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Transient Loss of Consciousness (TLOC). . . . . . . Classification of Transient Loss of Consciousness (TLOC). SyncopeNeurally-mediated reflex syndromesOrthostatic hypotensionCardiac arrhythmias Structural cardiovascular disease . Disorders Mimicking SyncopeWith loss of consciousness, i.e., seizure disorders, concussionWithout loss of consciousness, i.e., psychogenic
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1. SyncopeA Diagnostic and Treatment Strategy
2. Transient Loss of Consciousness, or TLOC, is just that.
It can be as simple as a benign ‘faint’ or a symptom of an underlying disease that may lead to sudden death. Or it may not be syncope at all.
Transient Loss of Consciousness, or TLOC, is just that.
It can be as simple as a benign ‘faint’ or a symptom of an underlying disease that may lead to sudden death. Or it may not be syncope at all.
3. Classification of Transient Loss of Consciousness (TLOC) Syncope
Neurally-mediated reflex syndromes
Orthostatic hypotension
Cardiac arrhythmias
Structural cardiovascular disease Disorders Mimicking Syncope
With loss of consciousness, i.e., seizure disorders, concussion
Without loss of consciousness, i.e., psychogenic “pseudo-syncope” Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
4. Syncope – A Symptom, Not a Diagnosis Self-limited loss of consciousness and postural tone
Relatively rapid onset
Variable warning symptoms
Spontaneous, complete, and usually prompt recovery without medical or surgical intervention Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
5. Presentation Overview I. Etiology, Prevalence, Impact
II. Diagnosis
III. Specific Conditions and Treatment
IV. Special Issues
6. Section I:Etiology, Prevalence, Impact
7. Causes of True Syncope This slide provides a simple classification of the principal causes of syncope, listed from the most commonly observed (left) to the least common (right). This ranking may be helpful in thinking about the strategy for evaluating syncope in individual patients.
Within the boxes, the most common causes of syncope are indicated for each of the major diagnostic groups.
The terms ‘neurally-mediated syncope’, ‘neurally-mediated reflex syncope,’ and ‘neurocardiogenic syncope’ are generally used synonymously. For purposes of this presentation, ‘neurally-mediated syncope’ is used to define a broad category; ‘neurocardiogenic’ or ‘vasovagal syncope’ refer to a specific condition.
VVS—Vasovagal Syncope
CSS—Carotid Sinus Syndrome
ANS—Autonomic Nervous System
HCM—Hypertrophic Cardiomyopathy
DG Benditt, MD. University of Minnesota Cardiac Arrhythmia CenterThis slide provides a simple classification of the principal causes of syncope, listed from the most commonly observed (left) to the least common (right). This ranking may be helpful in thinking about the strategy for evaluating syncope in individual patients.
Within the boxes, the most common causes of syncope are indicated for each of the major diagnostic groups.
The terms ‘neurally-mediated syncope’, ‘neurally-mediated reflex syncope,’ and ‘neurocardiogenic syncope’ are generally used synonymously. For purposes of this presentation, ‘neurally-mediated syncope’ is used to define a broad category; ‘neurocardiogenic’ or ‘vasovagal syncope’ refer to a specific condition.
VVS—Vasovagal Syncope
CSS—Carotid Sinus Syndrome
ANS—Autonomic Nervous System
HCM—Hypertrophic Cardiomyopathy
DG Benditt, MD. University of Minnesota Cardiac Arrhythmia Center
8. Syncope Mimics Acute intoxication (e.g., alcohol)
Seizures
Sleep disorders
Somatization disorder (psychogenic pseudo-syncope)
Trauma/concussion
Hypoglycemia
Hyperventilation Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
9. Impact of Syncope 1Kenny RA, Kapoor WN. Epidemiology and social costs. In: Benditt D, Blanc J-J, et al. eds. The Evaluation and Treatment of Syncope. Elmsford, NY: Futura;2003:23-27.
2Kapoor W. Evaluation and outcome of patients with syncope. Medicine. 1990;69:160-175.
3Brignole M, Disertori M, Menozzi C, et al. Management of syncope referred urgently to general hospitals with and without syncope units. Europace. 2003;5:293-298.
4 Blanc J-J, L’ Her C, Touiza A, et al. Prospective evaluation and outcome of patients admitted for syncope over a 1 year period. Eur Heart J. 2002;23:815-820.
5Campbell A, Reinken J, Allan B, et al. Falls in old age: A study of frequency and related clinical factors. Age and Ageing. 1981;10:264-270.
1Kenny RA, Kapoor WN. Epidemiology and social costs. In: Benditt D, Blanc J-J, et al. eds. The Evaluation and Treatment of Syncope. Elmsford, NY: Futura;2003:23-27.
2Kapoor W. Evaluation and outcome of patients with syncope. Medicine. 1990;69:160-175.
3Brignole M, Disertori M, Menozzi C, et al. Management of syncope referred urgently to general hospitals with and without syncope units. Europace. 2003;5:293-298.
4 Blanc J-J, L’ Her C, Touiza A, et al. Prospective evaluation and outcome of patients admitted for syncope over a 1 year period. Eur Heart J. 2002;23:815-820.
5Campbell A, Reinken J, Allan B, et al. Falls in old age: A study of frequency and related clinical factors. Age and Ageing. 1981;10:264-270.
10. Impact of Syncope: US Trends National Hospital Discharge Survey (NHDS) 2003.
National Ambulatory Medical Care Survey (NAMCS) 2002.
Syncope is a growing problem. More patients are being seen in outpatient visits and are being admitted with this problem.
National Hospital Discharge Survey (NHDS) 2003.
National Ambulatory Medical Care Survey (NAMCS) 2002.
Syncope is a growing problem. More patients are being seen in outpatient visits and are being admitted with this problem.
11. Impact of Syncope: US Trends The National Hospital Ambulatory Medical Care Survey (NHAMCS) is a national probability survey, conducted by the National Center for Health Statistics (NCHS). The NCHS is a part of the Centers for Disease Control and Prevention (CDC), U.S. Department of Health and Human Services, 2002.
Likewise, the trends indicate an increase in emergency room visits and a slight increase in hospital outpatient visits.The National Hospital Ambulatory Medical Care Survey (NHAMCS) is a national probability survey, conducted by the National Center for Health Statistics (NCHS). The NCHS is a part of the Centers for Disease Control and Prevention (CDC), U.S. Department of Health and Human Services, 2002.
Likewise, the trends indicate an increase in emergency room visits and a slight increase in hospital outpatient visits.
12. Impact of Syncope: NHS Hospitals, England, 2002-2003* 74,813 hospital consults for syncope and collapse
80% required hospital admission
Average length of stay: 6.1 days
327,201 hospital bed days, second only to senility Hospital Episode Statistics, Department of Health, England. 2002-2003.Hospital Episode Statistics, Department of Health, England. 2002-2003.
13. Impact of Syncope: Costs Estimated hospital costs exceeded $10 billion US1
Estimated physician office expenses exceeded $470 million2
Ł104,285 spent on 1,334 patients with syncopal codes (UK) (EaSyAS)3
Hospital admission: 67% of investigational costs
Over $7 billion is spent annually in the US to treat falls in older adults4 1Kenny RA, Kapoor WN. Epidemiology and social costs. In: Benditt D, Blanc J-J, et al. eds. The Evaluation and Treatment of Syncope. Elmsford, NY: Futura;2003:23-27.
2 Solucient Outpatient View: OutPatientView v. 6.0. Solucient LLC, Evanston IL.
3Farwell D and Sulke N. How do we diagnose syncope? J Cardiovasc Electrophysiol. 2002;13(Supp):S9-S13.
4Olshansky B. Syncope: Overview and approach to management. In: Grubb B and Olshansky B. eds. Syncope: Mechanisms and Management. Armonk, NY:Futura;1998:15-71.1Kenny RA, Kapoor WN. Epidemiology and social costs. In: Benditt D, Blanc J-J, et al. eds. The Evaluation and Treatment of Syncope. Elmsford, NY: Futura;2003:23-27.
2 Solucient Outpatient View: OutPatientView v. 6.0. Solucient LLC, Evanston IL.
3Farwell D and Sulke N. How do we diagnose syncope? J Cardiovasc Electrophysiol. 2002;13(Supp):S9-S13.
4Olshansky B. Syncope: Overview and approach to management. In: Grubb B and Olshansky B. eds. Syncope: Mechanisms and Management. Armonk, NY:Futura;1998:15-71.
14. Impact of Syncope: Quality of Life Syncope results in substantial cost to patients and to society. For example, syncope patients live with lifestyle altering restrictions that affect daily activities, mobility, and employment.
Linzer M, Pontinen M, Gold DT, et al. Impairment of physical and psychological function in recurrent syncope. J Clin Epidemiol. 1991;44:1037-1043.
Linzer M, Gold DT, Pontinen M, et al. Recurrent syncope as a chronic disease: Preliminary validation of a disease-specific measure of functional impairment. J Gen Int Med. 1994;9:181-186.Syncope results in substantial cost to patients and to society. For example, syncope patients live with lifestyle altering restrictions that affect daily activities, mobility, and employment.
Linzer M, Pontinen M, Gold DT, et al. Impairment of physical and psychological function in recurrent syncope. J Clin Epidemiol. 1991;44:1037-1043.
Linzer M, Gold DT, Pontinen M, et al. Recurrent syncope as a chronic disease: Preliminary validation of a disease-specific measure of functional impairment. J Gen Int Med. 1994;9:181-186.
15. Quality of Life: UK Population Norms vs. Syncope Patients To measure health-related quality of life (HRQL), Rose1 and colleagues used the EQ-5D. This tool has been designed as an international, standardized, generic instrument for describing and valuing health-related quality of life.2 The study showed evidence of substantially impaired HRQL in syncope patients, compared to the reference population norms in all five dimensions of health.
The increase in the prevalence of impaired health was approximately 10-fold for mobility, usual activities, and self-care, and 2-fold for anxiety/depression.
1Rose M, Koshman ML, Spreng S, et al. The relationship between health-related quality of life and frequency of spells in patients with syncope. J Clin Epidemiol. 2000;53:1209-1216.
2The EuroQol Group. EuroQol: A new facility for the measurement of health related quality of life. Health Policy. 1990;16:199-208.To measure health-related quality of life (HRQL), Rose1 and colleagues used the EQ-5D. This tool has been designed as an international, standardized, generic instrument for describing and valuing health-related quality of life.2 The study showed evidence of substantially impaired HRQL in syncope patients, compared to the reference population norms in all five dimensions of health.
The increase in the prevalence of impaired health was approximately 10-fold for mobility, usual activities, and self-care, and 2-fold for anxiety/depression.
1Rose M, Koshman ML, Spreng S, et al. The relationship between health-related quality of life and frequency of spells in patients with syncope. J Clin Epidemiol. 2000;53:1209-1216.
2The EuroQol Group. EuroQol: A new facility for the measurement of health related quality of life. Health Policy. 1990;16:199-208.
16. Syncope Mortality Low mortality vs. high mortality
Neurally-mediated syncope vs. syncope with a cardiac cause
17. Implications of Syncope for Driving a Vehicle Those who drive and have recurrent syncope risk their lives and the lives of others
Places considerable burden on the physician
Essential to know local laws and physician responsibilities
Some states – Invasion of privacy to notify motor vehicle department*
Other states – Reporting is mandatory* If the patient has sufficient warning of impending syncope – Driving may be permitted Olshansky B, Grubb B. Driving and Syncope. In: Olshansky B and Grubb B, eds. Syncope: Mechanisms and Management. Armonk, NY: Futura Publishing Co;1998:371-385.
*Medtronic, Inc. When may patients with implanted defibrillators drive? Follow-up Forum. Winter. 1995/96;1(3):8-10.
Olshansky B, Grubb B. Driving and Syncope. In: Olshansky B and Grubb B, eds. Syncope: Mechanisms and Management. Armonk, NY: Futura Publishing Co;1998:371-385.
*Medtronic, Inc. When may patients with implanted defibrillators drive? Follow-up Forum. Winter. 1995/96;1(3):8-10.
18. Challenges of Syncope Diagnosis
Complex
Quality of life implications
Work
Mobility (automobiles)
Psychological
Cost
Cost/year
Cost/diagnosis
Syncope impacts patient quality of life and health care costs in important ways.
Establishing a precise diagnosis is often challenging due to the unpredictability of events and the limited positive predictive value of most available tests. The ‘gold standard’ remains the recording of the cardiac rhythm (and if possible the arterial pressure) during a spontaneous faint.Syncope impacts patient quality of life and health care costs in important ways.
Establishing a precise diagnosis is often challenging due to the unpredictability of events and the limited positive predictive value of most available tests. The ‘gold standard’ remains the recording of the cardiac rhythm (and if possible the arterial pressure) during a spontaneous faint.
19. Section II:Diagnosis
20. Diagnostic Objectives Distinguish true syncope from syncope mimics
Determine presence of heart disease
Establish the cause of syncope with sufficient certainty to:
Assess prognosis confidently
Initiate effective preventive treatment
21. A Diagnostic Plan is Essential Initial Examination
Detailed patient history
Physical exam
ECG
Supine and upright blood pressure
Monitoring
Holter
Event
Insertable Loop Recorder (ILR)
Cardiac Imaging
Special Investigations
Head-up tilt test
Hemodynamics
Electrophysiology study Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
22. Diagnostic Flow Diagram for TLOC Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
23. Initial Exam: Detailed Patient History Circumstances of recent event
Eyewitness account of event
Symptoms at onset of event
Sequelae
Medications
Circumstances of more remote events
Concomitant disease, especially cardiac
Pertinent family history
Cardiac disease
Sudden death
Metabolic disorders
Past medical history
Neurological history
Syncope The history must include detailed summary of events leading up to and following syncope events. Additionally, it is important to ascertain whether there is any evidence of underlying structural heart disease. The direction of subsequent evaluation differs in patients with and without heart disease.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
Raviele A, Alboni P, Sutton D, Kenny RA. Initial evaluation of the syncope patient. In: Benditt D, Blanc J-J, Brignole M, Sutton R, eds. The Evaluation and Treatment of Syncope. Elmsford, NY: Futura. 2003:38-45.The history must include detailed summary of events leading up to and following syncope events. Additionally, it is important to ascertain whether there is any evidence of underlying structural heart disease. The direction of subsequent evaluation differs in patients with and without heart disease.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
Raviele A, Alboni P, Sutton D, Kenny RA. Initial evaluation of the syncope patient. In: Benditt D, Blanc J-J, Brignole M, Sutton R, eds. The Evaluation and Treatment of Syncope. Elmsford, NY: Futura. 2003:38-45.
