part II): 782.

20 Syncope Evaluation and Differential Diagnosis  Complete Description  From patient and observers  Type of Onset  Duration of Attacks  Posture  Associated Symptoms  Sequelae History – What to Look for

21 12-Lead ECG  Normal or Abnormal?  Acute MI  Severe Sinus Bradycardia/pause  AV Block  Tachyarrhythmia (SVT, VT)  Preexcitation (WPW), Long QT, Brugada  Short sampling window (approx. 12 sec)

22 Carotid Sinus Massage  Site:  Carotid arterial pulse just below thyroid cartilage  Method:  Right followed by left, pause between  Massage, NOT occlusion  Duration: 5-10 sec  Posture – supine & erect

23 Carotid Sinus Massage  Outcome:  3 sec asystole and/or 50 mmHg fall in systolic blood pressure with reproduction of symptoms = Carotid Sinus Syndrome (CSS)  Contraindications  Carotid bruit, known significant carotid arterial disease, previous CVA, MI last 3 months  Risks  1 in 5000 massages complicated by TIA

24 Conventional AECG Low Yield, Poor Symptom / Arrhythmia Concordance*  8 studies, 2612 patients  19% pts had symptoms with AECG  Only 4% had arrhythmia with symptoms  79% pts were without symptoms  14% had arrhythmia despite absence of symptoms * ACC/AHA Task Force, JACC 1999;

25 MethodComments Holter (24-48 hours)Useful for infrequent events Event Recorder  Useful for infrequent events  Limited value in sudden LOC Loop Recorder  Useful for infrequent events  Implantable type more convenient (ILR) Wireless (internet) Event Monitoring In development Ambulatory ECG

26 Head-up Tilt Test (HUT)  Unmasks VVS susceptibility  Reproduces symptoms  Patient learns VVS warning symptoms  Physician is better able to give prognostic / treatment advice

27 Head-Up Tilt Test (HUT) DG Benditt, UM Cardiac Arrhythmia Center

28 Electroencephalogram  Not a first line of testing  Syncope from Seizures  Abnormal in the interval between two attacks – Epilepsy  Normal – Syncope

29 Value of Event Recorder in Syncope Linzer M. Am J Cardiol. 1990;66: * Asterisk denotes event marker

30 Patient ActivatorReveal ® Plus ILR9790 Programmer Reveal ® Plus Insertable Loop Recorder

31 ILR Recordings* 56 yo woman with syncope accompanied with seizures. Infra-Hisian AV Block: Dual chamber pacemaker 65 yo man with syncope accompanied with brief retrograde amnesia. VT and VF: ICD and meds *Medtronic data on file

32 Randomized Assessment of Syncope Trial Usual care including: External loop recorder Tilt test, EPS and others Unexplained Syncope after history, physical exam, ECG, Holter Low Risk (EF > 35%) ILR Diagnosis ILR External loop recorder Tilt test, EPS, others Krahn A, Klein GJ, Skanes Y. Circulation 2001; 104:46-51.

33 RAST Methods  Prospective randomized trial  60 patients with unexplained syncope referred for cardiac investigation  Inclusion:  Recurrent unexplained syncope  Referred to the arrhythmia service for cardiac investigation  No clinical diagnosis after history, physical, ECG and at least 24 hours of cardiac monitoring  Exclusion:  LVEF < 35%  Unable to give informed consent  Major morbidity precluding one year of follow-up Krahn A, Klein GJ, Skanes Y. Circulation 2001; 104:46-51.

34 RAST Results Unexplained Syncope n=60 ILR n=30 Conventional n=30 In Follow-up n=3 Diagnosed n=14 Undiagnosed n=13 Diagnosed n=6 Undiagnosed n=24 Krahn A, Klein GJ, Skanes Y. Circulation 2001; 104:46-51.