24. Initial Exam: Thorough Physical Vital signs
Heart rate
Orthostatic blood pressure change
Cardiovascular exam: Is heart disease present?
ECG: Long QT, pre-excitation, conduction system disease
Echo: LV function, valve status, HCM
Neurological exam
Carotid sinus massage
Perform under clinically appropriate conditions preferably during head-up tilt test
Monitor both ECG and BP HCM—Hypertrophic Cardiomyopathy
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.HCM—Hypertrophic Cardiomyopathy
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
25. Carotid Sinus Massage (CSM) Method1
Massage, 5-10 seconds
Don’t occlude
Supine and upright posture (on tilt table)
Outcome
3 second asystole and/or 50 mmHg fall in systolic BP with reproduction of symptoms = Carotid Sinus Syndrome Absolute contraindications2
Carotid bruit, known significant carotid arterial disease, previous CVA, MI last 3 months
Complications
Primarily neurological
Less than 0.2%3
Usually transient Carotid sinus massage (CSM) is an often overlooked, yet highly cost effective test, especially in older syncope patients. CSM must be applied with care, and the method described here1 has proven both safe and effective.
Note that an abnormal response to CSM (i.e., Carotid Sinus Hypersensitivity, CSH) is not diagnostic of Carotid Sinus Syndrome (CSS). Reproduction of symptoms is a crucial diagnostic element. To achieve symptom reproduction, it may be useful to conduct CSM with the patient in the upright posture. If the latter is to be done, the patient should be safely secured to a tilt table in order to prevent injury from a fall.
1Kenny RA, O’Shea D, Parry SW. The Newcastle protocols for head-up tilt table testing in the diagnosis of vasovagal syncope, carotid sinus hypersensitivity, and related disorders. Heart. 2000;83:564-569.
2Linzer M, Yang EH, Estes M, et al. Diagnosing Syncope: Part 1: Value of history, physical examination, and electrocardiography. Ann Intern Med. 1997;126(12):989-996.
3Munro N, McIntosh S, Lawson J, et al. Incidence of complications after carotid sinus massage in older patients with syncope. J Am Geriatr Soc. 1994;42:1248-1251.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
Carotid sinus massage (CSM) is an often overlooked, yet highly cost effective test, especially in older syncope patients. CSM must be applied with care, and the method described here1 has proven both safe and effective.
Note that an abnormal response to CSM (i.e., Carotid Sinus Hypersensitivity, CSH) is not diagnostic of Carotid Sinus Syndrome (CSS). Reproduction of symptoms is a crucial diagnostic element. To achieve symptom reproduction, it may be useful to conduct CSM with the patient in the upright posture. If the latter is to be done, the patient should be safely secured to a tilt table in order to prevent injury from a fall.
1Kenny RA, O’Shea D, Parry SW. The Newcastle protocols for head-up tilt table testing in the diagnosis of vasovagal syncope, carotid sinus hypersensitivity, and related disorders. Heart. 2000;83:564-569.
2Linzer M, Yang EH, Estes M, et al. Diagnosing Syncope: Part 1: Value of history, physical examination, and electrocardiography. Ann Intern Med. 1997;126(12):989-996.
3Munro N, McIntosh S, Lawson J, et al. Incidence of complications after carotid sinus massage in older patients with syncope. J Am Geriatr Soc. 1994;42:1248-1251.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
26. Other Diagnostic Tests Ambulatory ECG
Holter monitoring
Event recorder
Intermittent vs. Loop
Insertable Loop Recorder (ILR)
Head-Up Tilt (HUT)
Includes drug provocation (NTG, isoproterenol)
Carotid Sinus Massage (CSM)
Adenosine Triphosphate Test (ATP)
Electrophysiology Study (EPS) NTG = nitroglycerin
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
NTG = nitroglycerin
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
27. Heart Monitoring Options Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
28. Diagnostic Assessment: Yields (N=3411 to 4332) 1Alboni P, Brignole M, Menozzi C, et al. Diagnostic value of history in patients with syncope with or without heart disease. J Am Coll Cardiol. 2001;37:1921-1928.
2Kapoor W. Evaluation and outcome of patients with syncope. Medicine. 1990;69:160-175.
3Krahn AD, Klein GJ, Yee R, et al. for the Reveal Investigators. Use of an extended monitoring strategy in patients with problematic syncope. Circulation. 1999;99;406-410.
4Krahn AD, Klein GJ, Yee R, et al. Randomized Assessment of Syncope Trial. Conventional diagnostic testing versus a prolonged monitoring strategy. Circulation. 2001;104:46-51.
5Krahn AD, Klein GJ, Yee R, et al. The high cost of syncope: Cost implications of a new insertable loop recorder in the investigation of recurrent syncope. Am Heart J. 1999;137:870-877.
6Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
1Alboni P, Brignole M, Menozzi C, et al. Diagnostic value of history in patients with syncope with or without heart disease. J Am Coll Cardiol. 2001;37:1921-1928.
2Kapoor W. Evaluation and outcome of patients with syncope. Medicine. 1990;69:160-175.
3Krahn AD, Klein GJ, Yee R, et al. for the Reveal Investigators. Use of an extended monitoring strategy in patients with problematic syncope. Circulation. 1999;99;406-410.
4Krahn AD, Klein GJ, Yee R, et al. Randomized Assessment of Syncope Trial. Conventional diagnostic testing versus a prolonged monitoring strategy. Circulation. 2001;104:46-51.
5Krahn AD, Klein GJ, Yee R, et al. The high cost of syncope: Cost implications of a new insertable loop recorder in the investigation of recurrent syncope. Am Heart J. 1999;137:870-877.
6Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
29. Neurological Tests: Rarely Diagnostic for Syncope EEG, Head CT, Head MRI
May help diagnose seizure Neurological studies (Head CT and MRI, EEG) are rarely useful in the diagnostic evaluation for syncope. Imaging may be justified if there is concern that syncope may have resulted in a head injury. Otherwise, without apparent abnormal neurological signs, such testing should be relegated to low priority.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
Neurological studies (Head CT and MRI, EEG) are rarely useful in the diagnostic evaluation for syncope. Imaging may be justified if there is concern that syncope may have resulted in a head injury. Otherwise, without apparent abnormal neurological signs, such testing should be relegated to low priority.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
30. Head-Up Tilt Test (HUT) Protocols vary
Useful as diagnostic adjunct in atypical syncope cases
Useful in teaching patients to recognize prodromal symptoms
Not useful in assessing treatment
The rationale for undertaking tilt table testing in patients suspected of having vasovagal (VVS) syncope is summarized here. The test may provide useful diagnostic information and also an opportunity for patients to become more familiar with the condition and its possible warning signs.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.The rationale for undertaking tilt table testing in patients suspected of having vasovagal (VVS) syncope is summarized here. The test may provide useful diagnostic information and also an opportunity for patients to become more familiar with the condition and its possible warning signs.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
31. Head-up Tilt Test
32. Head-Up Tilt Test:ECG Leads and Intra-Arterial Pressure Tracing This strip from ECG leads and an intra-arterial pressure tracing illustrates the final moments of a tilt table test just prior to induced syncope. Note that blood pressure tended to fall (1) in advance of the bradycardia (2). Even after the patient is returned to supine posture and the heart rate returns to normal, it may take time for the arterial pressure to fully recover due to persistent vasodilatation.
DG Benditt, MD. University of Minnesota Cardiac Arrhythmia CenterThis strip from ECG leads and an intra-arterial pressure tracing illustrates the final moments of a tilt table test just prior to induced syncope. Note that blood pressure tended to fall (1) in advance of the bradycardia (2). Even after the patient is returned to supine posture and the heart rate returns to normal, it may take time for the arterial pressure to fully recover due to persistent vasodilatation.
DG Benditt, MD. University of Minnesota Cardiac Arrhythmia Center
33. Adenosine Triphosphate (ATP) Test Ongoing investigation in the US
Provokes a short and potent cardioinhibitory vasovagal response
Advantages
Simple
Inexpensive
Correlation with pacing benefit Seems to identify a unique mechanism of syncope found in patients with:
Advanced age
More hypertension
More ECG abnormalities
1Brignole M, Gaggioli G, Menozzi C, et al. Clinical features of adenosine sensitive syncope and tilt induced vasovagal syncope. Heart. 2000;83:24-28.
2Donateo P, Brignole M, Menozzi C, et al. Mechanism of syncope in patients with positive adenosine triphosphate tests. J Am Coll Cardiol. 2003;41:93-98.
3Flammang D, Erickson M, McCarville S. Contribution of head-up tilt testing and ATP testing in assessing the mechanisms of vasovagal syndrome. Circulation. 1999;99:2427-2433.
1Brignole M, Gaggioli G, Menozzi C, et al. Clinical features of adenosine sensitive syncope and tilt induced vasovagal syncope. Heart. 2000;83:24-28.
2Donateo P, Brignole M, Menozzi C, et al. Mechanism of syncope in patients with positive adenosine triphosphate tests. J Am Coll Cardiol. 2003;41:93-98.
3Flammang D, Erickson M, McCarville S. Contribution of head-up tilt testing and ATP testing in assessing the mechanisms of vasovagal syndrome. Circulation. 1999;99:2427-2433.
34. Insertable Loop Recorder (ILR) The Reveal® Plus Insertable Loop Recorder system offers long-term, continuous, subcutaneous ECG monitoring and event-specific recording. The system includes an implanted loop recorder, a hand-held patient Activator, and a programmer with telemetry head that communicates noninvasively with the implanted device.
When a patient experiences an episode, the device stores an ECG using the Activator or through the use of a auto-activating feature.
The Reveal® Plus ILR can monitor continuously for up to 14 months. The probability of capturing an event is high—approximately 65-88%.1,2
The ECG captured during the episode may “reveal” the ECG during the patient’s episode or may allow the clinician to rule in or rule out arrhythmic causes.
The stored ECG data is retrieved, viewed, and printed or saved to a disk, using a Medtronic programmer. The Reveal ILR can then be re-started for continued monitoring.
1Krahn A, et al. Final results from a pilot study with an insertable loop recorder to determine the etiology of syncope in patients with negative noninvasive and invasive testing. Am J Cardiol. 1998;82:117-119.
2Krahn A, Klein GJ, Yee R, Skanes AC. Randomized assessment of syncope trial. Conventional diagnostic testing versus a prolonged monitoring strategy. Circulation. 2001;104:46-51.
The Reveal® Plus Insertable Loop Recorder system offers long-term, continuous, subcutaneous ECG monitoring and event-specific recording. The system includes an implanted loop recorder, a hand-held patient Activator, and a programmer with telemetry head that communicates noninvasively with the implanted device.
When a patient experiences an episode, the device stores an ECG using the Activator or through the use of a auto-activating feature.
The Reveal® Plus ILR can monitor continuously for up to 14 months. The probability of capturing an event is high—approximately 65-88%.1,2
The ECG captured during the episode may “reveal” the ECG during the patient’s episode or may allow the clinician to rule in or rule out arrhythmic causes.
The stored ECG data is retrieved, viewed, and printed or saved to a disk, using a Medtronic programmer. The Reveal ILR can then be re-started for continued monitoring.
1Krahn A, et al. Final results from a pilot study with an insertable loop recorder to determine the etiology of syncope in patients with negative noninvasive and invasive testing. Am J Cardiol. 1998;82:117-119.
2Krahn A, Klein GJ, Yee R, Skanes AC. Randomized assessment of syncope trial. Conventional diagnostic testing versus a prolonged monitoring strategy. Circulation. 2001;104:46-51.
35. Insertable Loop Recorder (ILR) The ILR is an implantable patient – and automatically – activated monitoring system that records subcutaneous ECG and is indicated for:
Patients with clinical syndromes or situations at increased risk of cardiac arrhythmias
Patients who experience transient symptoms that may suggest a cardiac arrhythmia
36. Insertable Loop Recorder (ILR)
37. Symptom-Rhythm Correlation with the ILR These are examples of ECG recordings obtained by the Reveal® ILR system in two symptomatic patients.
The gold standard for determining if a syncope episode may be due to an arrhythmia is to record the rhythm during symptoms, i.e., symptom-rhythm correlation. The ILR may help rule-in or rule-out arrhythmogenic causes.
These strips depict findings from an ILR interrogation as they appear on the programmer screen. In order to view the event in greater detail, one taps the screen over the ECG of interest.
On-screen calipers are available at every zoom level to measure cycle length in milliseconds or beats per minute.
Note that the ‘A’ represents an auto-activated event; the ‘P’ indicates when the patient activated the device.
Left strip: Infra-Hisian AV block: dual chamber pacemaker.
Right strip: VT and VF: ICD, meds.
Medtronic data on file.
These are examples of ECG recordings obtained by the Reveal® ILR system in two symptomatic patients.
The gold standard for determining if a syncope episode may be due to an arrhythmia is to record the rhythm during symptoms, i.e., symptom-rhythm correlation. The ILR may help rule-in or rule-out arrhythmogenic causes.
These strips depict findings from an ILR interrogation as they appear on the programmer screen. In order to view the event in greater detail, one taps the screen over the ECG of interest.
On-screen calipers are available at every zoom level to measure cycle length in milliseconds or beats per minute.
Note that the ‘A’ represents an auto-activated event; the ‘P’ indicates when the patient activated the device.
Left strip: Infra-Hisian AV block: dual chamber pacemaker.
Right strip: VT and VF: ICD, meds.
Medtronic data on file.