35 RAST Crossover Results Krahn A, Klein GJ, Skanes Y. Circulation 2001; 104: Unexplained Syncope n=60 13/30 Undiagnosed after monitoring 6 accepted crossover to conventional 24/30 Undiagnosed after conventional 21 accepted crossover to ILR Diagnosed n=1 Undiagnosed n=5 Diagnosed n=8 Undiagnosed n=5 In follow-up n=8

36 RAST - Diagnoses number of patients Krahn A, Klein GJ, Skanes Y. Circulation 2001; 104:46-51.

37 Conventional EP Testing in Syncope  Limited utility in syncope evaluation  Most useful in patients with structural heart disease  Heart disease…… %  No Heart disease…18-50%  Relatively ineffective for assessing bradyarrhythmias Brignole M, Alboni P, Benditt DG, et al. Eur Heart Journal 2001; 22:

38 EP Testing in Syncope: Useful Diagnostic Observations  Inducible monomorphic VT  SNRT > 3000 ms or CSRT > 600 ms  Inducible SVT with hypotension  HV interval ≥ 100 ms (especially in absence of inducible VT)  Pacing induced infra-nodal block

39  Objectives: Understand the mechanism of syncope in tilt-positive and tilt- negative (isolated) patients Use the ILR to assess the correlation of rhythms captured during tilt testing and spontaneous recurrent episodes  Inclusion Criteria: Patients with three or more syncopal episodes in the last 2 years Groups matched in age, sex, history of syncope, ECG, Echo abnormalities, SHD and arrhythmias ISSUE Study International Study of Syncope of Uncertain Etiology Moya A. Circulation. 2001; 104:

40 ISSUE Study Design  Multicenter, prospective 111 syncope patients 3 episodes in 2 years, first and last episode >6 months apart History, physical exam, ECG, CSM, echo, Holter (24 hr), other tests as appropriate Tilt test followed by implant of Reveal Insertable Loop Recorder Follow-up to recurrent spontaneous episode Moya A. Circulation. 2001; 104:

41 ISSUE Study Results Results Tilt-Negative Syncope (Isolated) n=82 Tilt-Positive Syncope n=29 Recurrent Event Occurrence (#)34% (28)34% (10) Mean Time to Recurrent Event (range) 105 days (47-226)59 (22-98) ILR ECG Documented (#)29% (24)28% (8)  Tachyarrhythmia 2% (2)  Bradycardia 16% (13)21% (6) –Sinus Brady 2% (2)3% (1) –Sinus Arrest 12% (10)17% (5) –AV Block 1% (1) Total Arrhythmic18% (15)21% (6) Normal Sinus Rhythm11% (9)7% (2) Moya A. Circulation. 2001; 104:

42 ISSUE Study  Conclusions: Homogeneous findings from tilt-negative and tilt- positive syncope patients were observed (clinical characteristics and outcomes). Most frequent finding was asystole secondary to progressive sinus bradycardia, suggesting a neuromediated origin In this study tilt-negative patients had as many arrhythmias (18%) as tilt-positive patients (21%) In tilt-positive patients the spontaneous episode ECG was more frequently asystolic than what was predicted by tilt test Moya A. Circulation. 2001; 104:

43 ISSUE Study Implications  HUT outcome was not predictive of vasodepressor vs. cardioinhibitory response  Bradycardia is common in spontaneous VVS - independent of HUT outcome  Bradycardia is more prevalent in spontaneous events vs. HUT induced VVS Clinical Implication: Consider a strategy of postponing treatment until a spontaneous episode can be documented Moya A. Circulation. 2001; 104:

44 Symptom-Rhythm Correlation Auto Activation Point Patient Activation Point

45 Diagnostic Limitations  Difficult to correlate spontaneous events and laboratory findings  Often must settle for an attributable cause  Unknowns remain 20-30% 1 1 Kapoor W. In Grubb B, Olshansky B (eds) Syncope: Mechanisms and Management. Armonk NY; Futura Publishing Co, Inc: 1998; 1-13.

46 Unexplained Syncope Diagnosis History and Physical Exam Surface ECG Neurological Testing Head CT Scan Carotid Doppler MRI Skull Films Brain Scan EEG CV Syncope Workup Holter ELR or ILR Tilt Table Echo EPS Other CV Testing Angiogram Exercise Test SAECG Psychological Evaluation ENT Evaluation Endocrine Evaluation Adapted from: W.Kapoor.An overview of the evaluation and management of syncope. From Grubb B, Olshansky B (eds) Syncope: Mechanisms and Management. Armonk, NY: Futura Publishing Co., Inc.1998.

47 Typical Cardiovascular Diagnostic Pathway History and Physical, ECG Syncope Known SHD No SHD Echo EPS + Treat > 30 days; > 2 Events Tilt ILR Tilt Holter/ ELR ILR Tilt/ILR < 30 days - Adapted from: Linzer M, et al. Annals of Int Med, : Syncope: Mechanisms and Management. Grubb B, Olshansky B (eds) Futura Publishing 1999 Zimetbaum P, Josephson M. Annals of Int Med, : Krahn A et al. ACC Current Journal Review,1999. Jan/Feb:80-84.

48 Section IV: Specific Conditions

49 Neurally-Mediated Reflex Syncope (NMS)  Vasovagal syncope (VVS)  Carotid sinus syndrome (CSS)  Situational syncope  post-micturition  cough  swallow  defecation  blood drawing  etc.

50 NM Reflex Syncope: Pathophysiology  Multiple triggers  Variable contribution of vasodilatation and bradycardia

51 NMS – Basic Pathophysiology Cerebral Cortex Vascular Bed Bradycardia/ Hypotension Baro- receptors Heart Feedback via Carotid Baroreceptors Other Mechanoreceptors Parasympathetic (+) sympathetic (+) ¯ Heart Rate ¯ AV Conduction _ Vasodilatation Benditt DG, Lurie KG, Adler SW, et al. Pathophysiology of vasovagal syncope. In: Neurally mediated syncope: Pathophysiology, investigations and treatment. Blanc JJ, Benditt D, Sutton R. Bakken Research Center Series, v. 10. Armonk, NY: Futura, 1996

52  Neurally Mediated Physiologic Reflex Mechanism with two Components:  Cardioinhibitory ( HR )  Vasodepressor ( BP )  Both components are usually present Vasovagal Syncope (VVS): Clinical Pathophysiology

53 Prevalence of VVS  Prevalence is poorly known  Various studies report 8% to 37% (mean 18%) of cases of syncope (Linzer 1997)  In general:  VVS patients younger than CSS patients  Ages range from adolescence to elderly (median 43 years)  Pallor, nausea, sweating, palpitations are common  Amnesia for warning symptoms in older patients

54 DG Benditt, UM Cardiac Arrhythmia Center 16.3 sec Continuous Tracing 1 sec Spontaneous VVS

55 Management Strategies for VVS  Optimal management strategies for VVS are a source of debate  Patient education, reassurance, instruction  Fluids, salt, diet  Tilt Training  Support hose  Drug therapies  Pacing  Class II indication for VVS patients with positive HUT and cardioinhibitory or mixed reflex

56 VVS: Tilt-Training  Objectives  Enhance Orthostatic Tolerance  Diminish Excessive Autonomic Reflex Activity  Reduce Syncope Susceptibility / Recurrences  Technique  Prescribed Periods of Upright Posture  Progressive Increased Duration

57 Carotid Sinus Syndrome (CSS)  Syncope clearly associated with carotid sinus stimulation is rare (≤1% of syncope)  CSS may be an important cause of unexplained syncope / falls in older individuals

58 Etiology of CSS  Sensory nerve endings in the carotid sinus walls respond to deformation  “Deafferentation” of neck muscles may contribute  Increased afferent signals to brain stem  Reflex increase in efferent vagal activity and diminution of sympathetic tone results in bradycardia and vasodilation Carotid Sinus

59 Carotid Sinus Hypersensitivity(CSH)  Abnormal response to CSM  Absence of symptoms attributable to CSS  CSH reported frequent in ‘fallers’ (Kenny) CSH  CSS

60 CSS and Falls in the Elderly  30% of people >65 yrs of age fall each year 1  Total is 9,000,000 people in USA  Approximately 10% of falls in elderly persons are due to syncope 2  50% of fallers have documented recurrence 3  Prevalence of CSS among frequent and unexplained fallers unknown but…  CSH present in 23% of >50 yrs fallers presenting at ER 3 1 Falling in the Elderly: U.S. Prevalence Data. Journal of the American Geriatric Society, Campbell et al: Age and Aging 1981;10: Richardson DA, Bexton RS, et al. Prevalence of cardioinhibitory carotid sinus hypersensitivity in patients 50 years or over presenting to the Accident and Emergency Department with “unexplained” or “recurrent” falls. PACE 1997