38. Randomized Assessment of Syncope Trial (RAST) Results:
Combining primary strategy with crossover, the diagnostic yield is 43% ILR only vs. 20% conventional only1
Cost/diagnosis is 26% less than conventional testing2 Dr. Andrew Krahn and his team at the University of Western Ontario authored the Randomized Assessment of Syncope Trial (RAST) in 20011 then followed up with a cost analysis of the same study in 2003.2
Prospective, randomized trial
60 patients with unexplained syncope after history, physical exam, ECG, and Holter monitor.
EF > 35% (lower risk)
2 testing strategies: conventional, using an exterior loop recorder (ELR) or Holter, tilt test, and electrophysiology study, or prolonged ILR monitoring.
If patients remained undiagnosed after their assigned strategy, they were offered crossover to the alternate strategy.
Overall, prolonged monitoring was more likely to result in a diagnosis than conventional testing, 43% vs. 20%, p=0.026.
Subsequent cost studies showed a 26% reduction in cost per diagnosis ($2,016) with a strategy of primary monitoring (p=0.002).
Prior to this study, the ILR was generally used as a last resort after other evaluation.
1 Krahn AD, et al. Randomized Assessment of Syncope Trial: Conventional diagnostic testing versus a prolonged monitoring strategy. Circulation. 2001:104(1):46-51.
2 Krahn AD, et al. Cost implications of testing strategy in patients with syncope (RAST). JACC. 2003;42:495-501.Dr. Andrew Krahn and his team at the University of Western Ontario authored the Randomized Assessment of Syncope Trial (RAST) in 20011 then followed up with a cost analysis of the same study in 2003.2
Prospective, randomized trial
60 patients with unexplained syncope after history, physical exam, ECG, and Holter monitor.
EF > 35% (lower risk)
2 testing strategies: conventional, using an exterior loop recorder (ELR) or Holter, tilt test, and electrophysiology study, or prolonged ILR monitoring.
If patients remained undiagnosed after their assigned strategy, they were offered crossover to the alternate strategy.
Overall, prolonged monitoring was more likely to result in a diagnosis than conventional testing, 43% vs. 20%, p=0.026.
Subsequent cost studies showed a 26% reduction in cost per diagnosis ($2,016) with a strategy of primary monitoring (p=0.002).
Prior to this study, the ILR was generally used as a last resort after other evaluation.
1 Krahn AD, et al. Randomized Assessment of Syncope Trial: Conventional diagnostic testing versus a prolonged monitoring strategy. Circulation. 2001:104(1):46-51.
2 Krahn AD, et al. Cost implications of testing strategy in patients with syncope (RAST). JACC. 2003;42:495-501.
39. Conventional EP Testing in Syncope Greater diagnostic value in older patients or those with SHD
Less diagnostic value in healthy patients without SHD
Useful diagnostic observations:
Inducible monomorphic VT
SNRT > 3000 ms or CSNRT > 600 ms
Inducible SVT with hypotension
HV interval = 100 ms (especially in absence of inducible VT)
Pacing induced infra-nodal block
Conventional EP testing (i.e., electrical stimulation without autonomic studies such as HUT) has not been highly effective in substantiating a basis for syncope. In this regard, EPS has been more effective in patients with structural cardiovascular disease than in those with normal cardiovascular status.
The most important findings at EPS in regard to the evaluation of syncope patients are listed in this slide.
SHD—Structural Heart Disease
SNRT—Sinus Node Recovery Time
CSNRT—Corrected Sinus Node Recovery Time
Benditt D. Syncope. In: Topol E, ed. Textbook of Cardiovascular Medicine. Philadelphia, PA: Lippencott Williams & Wilkins;2002:1529-1542.
Lu F and Bergfeldt L. Role of electrophysiologic testing in the syncope evaluation. In: Benditt D, et al. The Evaluation and Treatment of Syncope. Futura. 2003;80-95.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.Conventional EP testing (i.e., electrical stimulation without autonomic studies such as HUT) has not been highly effective in substantiating a basis for syncope. In this regard, EPS has been more effective in patients with structural cardiovascular disease than in those with normal cardiovascular status.
The most important findings at EPS in regard to the evaluation of syncope patients are listed in this slide.
SHD—Structural Heart Disease
SNRT—Sinus Node Recovery Time
CSNRT—Corrected Sinus Node Recovery Time
Benditt D. Syncope. In: Topol E, ed. Textbook of Cardiovascular Medicine. Philadelphia, PA: Lippencott Williams & Wilkins;2002:1529-1542.
Lu F and Bergfeldt L. Role of electrophysiologic testing in the syncope evaluation. In: Benditt D, et al. The Evaluation and Treatment of Syncope. Futura. 2003;80-95.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
40. Diagnostic Limitations of EPS Difficult to correlate spontaneous events and laboratory findings
Positive findings1
Without SHD: 6-17%
With SHD: 25-71%
Less effective in assessing bradyarrhythmias than tachyarrhythmias2
EPS findings must be consistent with clinical history
Beware of false positive
*SHD—Structural Heart Disease
1Linzer M, Yang E, Estes M, et al. Diagnosing Syncope. Part 2: Unexplained Syncope. Ann Int Med. 1997;127:76-86.
2Lu F and Bergfeldt L. Role of electrophysiologic testing in the syncope evaluation. In: Benditt D, et al. The Evaluation and Treatment of Syncope. Futura. 2003;80-95.*SHD—Structural Heart Disease
1Linzer M, Yang E, Estes M, et al. Diagnosing Syncope. Part 2: Unexplained Syncope. Ann Int Med. 1997;127:76-86.
2Lu F and Bergfeldt L. Role of electrophysiologic testing in the syncope evaluation. In: Benditt D, et al. The Evaluation and Treatment of Syncope. Futura. 2003;80-95.
41. ISSUEInternational Study of Syncope of Uncertain Etiology Multicenter, international, prospective study
Analyzed the diagnostic contribution of an ILR in three predefined groups of patients with syncope of uncertain origin:
Isolated syncope: No SHD, Normal ECG1
Negative tilt
Positive tilt
Patients with heart disease and negative EP test2
Patients with bundle branch block and negative EP test3
1Moya A, Brignole M, Menozzi C. Mechanism of syncope in patient with isolated syncope and in patients with tilt-positive syncope. Circulation. 2001;104:1261-1267.
2Menozzi C, Brignole M, Garcia-Civera R, et al. Mechanism of syncope in patients with heart disease and negative electrophysiological test. Circulation. 2002;105:2741-2745.
3Brignole M, Menozzi C, Moya A, et al. Mechanism of syncope in patients with bundle branch block and negative electrophysiological test. Circulation. 2001;104:2045-2050.
1Moya A, Brignole M, Menozzi C. Mechanism of syncope in patient with isolated syncope and in patients with tilt-positive syncope. Circulation. 2001;104:1261-1267.
2Menozzi C, Brignole M, Garcia-Civera R, et al. Mechanism of syncope in patients with heart disease and negative electrophysiological test. Circulation. 2002;105:2741-2745.
3Brignole M, Menozzi C, Moya A, et al. Mechanism of syncope in patients with bundle branch block and negative electrophysiological test. Circulation. 2001;104:2045-2050.
42. ISSUEPatients with Isolated Syncope and Tilt-Positive Syncope Moya A, Brignole M, Menozzi C. Mechanism of syncope in patient with isolated syncope and in patients with tilt-positive syncope. Circulation. 2001;104:1261-1267.Moya A, Brignole M, Menozzi C. Mechanism of syncope in patient with isolated syncope and in patients with tilt-positive syncope. Circulation. 2001;104:1261-1267.
43. ISSUEIsolated Syncope vs. Tilt-Positive Syncope Conclusions
Results similar in the two arms, including syncope recurrence and ECG correlation
Tilt-negative patients had as many bradycardias (18%) astilt-positive patients (21%)
Most frequent finding was asystole secondary to progressive sinus bradycardia, suggesting a neuro-mediated origin
Homogeneous findings from tilt-negative and tilt-positive infer low sensitivity of tilt-testing
If isolated (tilt-negative) syncope and tilt-positive syncope have similar clinical presentation, outcome, and cause, a logical inference is that tilt-testing lacks sensitivity.
Moya A, Brignole M, Menozzi C. Mechanism of syncope in patient with isolated syncope and in patients with tilt-positive syncope. Circulation. 2001;104:1261-1267.If isolated (tilt-negative) syncope and tilt-positive syncope have similar clinical presentation, outcome, and cause, a logical inference is that tilt-testing lacks sensitivity.
Moya A, Brignole M, Menozzi C. Mechanism of syncope in patient with isolated syncope and in patients with tilt-positive syncope. Circulation. 2001;104:1261-1267.
44. ISSUE Patients with Heart Disease and a Negative EP Test Menozzi C, et al. Mechanism of syncope in patients with heart disease and negative electrophysiological test. Circulation. 2002;105:2741-2745.Menozzi C, et al. Mechanism of syncope in patients with heart disease and negative electrophysiological test. Circulation. 2002;105:2741-2745.
45. ISSUEPatients with Heart Disease and a Negative EP Test Conclusions
Patients with unexplained syncope, overt heart disease, and negative EP study had a favorable medium-term outcome
Mechanism of syncope was heterogeneous
Ventricular tachyarrhythmia was unlikely
“ILR-guided strategy seems reasonable, with specific therapy safely delayed until a definite diagnosis is made.”
Menozzi C, Brignole M, Garcia-Civera R, et al. Mechanism of syncope in patients with heart disease and negative electrophysiological test. Circulation. 2002;105:2741-2745.
Menozzi C, Brignole M, Garcia-Civera R, et al. Mechanism of syncope in patients with heart disease and negative electrophysiological test. Circulation. 2002;105:2741-2745.
46. ISSUEPatients with Bundle Branch Block and Negative EP Test Brignole M, Menozzi C, Moya A, et al. Mechanism of syncope in patients with bundle branch block and negative electrophysiological test. Circulation. 2001;104:2045-2050.
Brignole M, Menozzi C, Moya A, et al. Mechanism of syncope in patients with bundle branch block and negative electrophysiological test. Circulation. 2001;104:2045-2050.
47. ISSUEPatients with Bundle Branch Block and Negative EP Test Conclusion:
In patients with BBB and negative EP study, most syncopal recurrences have a homogeneous mechanism that is characterized by prolonged asystolic pauses mainly attributable to sudden-onset paroxysmal AV block
Brignole M, Menozzi C, Moya A, et al. Mechanism of syncope in patients with bundle branch block and negative electrophysiological test. Circulation. 2001;104:2045-2050.
Brignole M, Menozzi C, Moya A, et al. Mechanism of syncope in patients with bundle branch block and negative electrophysiological test. Circulation. 2001;104:2045-2050.
48. Section III:Specific Conditions and Treatment The next section deals with some of the more important causes of syncope. The next section deals with some of the more important causes of syncope.
49. Specific Conditions Cardiac arrhythmia
Brady/Tachy
Long QT syndrome
Torsade de pointes
Brugada
Drug-induced
Structural cardio-pulmonary
Neurally-mediated
Vasovagal Syncope (VVS)
Carotid Sinus Syndrome (CSS)
Orthostatic
50. Cardiac Syncope Includes cardiac arrhythmias and SHD
Often life-threatening
May be warning of critical CV disease
Tachy and brady arrhythmias
Myocardial ischemia, aortic stenosis, pulmonary hypertension, aortic dissection
Assess culprit arrhythmia or structural abnormality aggressively
Initiate treatment promptly Syncope occurring as a result of cardiac arrhythmias or in association with underlying structural heart disease requires careful and aggressive evaluation. Whereas syncope in patients with normal hearts is often relatively benign, syncope in the presence of cardiac disease is often indicative of a potentially life-threatening problem.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.Syncope occurring as a result of cardiac arrhythmias or in association with underlying structural heart disease requires careful and aggressive evaluation. Whereas syncope in patients with normal hearts is often relatively benign, syncope in the presence of cardiac disease is often indicative of a potentially life-threatening problem.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
51. “…cardiac syncope can be a harbinger of sudden death.” Survival with and without syncope
6-month mortality rate of greater than 10%
Cardiac syncope doubled the risk of death
Includes cardiac arrhythmias and SHD
Cardiac causes include both arrhythmias and structural heart problems, both of which contribute to high mortality rates. One of the goals, therefore, is to attempt to either rule out or rule in arrhythmic disorders.
The statistic of a 1-year mortality rate ranging from 18-33% was validated in the September 19th, 2002 issue of the New England Journal of Medicine. The incidence and prognosis of syncope was studied in more than 7,800 participants in the Framingham Heart Study from 1971 to 1998.
The study found a 6-month mortality rate of greater than 10%.1
Cardiac syncope doubled the risk of death .1
Syncope of unknown cause was the largest category of causes.2
50% of syncope cases could not be diagnosed after conventional evaluation of detailed history, physical exam, and ECG.3
Because the precise cause of syncope is identified in fewer than half the patients during initial evaluation, the challenge lies in identifying those at high risk for death.
Cardiac syncope is not benign.
1 Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med. 2002;347(12):878-885.
2 Kapoor WN. Evaluation and outcome of patients with syncope. Medicine. 1990;69:160-175.
3 Linzer M, Yang E, Estes N, et al. Diagnosing syncope. Ann Intern Med. 1997;126(12):989-996.Cardiac causes include both arrhythmias and structural heart problems, both of which contribute to high mortality rates. One of the goals, therefore, is to attempt to either rule out or rule in arrhythmic disorders.
The statistic of a 1-year mortality rate ranging from 18-33% was validated in the September 19th, 2002 issue of the New England Journal of Medicine. The incidence and prognosis of syncope was studied in more than 7,800 participants in the Framingham Heart Study from 1971 to 1998.
The study found a 6-month mortality rate of greater than 10%.1
Cardiac syncope doubled the risk of death .1
Syncope of unknown cause was the largest category of causes.2
50% of syncope cases could not be diagnosed after conventional evaluation of detailed history, physical exam, and ECG.3
Because the precise cause of syncope is identified in fewer than half the patients during initial evaluation, the challenge lies in identifying those at high risk for death.
Cardiac syncope is not benign.