61 Section V: Treatment Options

62 VVS: Pharmacologic Rx  Salt /Volume  Salt tablets, ‘sport’ drinks, fludrocortisone  Beta-adrenergic blockers  1 positive controlled trial (atenolol),  1 on-going RCT (POST)  Disopyramide  SSRIs  1 controlled trial  Vasoconstrictors (e.g., midodrine)  1 negative controlled trial (etilephrine)

63 Midodrine for Neurocardiogenic Syncope Journal of Cardiovascular Electrophysiology Vol. 12, No. 8, Perez-Lugones, et al. Months p < Symptom – Free Interval Fluid Midodrine

64 Status of Pacing in VVS  Perception of pacing for VVS changing:  VVS with +HUT and cardioinhibitory response a Class IIb indication 1  Recent clinical studies demonstrated benefits of pacing in select VVS patients:  VPS I  VASIS  SYDIT  VPS II –Phase I  ROME VVS Trial 1 Gregoratos G, et al. ACC/AHA Guidelines for Implantation of Cardiac Pacemakers and Antiarrhythmic Devices. Circulation. 1998; 97:

65 Status of Pacing in VVS  Benefits of specific device features evolving:  Some success with DDD/DDI hysteresis 1 “False positives” may result in prolonged high rate intervention Tied to lower rate intervention  Rate drop therapies designed for treating VVS syncope appear to be successful Sutton R, et al. Circulation. 2000; 102: Connolly S, et al. J Am Coll Cardiol 1999; 33: Ammirati F, et al. Circulation. 2002; 104: Ammirati F, et al. NASPE Abstract #307. PACE, Vol. 24, April 2002, Part II.

66 VPS-I Vasovagal Pacemaker Study I Connolly S, et al. J Am Coll Cardiol 1999; 33:  Study Design:  54 patients randomized, prospective, single center _ 27 DDD pacemaker with rate drop response (RDR) _ 27 no pacemaker  Patient Inclusion Criteria:  6 syncopal events ever  +HUT  Relative bradycardia* *a trough heart rate <60/min if no isoproterenol used, <70/min if up to 2 mcg/min isoproterenol used, or <80/min if over 2 mcg/min isoproterenol used

67 VPS- I Connolly S, et al. J Am Coll Cardiol 1999; 33:  Endpoints:  Time to first syncope  Outcome: RESULTS PACEMAKER (n= 27) CONTROL (n=27) Number of patients w/syncopal recurrence6 (22%)19 (70%) Mean time to first recurrence (days)11254 Relative risk reduction of syncope*85.4%- *2p =

68 VPS- I Connolly S, et al. J Am Coll Cardiol 1999; 33: Cumulative Risk (%) Control (No Pacemaker) 2P= Pacemaker Time in Months Number At Risk C P

69 VPS-I  Conclusion: Dual-chamber pacing with rate drop response reduces the likelihood of syncope in patients with recurrent VVS. Connolly S, et al. J Am Coll Cardiol 1999; 33:

70 VASIS Vasovagal Syncope International Study Sutton, R, et al. Circulation. 2000; 102:  Study Design:  42 patients, randomized, prospective, multicenter _ 19 DDI pacemaker (80 bpm) with rate hysteresis (45 bpm) _ 23 no pacemaker  Patient Inclusion Criteria:  > 3 syncopal events in 2 years and last event occurring within 6 months of enrollment and,  Positive VASIS type 2A or 2B cardioinhibitory response to HUT and,  Age > 40 years or drug refractory if < 40 years

71 VASIS Sutton, R, et al. Circulation. 2000; 102:  Outcome: RESULTS Pacemaker (n= 19) No Pacemaker (n=23) Number of patients w/syncopal recurrence1 (5%)14 (61%) Median time to first recurrence (months)*155 *P=  Endpoints:  Time to first syncope

72 VASIS Pacemaker No-Pacemaker p= Years % syncope-free # of pts Sutton, R, et al. Circulation. 2000; 102:

73 VASIS  Conclusion: Dual-chamber pacing (at a rate of 80 bpm ) with rate hysteresis reduces the likelihood of syncope in patients with tilt-positive, cardioinhibitory syncope. Sutton, R, et al. Circulation. 2000; 102:

74 SYDIT Syncope Diagnosis and Treatment Study  Study Design:  93 patients randomized, prospective, multicenter _ 46 DDD pacemaker with rate drop response (RDR) _ 47 Atenolol 100 MG/D  Patient Inclusion Criteria:  > 55 yrs  > 3 syncopal episodes in 2 years  + HUT with relative bradycardia (trough HR <60 bpm) Ammirati F, et al. Circulation. 2001; 104:52-57.