1 Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med. 2002;347(12):878-885.
2 Kapoor WN. Evaluation and outcome of patients with syncope. Medicine. 1990;69:160-175.
3 Linzer M, Yang E, Estes N, et al. Diagnosing syncope. Ann Intern Med. 1997;126(12):989-996.
52. Syncope Due to Structural Cardiovascular Disease: Principle Mechanisms Acute MI/Ischemia
2° neural reflex bradycardia – Vasodilatation, arrhythmias, low output (rare)
Hypertrophic cardiomyopathy
Limited output during exertion (increased obstruction, greater demand), arrhythmias, neural reflex
Acute aortic dissection
Neural reflex mechanism, pericardial tamponade Pulmonary embolus/pulmonary hypertension
Neural reflex, inadequate flow with exertion
Valvular abnormalities
Aortic stenosis – Limited output, neural reflex dilation in periphery
Mitral stenosis, atrial myxoma – Obstruction to adequate flow This slide lists important structural cardiovascular abnormalities to be considered during the diagnostic evaluation of syncope.
Obstruction of blood flow and arrhythmias are often the mechanisms for the syncope; all are high risk.
The list is not intended to be exhaustive of the possibilities, but provides some of the more commonly found conditions.
MI—myocardial infarction
HCM—hypertrophic cardiomyopathy
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.This slide lists important structural cardiovascular abnormalities to be considered during the diagnostic evaluation of syncope.
Obstruction of blood flow and arrhythmias are often the mechanisms for the syncope; all are high risk.
The list is not intended to be exhaustive of the possibilities, but provides some of the more commonly found conditions.
MI—myocardial infarction
HCM—hypertrophic cardiomyopathy
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
53. Syncope Due to Cardiac Arrhythmias Bradyarrhythmias
Sinus arrest, exit block
High grade or acute complete AV block
Can be accompanied by vasodilatation (VVS, CSS)
Tachyarrhythmias
Atrial fibrillation/flutter with rapid ventricular rate (eg, pre-excitation syndrome)
Paroxysmal SVT or VT
Torsade de pointes Both excessively slow as well as excessively rapid heart rates may result in sufficient drop in systemic pressure to cause syncope. In the case of tachycardias, the syncope tends to occur at the onset of the episode, before vascular constriction has an opportunity to occur. Syncope may also occur at termination of tachyarrhythmias, if a prolonged pause occurs prior to resumption of a stable rhythm.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.Both excessively slow as well as excessively rapid heart rates may result in sufficient drop in systemic pressure to cause syncope. In the case of tachycardias, the syncope tends to occur at the onset of the episode, before vascular constriction has an opportunity to occur. Syncope may also occur at termination of tachyarrhythmias, if a prolonged pause occurs prior to resumption of a stable rhythm.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
54. ILR Recordings These are Reveal® ILR recordings from patients with syncopal symptoms. The left recording was obtained in an 83 year old woman and suggests bradycardic episodes as a cause of syncope. The right recording was obtained in a younger patient with idiopathic ventricular tachycardia.
Reveal ® ILR recordings; Medtronic data on file.
These are Reveal® ILR recordings from patients with syncopal symptoms. The left recording was obtained in an 83 year old woman and suggests bradycardic episodes as a cause of syncope. The right recording was obtained in a younger patient with idiopathic ventricular tachycardia.
Reveal ® ILR recordings; Medtronic data on file.
55. Cardiac Rhythms During Unexplained Syncope The chart is a composite of several studies showing cardiac rhythms during syncope. Fortunately, most of the patients are in normal sinus rhythm. But since it is impossible to determine which patients have arrhythmias, one of the primary goals is to attempt to either rule out or rule in arrhythmic disorders.
The disconcerting piece is this seemingly small 6% - those with ventricular tachycardia, ventricular fibrillation, nonsustaining VT, or supraventricular VT—a cardiac cause that can lead to sudden death, as we saw from the Framingham data.*
The ‘Other’ category includes conditions such as vasovagal-related causes and failed activation.
Medtronic ILR Replacement Data includes Medtronic devices that were implanted when the ILR was explanted.
Seidl K, Rameken M, Breunung S, et al. Diagnostic assessment of recurrent unexplained syncope with a new subcutaneously implantable loop recorder. Europace. 2000;2(3):256-262.
Krahn AD, Klein GJ, Fitzpatrick A, et al. Predicting the outcome of patients with unexplained syncope undergoing prolonged monitoring. PACE. 2002;25:37-41.
Medtronic ILR Replacement Data. FY03, 04. On file.
* Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med. 2002;347(12):878-885.The chart is a composite of several studies showing cardiac rhythms during syncope. Fortunately, most of the patients are in normal sinus rhythm. But since it is impossible to determine which patients have arrhythmias, one of the primary goals is to attempt to either rule out or rule in arrhythmic disorders.
The disconcerting piece is this seemingly small 6% - those with ventricular tachycardia, ventricular fibrillation, nonsustaining VT, or supraventricular VT—a cardiac cause that can lead to sudden death, as we saw from the Framingham data.*
The ‘Other’ category includes conditions such as vasovagal-related causes and failed activation.
Medtronic ILR Replacement Data includes Medtronic devices that were implanted when the ILR was explanted.
Seidl K, Rameken M, Breunung S, et al. Diagnostic assessment of recurrent unexplained syncope with a new subcutaneously implantable loop recorder. Europace. 2000;2(3):256-262.
Krahn AD, Klein GJ, Fitzpatrick A, et al. Predicting the outcome of patients with unexplained syncope undergoing prolonged monitoring. PACE. 2002;25:37-41.
Medtronic ILR Replacement Data. FY03, 04. On file.
* Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med. 2002;347(12):878-885.
56. Long QT Syndromes Mechanism
Abnormalities of sodium and/or potassium channels
Susceptibility to polymorphic VT (Torsade de pointes)
Prevalence
Drug-induced forms – Common
Genetic forms – Relatively rare, but increasingly being recognized
“Concealed” forms:
May be common
Provide basis for drug-induced torsade
Schwartz P and Priori S. Long QT syndrome: Genotype-Phenotype correlations. In: Zipes D and Jalife J, eds. Cardiac Electrophysiology. From Cell to Bedside. Philadelphia, PA: Saunders;2004:651-659.
Schwartz P and Priori S. Long QT syndrome: Genotype-Phenotype correlations. In: Zipes D and Jalife J, eds. Cardiac Electrophysiology. From Cell to Bedside. Philadelphia, PA: Saunders;2004:651-659.
57. Syncope: Torsade de Pointes Torsade de pointes ventricular tachycardia often presents as syncope, although life-threatening sustained tachyarrhythmias may also occur. The underlying factors are most often either acquired or congenital long QT syndrome.
In this case, the patient had been treated with quinidine for several weeks in an attempt to suppress episodes of atrial fibrillation.
From the files of DG Benditt, MD. University of Minnesota Cardiac Arrhythmia Center
Torsade de pointes ventricular tachycardia often presents as syncope, although life-threatening sustained tachyarrhythmias may also occur. The underlying factors are most often either acquired or congenital long QT syndrome.
In this case, the patient had been treated with quinidine for several weeks in an attempt to suppress episodes of atrial fibrillation.
From the files of DG Benditt, MD. University of Minnesota Cardiac Arrhythmia Center
58. Long QT Syndromes: 12-Lead ECG From the files of DG Benditt, MD. University of Minnesota Cardiac Arrhythmia CenterFrom the files of DG Benditt, MD. University of Minnesota Cardiac Arrhythmia Center
59. Drug-Induced QT Prolongation(List is continuously being updated) 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, Ciprofloxacin and its relatives
Nonsedating antihistamines
Terfenadine*, Astemizole
Others
Cisapride*, Droperidol, Haloperidol Numerous drugs have been associated with QT interval prolongation leading to susceptibility to torsade de pointes ventricular tachycardia. Some of these agents have been removed from the market in the USA, as noted with an asterisk.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537. Numerous drugs have been associated with QT interval prolongation leading to susceptibility to torsade de pointes ventricular tachycardia. Some of these agents have been removed from the market in the USA, as noted with an asterisk.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
60. Treatment of Long QT Suspicion and recognition are critical
Emergency treatment
Intravenous magnesium
Pacing to overcome bradycardia or pauses
Isoproterenol to increase heart rate and shorten repolarization
ICD if prior SCA or strong family history
If drug induced:
Reverse bradycardia
Withdraw drug
Avoid ALL long-QT provoking agents
If genetic:
Avoid ALL long-QT provoking agents
For more information visit www.longqt.org Schwartz P and Priori S. Long QT syndrome: Genotype-Phenotype correlations. In: Zipes D and Jalife J, eds. Cardiac Electrophysiology. From Cell to Bedside. Philadelphia, PA: Saunders;2004:651-659.
Schwartz P and Priori S. Long QT syndrome: Genotype-Phenotype correlations. In: Zipes D and Jalife J, eds. Cardiac Electrophysiology. From Cell to Bedside. Philadelphia, PA: Saunders;2004:651-659.
61. Treatment of Syncope Due to Bradyarrhythmia Class I indication for pacing using dual chamber system wherever possible
Ventricular pacing in atrial fibrillation with slow ventricular response
The treatment of syncope associated with bradyarrhythmias resulting from intrinsic conduction system disease is usually cardiac pacing. On occasion, removal of an offending drug may be sufficient. The problem of neurally-mediated reflex bradyarrhythmias is dealt with separately.
ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices: Summary Article. Circulation. 2002;106:2145-2161.
The treatment of syncope associated with bradyarrhythmias resulting from intrinsic conduction system disease is usually cardiac pacing. On occasion, removal of an offending drug may be sufficient. The problem of neurally-mediated reflex bradyarrhythmias is dealt with separately.
ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices: Summary Article. Circulation. 2002;106:2145-2161.
62. 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 for paroxysmal AF
Atrial flutter – Ablate the IVC-TV isthmus of the re-entrant circuit for ‘typical’ flutter
Ventricular tachyarrhythmias
Ventricular tachycardia – ICD or ablation where appropriate
Torsade de pointes – Withdraw offending drug or implant ICD (long QT/Brugada/short QT)
Drug therapy may be an alternative in many cases This slide provides an overview of the multiple tachyarrhythmias that may cause syncope. An EP study has proven more valuable in assessing tachyarrhythmia causes of syncope than those due to bradycardia.
IVC-TV =Inferior Vena Cava-Tricuspid Valve
AVRT =Atrioventricular Reentry Tachycardia
AVNRT =Atrioventricular Nodal Reentry Tachycardia
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.This slide provides an overview of the multiple tachyarrhythmias that may cause syncope. An EP study has proven more valuable in assessing tachyarrhythmia causes of syncope than those due to bradycardia.
IVC-TV =Inferior Vena Cava-Tricuspid Valve
AVRT =Atrioventricular Reentry Tachycardia
AVNRT =Atrioventricular Nodal Reentry Tachycardia
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
63. Neurally-Mediated Reflex Syncope Vasovagal Syncope (VVS)
Carotid Sinus Syndrome (CSS)
Situational syncope
Post-micturition
Cough
Swallow
Defecation
Blood drawing, etc. The neurally-mediated reflex causes of syncope are a group of related conditions in terms of symptomatic hypotension being caused by a variable combination of bradycardia and vasodilatation.
Vasovagal syncope and carotid sinus syndrome are the most frequent conditions in this group. The others occur occasionally and are usually recognized only if a detailed medical history is obtained.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.The neurally-mediated reflex causes of syncope are a group of related conditions in terms of symptomatic hypotension being caused by a variable combination of bradycardia and vasodilatation.
Vasovagal syncope and carotid sinus syndrome are the most frequent conditions in this group. The others occur occasionally and are usually recognized only if a detailed medical history is obtained.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
64. Pathophysiology The physiology of syncope is depicted graphically in this slide. The afferent trigger signals (eg, pain, emotional upset, dehydration) are not depicted. In the efferent loop of the neural reflex:
Parasympathetic signals from the cerebral cortex reduce heart rate and slow (or block) AV conduction.
Decreased sympathetic activity results in vasodilatation.
Bradycardia and/or hypotension occur.
Carotid baroreceptors and other mechanoreceptors provide paradoxical feedback to the central nervous system, aggravating bradycardia and vasodilatation.
The result may be a downward spiral in heart rate and blood pressure leading to syncope.
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.
The physiology of syncope is depicted graphically in this slide. The afferent trigger signals (eg, pain, emotional upset, dehydration) are not depicted. In the efferent loop of the neural reflex:
Parasympathetic signals from the cerebral cortex reduce heart rate and slow (or block) AV conduction.
Decreased sympathetic activity results in vasodilatation.
Bradycardia and/or hypotension occur.
Carotid baroreceptors and other mechanoreceptors provide paradoxical feedback to the central nervous system, aggravating bradycardia and vasodilatation.
The result may be a downward spiral in heart rate and blood pressure leading to syncope.
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.
65. VVSClinical Pathophysiology Neurally-mediated physiologic reflex mechanism with two components:
1. Cardioinhibitory (? HR)
2. Vasodepressor (? BP) despite heart beats, no significant BP generated
Both components are usually present Vasovagal syncope, as in other forms of neurally-mediated reflex syncope, is due to systemic hypotension resulting in a transient period of inadequate cerebral blood flow.
Hypotension is the result of two pathophysiologic components:
Marked bradycardia or inappropriately slow heart rate for the blood pressure (i.e., cardioinhibitory feature)
Vasodilatation
The relative contribution of these two components varies among patients.
Wieling W, Gert van Dijk J, van Lieshout J, Benditt D. Pathophysiology and clinical presentation. In: Benditt D, Blanc J-J, et al. eds. The Evaluation and Treatment of Syncope. Elmsford, NY: Futura. 2003;11-22.
Vasovagal syncope, as in other forms of neurally-mediated reflex syncope, is due to systemic hypotension resulting in a transient period of inadequate cerebral blood flow.
Hypotension is the result of two pathophysiologic components:
Marked bradycardia or inappropriately slow heart rate for the blood pressure (i.e., cardioinhibitory feature)
Vasodilatation
The relative contribution of these two components varies among patients.