75 SYDIT  Endpoints:  Time to first syncope  Outcome: RESULTS PACED (n= 46) DRUG (n= 47) Number of patients w/syncopal recurrence*2 (4%)12 (25%) Median time to first recurrence (days) *P=0.004 Ammirati, et al. Circulation. 2001; 104:52-57.

76 Syncope-free Survival: Intention-to-Treat (n=46/paced, 47/drug). Ammirati F, et al. Circulation. 2001; 104: SYDIT 1.0 Time (days) P = drug pacemaker % of syncope free pts

77 SYDIT  Conclusion: Dual-chamber pacing + RDR is superior to Atenolol in prevention of recurrent syncope in highly symptomatic patients with relative bradycardia during tilt-induced syncope. Ammirati F, et al. Circulation. 2001; 104:52-57.

78 VPS-II: Phase I Vasovagal Pacemaker Study-II  Study Design:  100 patients, randomized, prospective, multicenter _ 50 DDD pacemaker with rate drop response (RDR) _ 50 ODO pacemaker (inactive mode)  Patient Inclusion Criteria:  > 6 syncope events ever or > 3 syncope events in 2 years or > 1 syncope event in 6 months and,  Positive HUT with syncope or presyncope and a heart rate blood pressure product <9000 Presented at the 23 rd Annual Scientific Sessions of the North American Society of Pacing and Electrophysiology. Late Breaking Clinical Trials, May 11, 2002.

79 VPS-II: Phase I  Endpoints:  Time to first syncope  Outcome: RESULTS DDD Pacemaker (n= 50) ODO Pacemaker (n= 50) Number of patients w/syncopal recurrence16 (32%)22 (44%) Relative Risk Reduction*28.7%- *P=0.153 Presented at the 23 rd Annual Scientific Sessions of the North American Society of Pacing and Electrophysiology. Late Breaking Clinical Trials, May 11, 2002.

80 ODO DDD P = (one-sided) Number at Risk ODO DDD Cumulative Risk of Syncope Presented at the 23 rd Annual Scientific Sessions of the North American Society of Pacing and Electrophysiology. Late Breaking Clinical Trials, May 11, VPS-II: Phase I

81  Conclusions:  Lower than anticipated syncope event rate in the control arm.  Higher than anticipated event rate in the treatment group.  Consequence: treatment effect was less than VPS-I.  Results favored pacing but the treatment effect was not statistically significant. Presented at the 23 rd Annual Scientific Sessions of the North American Society of Pacing and Electrophysiology. Late Breaking Clinical Trials, May 11, 2002.

82 VVS Pacing Trials Conclusions DDD pacing reduces the risk of syncope in patients with recurrent, refractory, highly-symptomatic, cardioinhibitory vasovagal syncope.

83 SAFE PACE Study Design  Randomized controlled trial (N=175):  Pacing (87) vs. No Pacing (88)  Single center: Royal Victoria Infirmary, Newcastle, UK  Recruitment began: April 1998  12 month follow-up per patient  Study concluded: May 2000 Kenny RA, J Am Coll Cardiol 2001; 38:

84 SAFE PACE Inclusion Criteria  Consecutive adults attending accident and emergency department > 50 Years - Experienced non-accidental fall Positive response to CSM Kenny RA, J Am Coll Cardiol 2001; 38:

85 SAFE PACE Screening Process Accident and Emergency Attendees > 50 Yrs Falls or Syncope Non-accidental Fall CSM Performed Cardioinhibitory or Mixed CSH RCT ControlPacemaker Kenny RA, J Am Coll Cardiol 2001; 38:

86 SAFE PACE Screening Results RCT (n=175) Control (n=88) Pacemaker (n=87) No pacing interventionMedtronic Thera DR (Rate Drop Response Algorithm) Kenny RA, J Am Coll Cardiol 2001; 38:

87 SAFE PACE Results Number of Falls Control n=87 Pacemaker n=84 % Participants w/Falls 60%58% Total Number of Falls* Mean Number of Falls** * Falls during 12 months post randomization ** Crude adjustment calculation Kenny RA, J Am Coll Cardiol 2001; 38: % Reduction [OR 0.42; 95% CI: 0.23, 0.75]

88 Control N=87 Pacemaker N=84 % Participants w/Syncopal Events 22%11% Total Number of Syncopal Events 4722 Mean Number Syncopal Events SAFE PACE Results Number of Syncopal Episodes 50% Reduction [OR 0.53; 95% CI 0.23; 1.20 ns] * Syncopal events 12 months past randomization ** Crude adjustment calculation Kenny RA, J Am Coll Cardiol 2001; 38:

89 Control n= 87 Pacemaker n= 84 % Participants w/Injurious Events 41%35% Total Number Injury Events Fractures -Soft Tissue Injury SAFE PACE Results Number of Injury Events 70% Reduction * Injurious events 12 months post randomization Kenny RA, J Am Coll Cardiol 2001; 38:

90 SAFE PACE Conclusions In patients with unexplained falls and a diagnosis of Cardioinhibitory CSH, cardiac pacing reduced the total number of:  Falls by 70%  Syncopal events by 53%  Injurious events by 70% Kenny RA, J Am Coll Cardiol 2001; 38:

91 Role of Pacing in CSS -- Syncope Recurrence Rate Brignole et. Al. Diagnosis, natural history and treatment. Eur JCPE. 1992; 4: % %6 % Recurrence Class I indication for pacing (AHA and BPEG) Limit pacing to CSS that is: Cardioinhibitory Mixed DDD/DDI superior to VVI (Mean follow-up = 6 months)

92 Section VI: Insights into More Efficient and Effective Diagnosis and Treatment

93 Principal Causes of Orthostatic Syncope  Drug-induced (very common)  diuretics  vasodilators  Primary autonomic failure  multiple system atrophy  Parkinsonism  Secondary autonomic failure  diabetes  alcohol  amyloid  Alcohol  orthostatic intolerance apart from neuropathy

94 Syncope Due to Arrhythmia or Structural CV Disease: General Rules  Often life-threatening and/or exposes patient to high risk of injury  May be warning of critical CV disease  Aortic stenosis, Myocardial ischemia, Pulmonary hypertension  Assess culprit arrhythmia / structural abnormality aggressively  Initiate treatment promptly

95 Principal Causes of Syncope due to Structural Cardiovascular Disease  Acute MI / Ischemia  Acquired coronary artery disease  Congenital coronary artery anomalies  HOCM  Acute aortic dissection  Pericardial disease / tamponade  Pulmonary embolus / pulmonary hypertension  Valvular abnormalities  Aortic stenosis, Atrial myxoma

96 Syncope Due to Cardiac Arrhythmias  Bradyarrhythmias  Sinus arrest, exit block  High grade or acute complete AV block  Tachyarrhythmias  Atrial fibrillation / flutter with rapid ventricular rate (e.g. WPW syndrome)  Paroxysmal SVT or VT  Torsades de pointes

97 Rhythms During Recurrent Syncope Krahn A, et al. Circulation. 1999; 99: Normal Sinus Rhythm 58% Normal Sinus Rhythm 58% Bradycardia 36% Tachyarrhythmia 6%

98 AECG: 74 yr Male, Syncope From the files of DG Benditt, UM Cardiac Arrhythmia Center

99 Syncope: Torsades From the files of DG Benditt, UM Cardiac Arrhythmia Center

100 83 yo woman Bradycardia: Pacemaker implanted 28 yo man in the ER multiple times after falls resulting in trauma VT: ablated and medicated Reveal ® ILR recordings; Medtronic data on file.

101 Infra-His Block From the files of DG Benditt, UM Cardiac Arrhythmia Center

102 Drug-Induced QT Prolongation  Antiarrhythmics  Class IA...Quinidine, Procainamide, Disopyramide  Class III…Sotalol, Ibutilide, Dofetilide, Amiodarone, (NAPA)  Antianginal Agents  (Bepridil)  Psychoactive Agents  Phenothiazines, Amitriptyline, Imipramine, Ziprasidone  Antibiotics  Erythromycin, Pentamidine, Fluconazole  Nonsedating antihistamines  (Terfenadine), Astemizole  Others  (Cisapride), Droperidol