Wieling W, Gert van Dijk J, van Lieshout J, Benditt D. Pathophysiology and clinical presentation. In: Benditt D, Blanc J-J, et al. eds. The Evaluation and Treatment of Syncope. Elmsford, NY: Futura. 2003;11-22.
66. VVSIncidence Most common form of syncope
8% to 37% (mean 18%) of syncope cases
Depends on population sampled
Young without SHD, ? incidence
Older with SHD, ? incidence
The incidence of vasovagal syncope is poorly known.
The published data that exists mostly dates from before the advent of tilt table testing.
Linzer surveyed the literature and found published prevalences varying from 8% to 37% (mean 18%) of cases of syncope.
Standards for diagnosis and reporting are still emerging.
Linzer MD, Yang EH, Estes M, et al. Diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiography. Ann Intern Med. 1997;126(12):989-996.The incidence of vasovagal syncope is poorly known.
The published data that exists mostly dates from before the advent of tilt table testing.
Linzer surveyed the literature and found published prevalences varying from 8% to 37% (mean 18%) of cases of syncope.
Standards for diagnosis and reporting are still emerging.
Linzer MD, Yang EH, Estes M, et al. Diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiography. Ann Intern Med. 1997;126(12):989-996.
67. VVS vs. CSS In general:
VVS patients younger than CSS patients
Ages range from adolescence to older adults (median 43 years) It is generally recognized that:
Vasovagal syncope patients are usually younger than Carotid Sinus Syndrome patients (age range is from adolescent to older adults, median 43 years)
Vasovagal syncope is more common in females.
Linzer MD, Yang EH, Estes M, et al. Diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiography. Ann Intern Med. 1997;126(12):989-996.
It is generally recognized that:
Vasovagal syncope patients are usually younger than Carotid Sinus Syndrome patients (age range is from adolescent to older adults, median 43 years)
Vasovagal syncope is more common in females.
Linzer MD, Yang EH, Estes M, et al. Diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiography. Ann Intern Med. 1997;126(12):989-996.
68. VVS Recurrences Studies suggest that vasovagal syncope tends to recur in a substantial percentage of patients.1 Individuals who have historically experienced multiple syncopes over a long period of time are the ones at greatest risk for future recurrences.2
1Savage D, Corwin L, McGee D, et al. Epidemiologic features of isolated syncope: the Framingham Study. Stroke. 1985;16:626-629.
2Sheldon R, Rose S, Flanagan P, et al. Risk factors for syncope recurrence after a positive tilt-table test in patients with syncope. Circulation. 1996;93:973-981.
Studies suggest that vasovagal syncope tends to recur in a substantial percentage of patients.1 Individuals who have historically experienced multiple syncopes over a long period of time are the ones at greatest risk for future recurrences.2
1Savage D, Corwin L, McGee D, et al. Epidemiologic features of isolated syncope: the Framingham Study. Stroke. 1985;16:626-629.
2Sheldon R, Rose S, Flanagan P, et al. Risk factors for syncope recurrence after a positive tilt-table test in patients with syncope. Circulation. 1996;93:973-981.
69. VVS Spontaneous Example of marked bradycardia recorded during a spontaneous vasovagal syncope. The asystolic periods may be impressive in their duration but do not in themselves constitute an indication for cardiac pacing.
From the files of DG Benditt, MD. University of Minnesota Cardiac Arrhythmia CenterExample of marked bradycardia recorded during a spontaneous vasovagal syncope. The asystolic periods may be impressive in their duration but do not in themselves constitute an indication for cardiac pacing.
From the files of DG Benditt, MD. University of Minnesota Cardiac Arrhythmia Center
70. VVSDiagnosis History and physical exam, ECG and BP
Head-Up Tilt (HUT) – Protocol:
Fast > 2 hours
ECG and continuous blood pressure, supine, and upright
Tilt to 70°, 20 minutes
Isoproterenol/Nitroglycerin if necessary
End point – Loss of consciousness Vasovagal syncope is most effectively diagnosed if the detailed medical history is ‘classic’. However, this is not often the case, and supporting evidence is needed. Such supportive evidence may include:
Patient history, physical examination, including ECG and blood pressure
Patient experiences syncope during tilt table testing. Test completion without syncope is a negative result.
The following is one tilt table protocol:
At least a 2 hour fast
Measure ECG, at least 3 leads, and continuous supine and upright blood pressure at time of symptoms.
Patient remains supine on the table for 15-30 minutes.
Tilt to 70 degrees for 20 minutes.
Lower to horizontal and administer isoproterenol at 1-5 µg/min until heart rate increases 25%.
Re-tilt for 10 minutes
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
Benditt D, Ferfuson D, Grubb B, et al. Tilt table testing for assessing syncope. ACC expert consensus document. J Am Coll Cardiol. 1996;28:263-275.
Vasovagal syncope is most effectively diagnosed if the detailed medical history is ‘classic’. However, this is not often the case, and supporting evidence is needed. Such supportive evidence may include:
Patient history, physical examination, including ECG and blood pressure
Patient experiences syncope during tilt table testing. Test completion without syncope is a negative result.
The following is one tilt table protocol:
At least a 2 hour fast
Measure ECG, at least 3 leads, and continuous supine and upright blood pressure at time of symptoms.
Patient remains supine on the table for 15-30 minutes.
Tilt to 70 degrees for 20 minutes.
Lower to horizontal and administer isoproterenol at 1-5 µg/min until heart rate increases 25%.
Re-tilt for 10 minutes
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
Benditt D, Ferfuson D, Grubb B, et al. Tilt table testing for assessing syncope. ACC expert consensus document. J Am Coll Cardiol. 1996;28:263-275.
71. VVS General Treatment Measures Optimal treatment strategies for VVS are a source of debate
Treatment goals
Acute intervention
Physical maneuvers, eg, crossing legs or tugging arms
Lowering head
Lying down
Long-term prevention
Tilt training
Education
Diet, fluids, salt
Support hose
Drug therapy
Pacing
Optimal management strategies for VVS are a source of debate. Long-term prevention measures include:
Patient education, reassurance, and instruction.
Control of fluids, salt, and diet may help reduce incidence.
Support hose may limit blood pooling in the legs and feet.
Drug therapy should be used as a second line option. Midodrine and beta-adrenergic blockers are the agents most thoroughly studied to date
Pacing may benefit some patients. Subsequent slides will examine the utility of pacing in very symptomatic VVS patients.
When the patient has a relatively long prodrome, evasive action may prevent injury if not syncope. This might include physical maneuvers such as crossing the legs, lowering the head, or lying down.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.Optimal management strategies for VVS are a source of debate. Long-term prevention measures include:
Patient education, reassurance, and instruction.
Control of fluids, salt, and diet may help reduce incidence.
Support hose may limit blood pooling in the legs and feet.
Drug therapy should be used as a second line option. Midodrine and beta-adrenergic blockers are the agents most thoroughly studied to date
Pacing may benefit some patients. Subsequent slides will examine the utility of pacing in very symptomatic VVS patients.
When the patient has a relatively long prodrome, evasive action may prevent injury if not syncope. This might include physical maneuvers such as crossing the legs, lowering the head, or lying down.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
72. VVS Tilt Training Protocol Objectives
Enhance orthostatic tolerance
Diminish excessive autonomic reflex activity
Reduce syncope susceptibility/recurrences
Technique
Prescribed periods of upright posture against a wall
Start with 3-5 min BID
Increase by 5 min each week until a duration of 30 min is achieved Reybrouck T, Heidbuchel H, Van de Werf F, Ector H, et al. Tilt training: A treatment for malignant and recurrent neurocardiogenic syncope. PACE. 2000;23(4 Pt. 1):493-498.Reybrouck T, Heidbuchel H, Van de Werf F, Ector H, et al. Tilt training: A treatment for malignant and recurrent neurocardiogenic syncope. PACE. 2000;23(4 Pt. 1):493-498.
73. VVS Tilt Training: Clinical Outcomes Treatment of recurrent VVS
Reybrouck, et al.*: Long-term study
38 patients performed home tilt training
After a period of regular tilt training, 82% remained free of syncope during the follow-up period
However, 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, et al. have demonstrated that the use of tilt training may be beneficial in a select population of patients who have frequent episodes of vasovagal syncope. It may also be of value in some forms of orthostatic hypotension. Results may be related to more of a placebo effect than an actual effect. Tilt training may have short-lived benefit when patients fail to comply with the regime for an extended period of time.
*Reybrouck T, Heidbuchel H, Van de Werf F, Ector H, et al. Long-term follow-up results of tilt-training therapy in patients with recurrent neurocardiogenic syncope. PACE. 2002;25:1441-1446.
Additional references on tilt-training:
Ector H, Reybrouck T, Heidbuchel H, Gewillig M, Van de Werf F. Tilt-training: A new treatment for recurrent neurocardiogenic syncope or severe orthostatic intolerance. PACE. 1998;21:193-196.
Di Girolamo E, Di Iorio C, Leonzio L, Sabatini P, Barsotti A. Usefulness of a tilt-training program for prevention of refractory neurocardiogenic syncope in adolescents. A controlled study. Circulation. 1999;100:1798-1801.
Reybrouck, et al. have demonstrated that the use of tilt training may be beneficial in a select population of patients who have frequent episodes of vasovagal syncope. It may also be of value in some forms of orthostatic hypotension. Results may be related to more of a placebo effect than an actual effect. Tilt training may have short-lived benefit when patients fail to comply with the regime for an extended period of time.
*Reybrouck T, Heidbuchel H, Van de Werf F, Ector H, et al. Long-term follow-up results of tilt-training therapy in patients with recurrent neurocardiogenic syncope. PACE. 2002;25:1441-1446.
Additional references on tilt-training:
Ector H, Reybrouck T, Heidbuchel H, Gewillig M, Van de Werf F. Tilt-training: A new treatment for recurrent neurocardiogenic syncope or severe orthostatic intolerance. PACE. 1998;21:193-196.
Di Girolamo E, Di Iorio C, Leonzio L, Sabatini P, Barsotti A. Usefulness of a tilt-training program for prevention of refractory neurocardiogenic syncope in adolescents. A controlled study. Circulation. 1999;100:1798-1801.
74. VVS Tilt Training: Clinical Outcomes Foglia-Manzillo, et al.*: Short-term study
68 patients
35 tilt training
33 no treatment (control)
Tilt table test conducted after 3 weeks
19 (59%) of tilt trained and 18 (60%) of controls had a positive test
Tilt training was not effective in reducing tilt testing positivity rate
Poor compliance in the majority of patients with recurrent VVS *Foglio-Manzillo G, Giada F, Gaggioli G, et al. Efficacy of tilt training in the treatment of neurally mediated syncope. A randomized study. Europace. 2004;6:199-204.
*Foglio-Manzillo G, Giada F, Gaggioli G, et al. Efficacy of tilt training in the treatment of neurally mediated syncope. A randomized study. Europace. 2004;6:199-204.
75. VVS Pharmacologic Treatment Fludrocortisone
Beta-adrenergic blockers
Preponderance of clinical evidence suggests minimal benefit1
SSRI (Selective Serotonin Re-Uptake Inhibitor)
1 small controlled trial2
Vasoconstrictors
1 negative controlled trial (etilefrine)3
2 positive controlled trials (midodrine)4,5 This slide summarizes the key pharmacologic treatment options in VVS patients. Drug therapy should be reserved as a second-line option.
1Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
2Di Girolamo E, Di Iorio C, Sabatini O, et al. Effects of paroxetine hydrochloride, a selective serotonin reuptake inhibitor, on refractory vasovagal syncope: a randomized, double-blind, placebo-controlled study. J Am Coll Cardiol. 1999;33:1227-1230.
3Raviele A, Brignole M, Sutton R, et al. Effect of etilefrine in preventing syncopal recurrence in patients with vasovagal syncope: a double-blind, randomized, placebo-controlled trial. The Vasovagal Syncope International Study. Circulation. 1999;99:1452-1457.
4Ward C, Gray J, Gilroy J, et al. Midodrine: a role in the management of neurocardiogenic syncope. Heart. 1998;79:45-49.
5Perez-Lugones A, Schweikert R, Pavia S, et al. Usefulness of midodrine in patients with severely symptomatic neurocardiogenic syncope: A randomized control study. J Cardiovasc Electrophysiol. 2001;12(8):935-938.
This slide summarizes the key pharmacologic treatment options in VVS patients. Drug therapy should be reserved as a second-line option.
1Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
2Di Girolamo E, Di Iorio C, Sabatini O, et al. Effects of paroxetine hydrochloride, a selective serotonin reuptake inhibitor, on refractory vasovagal syncope: a randomized, double-blind, placebo-controlled study. J Am Coll Cardiol. 1999;33:1227-1230.
3Raviele A, Brignole M, Sutton R, et al. Effect of etilefrine in preventing syncopal recurrence in patients with vasovagal syncope: a double-blind, randomized, placebo-controlled trial. The Vasovagal Syncope International Study. Circulation. 1999;99:1452-1457.
4Ward C, Gray J, Gilroy J, et al. Midodrine: a role in the management of neurocardiogenic syncope. Heart. 1998;79:45-49.
5Perez-Lugones A, Schweikert R, Pavia S, et al. Usefulness of midodrine in patients with severely symptomatic neurocardiogenic syncope: A randomized control study. J Cardiovasc Electrophysiol. 2001;12(8):935-938.
76. Midodrine for VVS Findings from a clinical trial in which salt/volume therapy and midodrine treatment were compared in VVS patients. Midodrine proved to be more effective than volume alone in this selected patient population.
Perez-Lugones A, Schweikert R, Pavia S, et al. Usefulness of midodrine in patients with severely symptomatic neurocardiogenic syncope: A randomized control study. J Cardiovasc Electrophysiol. 2001;12(8):935-938.Findings from a clinical trial in which salt/volume therapy and midodrine treatment were compared in VVS patients. Midodrine proved to be more effective than volume alone in this selected patient population.
Perez-Lugones A, Schweikert R, Pavia S, et al. Usefulness of midodrine in patients with severely symptomatic neurocardiogenic syncope: A randomized control study. J Cardiovasc Electrophysiol. 2001;12(8):935-938.
77. The Role of Pacing as Therapy for Syncope VVS with +HUT and cardioinhibitory response:Class IIb indication for pacing
Three randomized, prospective trials reported benefits of pacing in select VVS patients:
VPS I1
VASIS2
SYDIT3
Subsequent study results less clear
VPS II4
Synpace5
INVASY6 The role of pacing therapy for the treatment of vasovagal syncope is controversial. Some studies have shown a benefit1-3 and others have not.4-6 Outcomes with pacing depend in part on the patient population and the selection criteria for a pacemaker. Older patients, and those with long asystolic pauses and little vasodilatation, are the most likely to benefit from a pacemaker. This should be considered the therapy of last resort if no other medical therapy is effective for the patient.7
1Connolly SJ, Sheldon R, Roberts RS, Gent M. Vasovagal pacemaker study investigators. The North American vasovagal pacemaker study (VPS): A randomized trial of permanent cardiac pacing for the prevention of vasovagal syncope. J Am Coll Cardiol. 1999;33:16-20.
2Sutton R, Brignole M, Menozzi C, et al. Dual-chamber pacing is efficacious in treatment of neurally-mediated tilt-positive cardioinhibitory syncope. Pacemaker versus no therapy: a multicenter randomized study. Circulation. 2000;102:294-299.
3Ammirati F, Colivicchi F, Santini M. Permanent cardiac pacing versus medical treatment for the prevention of recurrent vasovagal syncope. Circulation. 2001;104:52-57.
4Connolly S, Sheldon R, Thorpe K, et al. Pacemaker therapy for prevention of syncope in patients with recurrent severe vasovagal syncope (VPS II) JAMA. 2003;289:2224–2229.
5Giada F, Raviele A, Menozzi C, et al. The vasovagal syncope and pacing trial (Synpace). A randomized placebo-controlled study of permanent pacing for treatment of recurrent vasovagal syncope. PACE. 2003;26:1016 (abstract).
6Occhetta E, Bortnik M, Audoglio R, et al. Closed loop stimulation in prevention of vasovagal syncope. Inotropy controlled pacing in vasovagal syncope (INVASY): a multicentre randomized, single blind, controlled study. Europace. 2004;6:538-547.
7Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.The role of pacing therapy for the treatment of vasovagal syncope is controversial. Some studies have shown a benefit1-3 and others have not.4-6 Outcomes with pacing depend in part on the patient population and the selection criteria for a pacemaker. Older patients, and those with long asystolic pauses and little vasodilatation, are the most likely to benefit from a pacemaker. This should be considered the therapy of last resort if no other medical therapy is effective for the patient.7
1Connolly SJ, Sheldon R, Roberts RS, Gent M. Vasovagal pacemaker study investigators. The North American vasovagal pacemaker study (VPS): A randomized trial of permanent cardiac pacing for the prevention of vasovagal syncope. J Am Coll Cardiol. 1999;33:16-20.
2Sutton R, Brignole M, Menozzi C, et al. Dual-chamber pacing is efficacious in treatment of neurally-mediated tilt-positive cardioinhibitory syncope. Pacemaker versus no therapy: a multicenter randomized study. Circulation. 2000;102:294-299.
3Ammirati F, Colivicchi F, Santini M. Permanent cardiac pacing versus medical treatment for the prevention of recurrent vasovagal syncope. Circulation. 2001;104:52-57.
4Connolly S, Sheldon R, Thorpe K, et al. Pacemaker therapy for prevention of syncope in patients with recurrent severe vasovagal syncope (VPS II) JAMA. 2003;289:2224–2229.
5Giada F, Raviele A, Menozzi C, et al. The vasovagal syncope and pacing trial (Synpace). A randomized placebo-controlled study of permanent pacing for treatment of recurrent vasovagal syncope. PACE. 2003;26:1016 (abstract).
6Occhetta E, Bortnik M, Audoglio R, et al. Closed loop stimulation in prevention of vasovagal syncope. Inotropy controlled pacing in vasovagal syncope (INVASY): a multicentre randomized, single blind, controlled study. Europace. 2004;6:538-547.
7Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
78. VPS I (North American Vasovagal Pacemaker Study) Objective: To evaluate pacemaker therapy for severe recurrent vasovagal syncope
Randomized, prospective, single center
N=54 patients
27: DDD pacemaker with rate drop response
27: No pacemaker
Inclusion: Vasodepressor response
Primary outcome: First recurrence of syncope
54 patients were enrolled in the prospective North American Vasovagal Pacemaker study. Patients were randomized to rate drop response feature or to current therapy.
These were patients who had standard vasovagal syncope with frequent episodes and a positive tilt table test. The tilt table test was positive by criteria of relative bradycardia and hypotension, the standard response on the tilt table test. Patients with long asystolic pauses were not included.
Connolly SJ, Sheldon R, Roberts RS, Gent M. Vasovagal pacemaker study investigators. The North American vasovagal pacemaker study (VPS): A randomized trial of permanent cardiac pacing for the prevention of vasovagal syncope. J Am Coll Cardiol. 1999;33:16-20.
54 patients were enrolled in the prospective North American Vasovagal Pacemaker study. Patients were randomized to rate drop response feature or to current therapy.
These were patients who had standard vasovagal syncope with frequent episodes and a positive tilt table test. The tilt table test was positive by criteria of relative bradycardia and hypotension, the standard response on the tilt table test. Patients with long asystolic pauses were not included.
Connolly SJ, Sheldon R, Roberts RS, Gent M. Vasovagal pacemaker study investigators. The North American vasovagal pacemaker study (VPS): A randomized trial of permanent cardiac pacing for the prevention of vasovagal syncope. J Am Coll Cardiol. 1999;33:16-20.
79. VPS I (North American Vasovagal Pacemaker Study) Final analysis found:
6/27 (22%) with pacemakers had syncope recurrence
19/27 (70%) without pacemakers had syncope recurrence
The study reported an 84% relative risk reduction (RRR) in pacemaker group versus standard therapy.
The study was halted when early stopping criteria were achieved (p<0.001 in favor of pacing).
Connolly SJ, Sheldon R, Roberts RS, Gent M. Vasovagal pacemaker study investigators. The North American vasovagal pacemaker study (VPS): A randomized trial of permanent cardiac pacing for the prevention of vasovagal syncope. J Am Coll Cardiol . 1999;33:16-20.
Final analysis found:
6/27 (22%) with pacemakers had syncope recurrence
19/27 (70%) without pacemakers had syncope recurrence
The study reported an 84% relative risk reduction (RRR) in pacemaker group versus standard therapy.
The study was halted when early stopping criteria were achieved (p<0.001 in favor of pacing).
Connolly SJ, Sheldon R, Roberts RS, Gent M. Vasovagal pacemaker study investigators. The North American vasovagal pacemaker study (VPS): A randomized trial of permanent cardiac pacing for the prevention of vasovagal syncope. J Am Coll Cardiol . 1999;33:16-20.
80. VASIS (VAsovagal Syncope International Study) Objective: To evaluate pacemaker therapy for severe cardioinhibitory tilt-positive neurally mediated syncope
Randomized, prospective, multi-center
N=42 patients
19: DDI pacemaker (80 bpm) with rate hysteresis (45 bpm)
23: No pacemaker
Inclusion: Positive cardioinhibitory response
Primary outcome: First recurrence of syncope
The VASIS trial examined the effectiveness of cardiac pacing in patients with recurrent VVS symptoms and evidence of a bradycardia component during evaluation. Differences between this study and the VPS 1 Trial were that these patients had cardioinhibitory tilt-positive neurally-mediated syncope.
Sutton R, Brignole M, Menozzi C, et al. Dual-chamber pacing is efficacious in treatment of neurally-mediated tilt-positive cardioinhibitory syncope. Pacemaker versus no therapy: a multicenter randomized study. Circulation. 2000;102:294-299.
The VASIS trial examined the effectiveness of cardiac pacing in patients with recurrent VVS symptoms and evidence of a bradycardia component during evaluation. Differences between this study and the VPS 1 Trial were that these patients had cardioinhibitory tilt-positive neurally-mediated syncope.
Sutton R, Brignole M, Menozzi C, et al. Dual-chamber pacing is efficacious in treatment of neurally-mediated tilt-positive cardioinhibitory syncope. Pacemaker versus no therapy: a multicenter randomized study. Circulation. 2000;102:294-299.
81. VASIS (VAsovagal Syncope International Study) As was the case in the VPS 1 study, pacing was more effective than conventional therapy in terms of preventing syncope recurrences.
The VASIS intention-to-treat data are presented in Kaplan-Meier format.
Sutton R, Brignole M, Menozzi C, et al. Dual-chamber pacing is efficacious in treatment of neurally-mediated tilt-positive cardioinhibitory syncope. Pacemaker versus no therapy: a multicenter randomized study. Circulation. 2000;102:294-299.
As was the case in the VPS 1 study, pacing was more effective than conventional therapy in terms of preventing syncope recurrences.
The VASIS intention-to-treat data are presented in Kaplan-Meier format.
Sutton R, Brignole M, Menozzi C, et al. Dual-chamber pacing is efficacious in treatment of neurally-mediated tilt-positive cardioinhibitory syncope. Pacemaker versus no therapy: a multicenter randomized study. Circulation. 2000;102:294-299.
82. SYDIT (SYncope DIagnosis and Treatment) Objective: To compare the effects of cardiac pacing with pharmacological therapy in patients with recurrent vasovagal syncope
Randomized, prospective, multi-center
N=93 patients
46: DDD pacemaker with rate drop response
47: Atenolol 100 mg/d
Inclusion: Positive HUT with relative bradycardia
Primary outcome: First recurrence of syncope
SYDIT is a randomized, prospective, multi-center trial of 93 patients that compared the effects of cardiac pacing with pharmacological therapy in patients with recurrent vasovagal syncope. Patients were randomized to DDD pacemaker with rate drop response, or atenolol, 100 mg/d. To be enrolled, patients had to have a positive HUT with relative bradycardia. The primary outcome was the first recurrence of syncope.
Ammirati F, Colivicchi F, Santini M. Permanent cardiac pacing versus medical treatment for the prevention of recurrent vasovagal syncope. Circulation. 2001;104:52-57.
SYDIT is a randomized, prospective, multi-center trial of 93 patients that compared the effects of cardiac pacing with pharmacological therapy in patients with recurrent vasovagal syncope. Patients were randomized to DDD pacemaker with rate drop response, or atenolol, 100 mg/d. To be enrolled, patients had to have a positive HUT with relative bradycardia. The primary outcome was the first recurrence of syncope.
Ammirati F, Colivicchi F, Santini M. Permanent cardiac pacing versus medical treatment for the prevention of recurrent vasovagal syncope. Circulation. 2001;104:52-57.
83. SYDIT (SYncope DIagnosis and Treatment) Final analysis found:
2 (4%) with pacemakers had syncope recurrence
12 (26%) without pacemakers had syncope recurrence
DDD pacing with rate drop response function is more effective than ß-blockage for the prevention of syncopal recurrences in patients with highly symptomatic vasovagal syncope with relative bradycardia during tilt-induced syncope.
The SYDIT intention-to-treat data are presented in Kaplan-Meier format.
Ammirati F, Colivicchi F, Santini M. Permanent cardiac pacing versus medical treatment for the prevention of recurrent vasovagal syncope. Circulation. 2001;104:52-57.
Final analysis found:
2 (4%) with pacemakers had syncope recurrence
12 (26%) without pacemakers had syncope recurrence
DDD pacing with rate drop response function is more effective than ß-blockage for the prevention of syncopal recurrences in patients with highly symptomatic vasovagal syncope with relative bradycardia during tilt-induced syncope.
The SYDIT intention-to-treat data are presented in Kaplan-Meier format.
Ammirati F, Colivicchi F, Santini M. Permanent cardiac pacing versus medical treatment for the prevention of recurrent vasovagal syncope. Circulation. 2001;104:52-57.
84. VPS II (Vasovagal Pacemaker Study II) Objective: To determine if pacing therapy reduces the risk of syncope in patients with vasovagal syncope
Randomized, double-blind, prospective, multi-center
N=100 patients
52: Only sensing without pacing
48: DDD pacemaker with rate drop response
Inclusion: Positive HUT with (HRxBP) < 6000/min x mm Hg
Primary outcome: First recurrence of syncope The VPS II trial was designed to investigate whether the dramatic changes observed with pacing therapy were due to the actual pacing or to a placebo effect. This was a highly select population of patients. To be included, patients had to experience frequent syncope and have a positive head up tilt test with a heart rate x blood pressure product less than 6000/min x mm Hg.
The objective was to determine if pacing therapy reduces the risk of syncope in patients with vasovagal syncope. The study was randomized, double-blind, prospective, multi-center, and included 100 patients. Fifty-two had a pacemaker implanted but set to sense only. The remaining patients had a pacemaker programmed to DDD pacing with rate drop response. The primary outcome of the study was time to the first recurrence of syncope.
Connolly S, Sheldon R, Thorpe K, et al. Pacemaker therapy for prevention of syncope in patients with recurrent severe vasovagal syncope (VPS II) JAMA. 2003;289:2224–2229.
The VPS II trial was designed to investigate whether the dramatic changes observed with pacing therapy were due to the actual pacing or to a placebo effect. This was a highly select population of patients. To be included, patients had to experience frequent syncope and have a positive head up tilt test with a heart rate x blood pressure product less than 6000/min x mm Hg.
The objective was to determine if pacing therapy reduces the risk of syncope in patients with vasovagal syncope. The study was randomized, double-blind, prospective, multi-center, and included 100 patients. Fifty-two had a pacemaker implanted but set to sense only. The remaining patients had a pacemaker programmed to DDD pacing with rate drop response. The primary outcome of the study was time to the first recurrence of syncope.
Connolly S, Sheldon R, Thorpe K, et al. Pacemaker therapy for prevention of syncope in patients with recurrent severe vasovagal syncope (VPS II) JAMA. 2003;289:2224–2229.