103 Treatment of Syncope Due to Bradyarrhythmia  Class I indication for pacing using dual- chamber system wherever adequate atrial rhythm is available  Ventricular pacing in atrial fibrillation with slow ventricular response

104 Treatment of Syncope Due to Tachyarrhythmia  Atrial Tachyarrhythmias;  AVRT due to accessory pathway – ablate pathway  AVNRT – ablate AV nodal slow pathway  Atrial fib  – Pacing, linear / focal ablation, ICD selected pts  Atrial flutter – Ablation of reentrant circuit  Ventricular Tachyarrhythmias;  Ventricular tachycardia – ICD or ablation where appropriate  Torsades de Pointes – withdraw offending Rx or ICD (long- QT/Brugada)  Drug therapy may be an alternative in many cases

105 Conclusion Syncope is a common symptom, often with dramatic consequences, which deserves thorough investigation and appropriate treatment of its cause.

106 Disclaimer INDICATIONS 9526 Reveal ® Plus Insertable Loop Recorder The Reveal Plus Insertable Loop Recorder (ILR) is an implantable patient activated monitoring system that records subcutaneous ECG and is indicated for patients who experience transient symptoms that may suggest a cardiac arrhythmia Programmer The Medtronic 9790 Programmers are portable, microprocessor based instruments used to program Medtronic implantable devices Activator The Model 6191 Activator is intended for use in combination with a Medtronic Model 9525 Reveal ® and the Model 9526 Reveal Plus Insertable Loop Recorders. CONTRAINDICATIONS There are no known contraindications for the implantation of the Reveal Plus ILR. However, the patient’s particular medical condition may dictate whether or not a subcutaneous, chronically implanted device can be tolerated. WARNINGS/PRECAUTIONS 9526 Reveal Plus Insertable Loop Recorder Patients with the Reveal Plus ILR should avoid sources of magnetic resonance imaging, diathermy, high sources of radiation, electrosurgical cautery, external defibrillation, lithotripsy, and radiofrequency ablation to avoid electrical reset of the device, and/or inappropriate sensing Activator Operation of the Model 6191 Activator near sources of electromagnetic interference, such as cellular phones, computer monitors, etc., may adversely affect the performance of this device. See the appropriate technical manual for detailed information regarding indications, contraindications, warnings, and precautions. Caution: Federal law (U.S.A.) restricts this device to sale by or on the order of a physician.

107 Disclaimer INDICATIONS Medtronic.Kappa 700 Series Pacemakers The Medtronic.Kappa 700 Series pacemakers are indicated for rate adaptive pacing in patients who may benefit from increased pacing rates concurrent with increases in activity and are also indicated for dual chamber and atrial tracking modes in patients who may benefit from maintenance of AV synchrony. Dual chamber modes are specifically indicated for treatment of conduction disorders that require restoration of both rate and AV synchrony, which include various degrees of AV block to maintain the atrial contribution to cardiac output and VVI intolerance (e.g., pacemaker syndrome) in the presence of persistent sinus rhythm Programmer The Medtronic 9790 Programmers are portable, microprocessor based instruments used to program Medtronic implantable devices The Model 9462 Remote Assistant is intended for use in combination with a Medtronic implantable pacemaker with Remote Assistant diagnostic capabilities. CONTRAINDICATIONS The Medtronic.Kappa 700 Series pacemakers are contraindicated for the following applications: · Dual chamber atrial pacing in patients with chronic refractory atrial tachyarrhythmias. · Asynchronous pacing in the presence (or likelihood) of competitive paced and intrinsic rhythms. · Unipolar pacing for patients with an implanted cardioverter-defibrillator (ICD) because it may cause unwanted delivery or inhibition of ICD therapy. WARNINGS/PRECAUTIONS Medtronic.Kappa 700 Series patients should avoid sources of magnetic resonance imaging, diathermy, high sources of radiation, electrosurgical cautery, external defibrillation, lithotripsy, and radiofrequency ablation to avoid electrical reset of the device, inappropriate sensing and/or therapy. See the appropriate technical manual for detailed information regarding indications, contraindications, warnings, and precautions. Caution: Federal law (U.S.A.) restricts this device to sale by or on the order of a physician.