85. VPS II (Vasovagal Pacemaker Study II) Final analysis found:
22/52 (42%) with only sensing had syncope recurrence within 6 months
16/48 (33%) with DDD pacemaker had syncope recurrence within 6 months
The relative risk reduction in time to syncope with DDD pacing was 30% (not statistically significant).
Results favored pacing but the treatment effect was not statistically significant. The study results raise the question of whether pacemakers have any role in the treatment of vasovagal syncope beyond a placebo effect.
The VPS II trial did not show any advantage of a pacemaker for this population but this population was select. Patients with long asystolic episodes may benefit from a pacemaker but first the episodes need to be documented. The patient should be considered resistant to other medical therapies.
The VPS II intention-to-treat data are presented in Kaplan-Meier format.
Connolly S, Sheldon R, Thorpe K, et al. Pacemaker therapy for prevention of syncope in patients with recurrent severe vasovagal syncope (VPS II). JAMA. 2003;289:2224–2229.
Final analysis found:
22/52 (42%) with only sensing had syncope recurrence within 6 months
16/48 (33%) with DDD pacemaker had syncope recurrence within 6 months
The relative risk reduction in time to syncope with DDD pacing was 30% (not statistically significant).
Results favored pacing but the treatment effect was not statistically significant. The study results raise the question of whether pacemakers have any role in the treatment of vasovagal syncope beyond a placebo effect.
The VPS II trial did not show any advantage of a pacemaker for this population but this population was select. Patients with long asystolic episodes may benefit from a pacemaker but first the episodes need to be documented. The patient should be considered resistant to other medical therapies.
The VPS II intention-to-treat data are presented in Kaplan-Meier format.
Connolly S, Sheldon R, Thorpe K, et al. Pacemaker therapy for prevention of syncope in patients with recurrent severe vasovagal syncope (VPS II). JAMA. 2003;289:2224–2229.
86. SYNPACE(Vasovagal SYNcope and PACing) Objective: To determine if pacing therapy will reduce syncope relapses in patients with recurrent vasovagal syncope, compared to those with a pacemaker programmed to OFF
Randomized, double-blind, prospective, multi-center, placebo-controlled
N=29 patients
16: DDD PM with rate drop response programmed ON
13: PM programmed OFF (OOO mode)
Inclusion: Recurrent VVS and +HUT with asystolic or mixed response
Primary outcome: First recurrence of syncope
PM=Pacemaker
SYNPACE is a randomized, double-blind, prospective, multi-center, placebo-controlled trial of 29 patients. The aim was to ascertain whether, in patients with recurrent tilt-induced vasovagal syncope, a dual chamber pacemaker programmed to ON reduced the number syncopal relapses and/or prolonged the time to the first recurrence, compared to patients with a pacemaker programmed to OFF.
Raviele A, Giada F, Sutton R, et al. The vasovagal syncope and pacing (Synpace) trial: Rationale and study design. Europace. 2001;3:336-341.
Raviele A, Giada F, Menozzi C, et al. Vasovagal Syncope and Pacing Trial Investigators. A randomized, double-blind, placebo-controlled study of permanent cardiac pacing for the treatment of recurrent tilt-induced vasovagal syncope. The vasovagal syncope and pacing trial (SYNPACE). Eur Heart J. 2004;25:1741-1748.
PM=Pacemaker
SYNPACE is a randomized, double-blind, prospective, multi-center, placebo-controlled trial of 29 patients. The aim was to ascertain whether, in patients with recurrent tilt-induced vasovagal syncope, a dual chamber pacemaker programmed to ON reduced the number syncopal relapses and/or prolonged the time to the first recurrence, compared to patients with a pacemaker programmed to OFF.
Raviele A, Giada F, Sutton R, et al. The vasovagal syncope and pacing (Synpace) trial: Rationale and study design. Europace. 2001;3:336-341.
Raviele A, Giada F, Menozzi C, et al. Vasovagal Syncope and Pacing Trial Investigators. A randomized, double-blind, placebo-controlled study of permanent cardiac pacing for the treatment of recurrent tilt-induced vasovagal syncope. The vasovagal syncope and pacing trial (SYNPACE). Eur Heart J. 2004;25:1741-1748.
87. SYNPACE(Vasovagal SYNcope and PACing) Final analysis found that during a median of 715 days of follow-up:
8/16 (50%) patients randomized to pacemaker programmed ON had recurrence of syncope
5/13 (38%) patients randomized to pacemaker programmed to OFF had recurrence of syncope
Median time to first syncope was longer in the pacemaker ON group, although not significantly so (p=0.38)
No significant difference in the subgroups of patients who had had a mixed response and in those who had had an asystolic response during head-up tilt testing
The SYNPACE intention-to-treat data are presented in Kaplan-Meier format.
Raviele A, Giada F, Menozzi C, et al. Vasovagal Syncope and Pacing Trial Investigators. A randomized, double-blind, placebo-controlled study of permanent cardiac pacing for the treatment of recurrent tilt-induced vasovagal syncope. The vasovagal syncope and pacing trial (SYNPACE). Eur Heart J. 2004;25:1741-1748.
Final analysis found that during a median of 715 days of follow-up:
8/16 (50%) patients randomized to pacemaker programmed ON had recurrence of syncope
5/13 (38%) patients randomized to pacemaker programmed to OFF had recurrence of syncope
Median time to first syncope was longer in the pacemaker ON group, although not significantly so (p=0.38)
No significant difference in the subgroups of patients who had had a mixed response and in those who had had an asystolic response during head-up tilt testing
The SYNPACE intention-to-treat data are presented in Kaplan-Meier format.
Raviele A, Giada F, Menozzi C, et al. Vasovagal Syncope and Pacing Trial Investigators. A randomized, double-blind, placebo-controlled study of permanent cardiac pacing for the treatment of recurrent tilt-induced vasovagal syncope. The vasovagal syncope and pacing trial (SYNPACE). Eur Heart J. 2004;25:1741-1748.
88. INVASY(INotropy Controlled Pacing in VAsovagal Syncope) Objective: To evaluate Closed Loop Stimulation (CLS), a form of rate-adaptive pacing using RV impedance, in preventing recurrence of VVS
Randomized, prospective, single-blind, multi-center
N=50 patients
41: CLS therapy
9: Control (pacemaker programmed in DDI)
Inclusion: Recurrent VVS and +HUT with cardioinhibition
Primary outcome: Recurrence of two VVSs during a minimum of 1 year of follow-up INVASY is a randomized, prospective, single-blind, multi-center trial with the objective to determine whether dual chamber, rate-adaptive Closed Loop Stimulation (CLS) could prevent recurrence of vasovagal syncope (VVS). The CLS algorithm is a form of rate-adaptive pacing which responds to myocardial contraction dynamics, by measuring variations in right ventricular intracardiac impedance.
Fifty patients with severe and recurrent VVS and positive head-up tilt test with cardioinhibition, received a CLS pacemaker. Randomization between DDD-CLS and DDI mode pacing was performed only during the first stage of the study which included 26 patients:
17/26—DDD-CLS mode
9/26—DDI mode (control group)
All 24 patients recruited in the second stage of the study were programmed in DDD-CLS mode.
Occhetta E, Bortnik M, Audoglio R, et al. Closed loop stimulation in prevention of vasovagal syncope. Inotropy controlled pacing in vasovagal syncope (INVASY): A multicentre randomized, single blind, controlled study. Europace. 2004;6:538-547.
INVASY is a randomized, prospective, single-blind, multi-center trial with the objective to determine whether dual chamber, rate-adaptive Closed Loop Stimulation (CLS) could prevent recurrence of vasovagal syncope (VVS). The CLS algorithm is a form of rate-adaptive pacing which responds to myocardial contraction dynamics, by measuring variations in right ventricular intracardiac impedance.
Fifty patients with severe and recurrent VVS and positive head-up tilt test with cardioinhibition, received a CLS pacemaker. Randomization between DDD-CLS and DDI mode pacing was performed only during the first stage of the study which included 26 patients:
17/26—DDD-CLS mode
9/26—DDI mode (control group)
All 24 patients recruited in the second stage of the study were programmed in DDD-CLS mode.
Occhetta E, Bortnik M, Audoglio R, et al. Closed loop stimulation in prevention of vasovagal syncope. Inotropy controlled pacing in vasovagal syncope (INVASY): A multicentre randomized, single blind, controlled study. Europace. 2004;6:538-547.
89. INVASY(INotropy Controlled Pacing in VAsovagal SYncope) Final analysis found:
7/9 patients in the DDI mode had recurrence of syncope during the first year
These 9 patients were then reprogrammed to the CLS mode and no more syncope occurred
0/41 patients programmed to CLS reported VVS
A main limitation of this study is the low number of control subjects.
The INVASY intention-to-treat data are presented in Kaplan-Meier format.
Occhetta E, Bortnik M, Audoglio R, et al. Closed loop stimulation in prevention of vasovagal syncope. Inotropy controlled pacing in vasovagal syncope (INVASY): a multicentre randomized, single blind, controlled study. Europace. 2004;6:538-547.Final analysis found:
7/9 patients in the DDI mode had recurrence of syncope during the first year
These 9 patients were then reprogrammed to the CLS mode and no more syncope occurred
0/41 patients programmed to CLS reported VVS
A main limitation of this study is the low number of control subjects.
The INVASY intention-to-treat data are presented in Kaplan-Meier format.
Occhetta E, Bortnik M, Audoglio R, et al. Closed loop stimulation in prevention of vasovagal syncope. Inotropy controlled pacing in vasovagal syncope (INVASY): a multicentre randomized, single blind, controlled study. Europace. 2004;6:538-547.
90. Role of Pacing as Therapy for Syncope: Summary Three earlier studies single blind – Bias?
Pacemaker implantation may modulate reflex syncope and autonomic responses1
Study results may differ based on pre-implant selection criteria and tilt-testing techniques
Pacing therapy is effective in some but not all (cardioinhibition vs. vasodepression)
In five pacing studies, syncope recurred in 33/156 (21%) of paced patients, 72/162 (44%) in non-paced patients (p<0.000)2
A comparison of the patient populations of the four pacemaker trials raises the question of whether the differences in study results could be due to differences in the study populations or in tilt-testing methods.
VPS and VPS II – < 30% of patients had relatively severe bradycardia
VASIS and SYDIT– patients tended to have more severe bradycardia with a vast majority having asystole
VASIS and SYDIT–tilt testing was fairly standardized
VPS and VPS II—tilt testing was not standardized
VASIS and SYDIT–patients were older
Does neurally-mediated syncope in older individuals have a different pathophysiological mechanism requiring different treatments1?
In the five pacing studies, 318 patients were evaluated. Syncope recurred in 33/156 (21%) of the paced patients and 72/162 (44%) of non-paced patients (p<0.000). Follow-up studies are necessary to address the limitations found in all of the studies,2 including pre-implant selection criteria of the patients who might benefit from pacemaker therapy.
1Kapoor W. Is there an effective treatment for neurally mediated syncope? JAMA. 2003;289:2272-2275.
2Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.A comparison of the patient populations of the four pacemaker trials raises the question of whether the differences in study results could be due to differences in the study populations or in tilt-testing methods.
VPS and VPS II – < 30% of patients had relatively severe bradycardia
VASIS and SYDIT– patients tended to have more severe bradycardia with a vast majority having asystole
VASIS and SYDIT–tilt testing was fairly standardized
VPS and VPS II—tilt testing was not standardized
VASIS and SYDIT–patients were older
Does neurally-mediated syncope in older individuals have a different pathophysiological mechanism requiring different treatments1?
In the five pacing studies, 318 patients were evaluated. Syncope recurred in 33/156 (21%) of the paced patients and 72/162 (44%) of non-paced patients (p<0.000). Follow-up studies are necessary to address the limitations found in all of the studies,2 including pre-implant selection criteria of the patients who might benefit from pacemaker therapy.
1Kapoor W. Is there an effective treatment for neurally mediated syncope? JAMA. 2003;289:2272-2275.
2Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
91. CSSCarotid Sinus Syndrome 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
Prevalence higher than previously believed
Carotid Sinus Hypersensitivity (CSH)
No symptoms
No treatment Carotid sinus syndrome (CSS) is an important and often overlooked cause of syncope, and in addition is believed to be a frequent cause of unexplained falls in older individuals. The underlying cause of CSS is considered to be a hypersensitive carotid sinus. Carotid Sinus Hypersensitivity (CSH) is diagnosed by using Carotid Sinus Massage (CSM). The method of carotid sinus massage, and the findings diagnostic of CSS were presented on previous slides.
Kenny RA, Richardson D, Steen N, et al. Carotid sinus syndrome: A modifiable risk factor for nonaccidental falls in older adults (SAFE PACE). J Am Coll Cardiol. 2001;38:1491-1496.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
Sutton R. Carotid sinus syndrome: clinical presentation, epidemiology, and natural history. In: Neurally Mediated Syncope: Pathophysiology, Investigation and Treatment. Blanc JJ, Benditt D, Sutton R. eds. Armonk, NY: Futura;1996:138.Carotid sinus syndrome (CSS) is an important and often overlooked cause of syncope, and in addition is believed to be a frequent cause of unexplained falls in older individuals. The underlying cause of CSS is considered to be a hypersensitive carotid sinus. Carotid Sinus Hypersensitivity (CSH) is diagnosed by using Carotid Sinus Massage (CSM). The method of carotid sinus massage, and the findings diagnostic of CSS were presented on previous slides.
Kenny RA, Richardson D, Steen N, et al. Carotid sinus syndrome: A modifiable risk factor for nonaccidental falls in older adults (SAFE PACE). J Am Coll Cardiol. 2001;38:1491-1496.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
Sutton R. Carotid sinus syndrome: clinical presentation, epidemiology, and natural history. In: Neurally Mediated Syncope: Pathophysiology, Investigation and Treatment. Blanc JJ, Benditt D, Sutton R. eds. Armonk, NY: Futura;1996:138.