108 Additional Slides

109 Falls -- Incidence, Recurrence, CHS* 1 Falling in the Elderly, Richardson, PACE, Incidence > 65 yrs. old RecurrenceCSH* present in fallers > 50 yrs. presenting at ER 30% 1 50% 1 23% 2 Percent of People * Carotid Sinus Hypersensitivity

110 VVS Pacing Trials Comparison Summary

111 Pacing in VVS Two randomized, controlled trials suggest benefit in selected patients with multiple (>5 lifetime) syncope recurrences and one or more of:  prominent cardioinhibitory features  asystolic pause >10 seconds  sustained HR<40/minute

112 VVS Recurrences  35% of patients report syncope recurrence during follow-up ≤3 years  Positive HUT with >6 lifetime syncope episodes: recurrence risk >50% over 2 years Sheldon et al. Circulation 1996; 93: Savage et al. STROKE 1985; 16:

113 SAFE PACE 2: Syncope and Falls in the Elderly  30% of individuals >65 yrs fall each year  5% of falls result in fractures  1% of falls result in hip fractures  SAFEPACE Pilot Study  18% prevalence of CSH in unexplained ‘fallers’  31% in ‘fallers’ >80 yrs Kenny RA, J Am Coll Cardiol 2001; 38:

114 Both Rate Drop Response Overview Detection Options Drop Detect Drop Detect Low Rate Detect Low Rate Detect Detects relative heart rate drops of a pre- determined size Detects heart rate that falls to a user-defined lower rate Detection occurs when either Drop Detection or Low Rate Detection criteria are met Rate Drop Detection in Medtronic Kappa® Series Pacemakers

115 Drop Detection with Intervention Drop Detection Method: Drop Size 25, Drop Rate Ventricular Rate Drop Size=25 bpm Drop Rate Peak Rate=90 bpm 2 consecutive beats< Drop Size and Drop Rate Rate Drop Detection in Medtronic Kappa® Series Pacemakers

116 Drop Detect Peak Rate Drop Detection Method: Drop Size Ventricular Rate Drop Size=25 bpm Peak Rate=90 bpm Rate Drop Detection in Medtronic Kappa® Series Pacemakers

117 Low Rate Detection Method: Lower Rate 40, Detection beats Ventricular Rate Lower Rate 2 consecutive paced beats at Lower Rate Low Rate Detect Rate Drop Detection in Medtronic Kappa® Series Pacemakers

118 Using Both Detection Algorithms  When both detection algorithms are used:  Detection occurs when either Drop Detection or Low Rate Detection criteria are met  Intervention Rate, Duration and Termination are programmed the same as when using the individual detection modes Rate Drop Detection in Medtronic Kappa® Series Pacemakers

119 Rate Drop Intervention Therapy  DDD or DDI pacing  Pacing intervention  Paces at programmed Intervention Rate for programmed duration  Pacing termination  Pacing rate decreases until there are three consecutive atrial senses or Lower Rate is reached Rate Drop Detection in Medtronic Kappa® Series Pacemakers

120 Challenges of Syncope  Cost  Cost/year  Cost/diagnosis  Quality of Life Implications  Work/financial  Mobility (automobiles)  Psychological  Diagnosis & Treatment  Diagnostic yield and repeatability of tests  Frequency and clustering of events  Difficulty in managing/treating/controlling future events  Appropriate risk stratification  Complex Etiology

121 Diagnosing VVS  Patient history and physical exam  Positive tilt table test (ACC Consensus Protocol)  Overnight fast  ECG  Blood pressure  Supine and upright  Tilt to degrees  Isoproterenol  Re-tilt DG Benditt, Tilt Table Testing, ° - 80°

122 VVS: Treatment Overview  Education  symptom recognition  reassurance  situation avoidance  Tilt-Training  prescribed upright posture  Pharmacologic Agents  salt/volume management  beta-adrenergic blockers  SSRIs  vasoconstrictors (e.g., midodrine)  Cardiac Pacemakers

123 Tilt-Training: Clinical Outcomes  42 HUT positive (21±13 min) VVS patients  Home training: two 30 minute sessions daily  Outcomes  41/42 pts --->45 min asymptomatic HUT  Clinical follow-up: 15.1±7.8 mos 36 pts syncope free 4 pts: presyncope 1 pt: syncope recurrences Reybrouck et al. PACE 2000; 23:493-8


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