92. CSSEtiology Sensory nerve endings in the carotid sinus walls respond to deformation
“Deafferentation” of neck muscles may contribute
Increased afferent signals tobrain stem
Reflex increase in efferent vagal activity and diminution of sympathetic tone results in bradycardia and vasodilatation
The etiology of CSS rests in part from afferent signals arising in the carotid baroreceptors, and inappropriate concomitant signals from nearby neck muscles.
Sensory nerve endings in the carotid sinus walls respond to deformation.
An increase in afferent traffic results in cardioinhibition and vasodilatation.
Deafferentation of nearby neck muscles may contribute. The CNS is not informed of neck movement and consequently the carotid baroreceptor afferents are interpreted as indicating a rise in central arterial pressure.
Blanc JJ, L’Heveder J, Mansourati J, et al. Pathophysiology of carotid sinus syndrome. In: Neurally mediated syncope: Pathophysiology, investigation and treatment. Blanc JJ, Benditt D, Sutton R. eds. Armonk, NY: Futura;1996:25-29.
Kenny RA, McIntosh SJ. Carotid sinus syndrome. In: Syncope in the Older Patient. Kenny RA ed. London: Chapman & Hall Medical; 1996:107-108.
The etiology of CSS rests in part from afferent signals arising in the carotid baroreceptors, and inappropriate concomitant signals from nearby neck muscles.
Sensory nerve endings in the carotid sinus walls respond to deformation.
An increase in afferent traffic results in cardioinhibition and vasodilatation.
Deafferentation of nearby neck muscles may contribute. The CNS is not informed of neck movement and consequently the carotid baroreceptor afferents are interpreted as indicating a rise in central arterial pressure.
Blanc JJ, L’Heveder J, Mansourati J, et al. Pathophysiology of carotid sinus syndrome. In: Neurally mediated syncope: Pathophysiology, investigation and treatment. Blanc JJ, Benditt D, Sutton R. eds. Armonk, NY: Futura;1996:25-29.
Kenny RA, McIntosh SJ. Carotid sinus syndrome. In: Syncope in the Older Patient. Kenny RA ed. London: Chapman & Hall Medical; 1996:107-108.
93. Falls:Incidence, Recurrence, CSH* Falls are the leading cause of injury among older adults, according to 1995 U.S. prevalence data.1
30% of the population older than 65 years of age falls each year, or about 9 million people in the U.S.
50% of these fallers have documented recurrence.
8% of the population greater than 70 years of age visit an ER for a fall.
40% of these visits result in hospitalization.
Carotid sinus hypersensitivity and CSS increasingly are being recognized as attributable causes for unexplained falls and syncope in older adults. What is the contribution of CSS to these falls? This is an area of active research, but already-published results are suggestive. In one study, 279 fallers 50 years or older presenting to an emergency room with frequent or unexplained falls (at least 3 in previous 12 months) underwent carotid sinus massage, and 65 (23%) exhibited cardioinhibitory carotid sinus hypersensitivity.2
1Falling in the elderly: U.S. prevalence data. J Am Geriatr Soc, December, 1995.
2Richardson D, Bexton R, Shaw F, 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;20:820-823.
Falls are the leading cause of injury among older adults, according to 1995 U.S. prevalence data.1
30% of the population older than 65 years of age falls each year, or about 9 million people in the U.S.
50% of these fallers have documented recurrence.
8% of the population greater than 70 years of age visit an ER for a fall.
40% of these visits result in hospitalization.
Carotid sinus hypersensitivity and CSS increasingly are being recognized as attributable causes for unexplained falls and syncope in older adults. What is the contribution of CSS to these falls? This is an area of active research, but already-published results are suggestive. In one study, 279 fallers 50 years or older presenting to an emergency room with frequent or unexplained falls (at least 3 in previous 12 months) underwent carotid sinus massage, and 65 (23%) exhibited cardioinhibitory carotid sinus hypersensitivity.2
1Falling in the elderly: U.S. prevalence data. J Am Geriatr Soc, December, 1995.
2Richardson D, Bexton R, Shaw F, 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;20:820-823.
94. CSS Role of Pacing – Syncope Recurrence Rate 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 CSS is a Class I indication for pacing (AHA and BPEG).
Pacing therapy may be effective for CSS that is either
Cardioinhibitory
or
Mixed cardioinhibitory/vasodepressor
AV sequential pacing (DDD/DDI) is clearly preferable to ventricular demand (VVI) pacing.
Wagshal AB, Wang SKS. Carotid sinus hypersensitivity. In: Syncope: Mechanisms and Management. Grubb BP, Olshansky B. eds. Armonk, NY: Futura;1998:281-295.
Brignole M, Menozzi C. Carotid sinus syndrome: Diagnosis, natural history and treatment. Eur J C P E. 1992;4:247-254.
CSS is a Class I indication for pacing (AHA and BPEG).
Pacing therapy may be effective for CSS that is either
Cardioinhibitory
or
Mixed cardioinhibitory/vasodepressor
AV sequential pacing (DDD/DDI) is clearly preferable to ventricular demand (VVI) pacing.
Wagshal AB, Wang SKS. Carotid sinus hypersensitivity. In: Syncope: Mechanisms and Management. Grubb BP, Olshansky B. eds. Armonk, NY: Futura;1998:281-295.
Brignole M, Menozzi C. Carotid sinus syndrome: Diagnosis, natural history and treatment. Eur J C P E. 1992;4:247-254.
95. SAFE PACESyncope And Falls in the Elderly – Pacing And Carotid Sinus Evaluation Objective
Determine whether cardiac pacing reduces falls in older adults with carotid sinus hypersensitivity
Randomized controlled trial (N=175)
Adults > 50 years, non-accidental fall, positive CSM
Pacing (n=87) vs. No Pacing (n=88) Results
More than 1/3 of adults over 50 years presented to the Emergency Department because of a fall
With pacing, falls ? 70%
Syncopal events ? 53%
Injurious events ? 70% The study was a randomized controlled trial, pacing versus no pacing, performed at the Royal Victoria Infirmary in Newcastle, between April 1998 and May 2000. Patients were followed for 12 months after randomization.
The inclusion criteria were consecutive adults, over the age of 50 years, presenting with a non-accidental fall, who exhibited a positive response to CSM and who had no evidence of cognitive impairment or dementia.
In patients with unexplained falls and a diagnosis of cardioinhibitory carotid sinus hypersensitivity, cardiac pacing reduced the total number of falls by 70%, total syncopal events by 53%, and total injurious events by 70%.
There was a statistically significant reduction in the total number of falls among the pacemaker patient group, with a 70% reduction in total falls compared with the control group.
Only 28 patients reported syncope; 22 syncopal events were reported by paced patients and 47 by controls. Although there was a 50% reduction in the overall number of syncopal episodes, this did not reach statistical significance.
There was also a 70% reduction in the total number of injury events, from 202 in the control group to 61 in paced patients.
Kenny RA, Richardson D, Steen N, et al. Carotid sinus syndrome: A modifiable risk factor for nonaccidental falls in older adults (SAFE PACE). J Am Coll Cardiol. 2001;38:1491-1496.
The study was a randomized controlled trial, pacing versus no pacing, performed at the Royal Victoria Infirmary in Newcastle, between April 1998 and May 2000. Patients were followed for 12 months after randomization.
The inclusion criteria were consecutive adults, over the age of 50 years, presenting with a non-accidental fall, who exhibited a positive response to CSM and who had no evidence of cognitive impairment or dementia.
In patients with unexplained falls and a diagnosis of cardioinhibitory carotid sinus hypersensitivity, cardiac pacing reduced the total number of falls by 70%, total syncopal events by 53%, and total injurious events by 70%.
There was a statistically significant reduction in the total number of falls among the pacemaker patient group, with a 70% reduction in total falls compared with the control group.
Only 28 patients reported syncope; 22 syncopal events were reported by paced patients and 47 by controls. Although there was a 50% reduction in the overall number of syncopal episodes, this did not reach statistical significance.
There was also a 70% reduction in the total number of injury events, from 202 in the control group to 61 in paced patients.
Kenny RA, Richardson D, Steen N, et al. Carotid sinus syndrome: A modifiable risk factor for nonaccidental falls in older adults (SAFE PACE). J Am Coll Cardiol. 2001;38:1491-1496.
96. SAFE PACE Conclusions
Strong association between non-accidental falls and cardioinhibitory CSH
These patients usually not referred for cardiac assessment
Cardiac pacing significantly reduced subsequent falls
CSH should be considered in all older adults who have non-accidental falls Kenny RA, Richardson D, Steen N, et al. Carotid sinus syndrome: A modifiable risk factor for nonaccidental falls in older adults (SAFE PACE). J Am Coll Cardiol. 2001;38:1491-1496.
Kenny RA, Richardson D, Steen N, et al. Carotid sinus syndrome: A modifiable risk factor for nonaccidental falls in older adults (SAFE PACE). J Am Coll Cardiol. 2001;38:1491-1496.
97. Orthostatic Hypotension Etiology
Drug-induced (very common)
Diuretics
Vasodilators
Primary autonomic failure
Multiple system atrophy
Parkinson’s Disease
Postural Orthostatic Tachycardia Syndrome (POTS) Secondary autonomic failure
Diabetes
Alcohol
Amyloid Orthostatic hypotension is an important cause of syncope. The medical history is usually sufficient to establish the diagnosis. However, defining the specific cause requires careful consideration of a number of important conditions.
The most important conditions predisposing to orthostatic syncope are listed here.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.Orthostatic hypotension is an important cause of syncope. The medical history is usually sufficient to establish the diagnosis. However, defining the specific cause requires careful consideration of a number of important conditions.
The most important conditions predisposing to orthostatic syncope are listed here.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
98. Treatment Strategies for Orthostatic Intolerance Patient education, injury avoidance
Hydration
Fluids, salt, diet
Minimize caffeine/alcohol
Sleeping with head of bed elevated
Tilt training, leg crossing, arm pull
Support hose
Drug therapies
Fludrocortisone, midodrine, erythropoietin
Tachy-Pacing (probably not useful)
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
99. Section IV: Special Issues
100. Syncope: Diagnostic Testing in Hospital Strongly Recommended Suspected/known ‘significant’ heart disease
ECG abnormalities suggesting potential life-threatening arrhythmic cause
Syncope during exercise
Severe injury or accident
Family history of premature sudden death Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
101. SEEDS: Syncope Evaluation in the Emergency Department Study Most recently the Syncope Evaluation in the Emergency Department Study (SEEDS) was performed at the Mayo Clinic.* It became clear that a careful evaluation performed in a syncope unit in the Emergency Department was much more beneficial than admission to the hospital.
Prospective randomized clinical trial: syncope unit evaluation vs. standard care.
N=103 consecutive patients
51 randomized to the syncope unit
52 received standard care
Presumptive diagnosis was established in 34 (67%) and 5 (10%) patients (P<0.001), for the syncope unit and standard care groups, respectively
Hospital admission was required for 22 (43%) and 51 (98%) patients (P<0.001)
Actuarial survival was 97% and 90% (P=0.30)
Survival free from recurrent syncope was 88% and 89% (P=0.72) at 2 years
Total patient-hospital days were reduced from 140 to 64
Conclusion: A syncope unit designed for this study significantly improved diagnostic yield in the emergency department and reduced hospital admission and total length of hospital stay without affecting recurrent syncope and all-cause mortality among intermediate-risk patients.
*Shen W, Decker W, Smars P, et al. Syncope evaluation in the emergency department study (SEEDS). Circulation. 2004;110:3636-3645.
Most recently the Syncope Evaluation in the Emergency Department Study (SEEDS) was performed at the Mayo Clinic.* It became clear that a careful evaluation performed in a syncope unit in the Emergency Department was much more beneficial than admission to the hospital.
Prospective randomized clinical trial: syncope unit evaluation vs. standard care.
N=103 consecutive patients
51 randomized to the syncope unit
52 received standard care
Presumptive diagnosis was established in 34 (67%) and 5 (10%) patients (P<0.001), for the syncope unit and standard care groups, respectively
Hospital admission was required for 22 (43%) and 51 (98%) patients (P<0.001)
Actuarial survival was 97% and 90% (P=0.30)
Survival free from recurrent syncope was 88% and 89% (P=0.72) at 2 years
Total patient-hospital days were reduced from 140 to 64
Conclusion: A syncope unit designed for this study significantly improved diagnostic yield in the emergency department and reduced hospital admission and total length of hospital stay without affecting recurrent syncope and all-cause mortality among intermediate-risk patients.
*Shen W, Decker W, Smars P, et al. Syncope evaluation in the emergency department study (SEEDS). Circulation. 2004;110:3636-3645.
102. The Integrated Syncope Unit To optimize the effectiveness of the evaluation and treatment of syncope patients at a given center
Best accomplished by:
Cohesive, structured care pathway
Multidisciplinary approach
Core equipment available
Preferential access to other tests or therapy
Majority of syncope evaluations – Out-patient or day cases The role of a local integrated syncope service is to set standards for, and optimize effectiveness of, the evaluation and treatment of syncope patients at a given center.1
A cohesive, structured care pathway, either delivered within a single syncope facility or as a more multi-faceted service, is recommended for the global assessment of the patient with syncope.
Experience and training in key components of cardiology, neurology, emergency, and geriatric medicine are pertinent.
Core equipment for the facility includes: surface ECG recording, phasic blood pressure monitoring, tilt table testing equipment, external and internal (insertable) ECG loop recorder systems, 24 hour ambulatory blood pressure monitoring, 24 hour ambulatory ECG, and autonomic function testing.
Preferential access to other tests or therapy for syncope should be guaranteed and standardized.
The majority of syncope patients should be investigated as out-patients or day cases.2
1Kenny RA, Brignole M. Organizing management of syncope in the hospital and clinic (the syncope unit). In: Benditt D, Blanc J-J, et al. eds. The Evaluation and Treatment of Syncope. Elmsford, NY: Futura;2003:55-60.
2Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope— Update 2004. Europace. 2004;6:467-537.The role of a local integrated syncope service is to set standards for, and optimize effectiveness of, the evaluation and treatment of syncope patients at a given center.1
A cohesive, structured care pathway, either delivered within a single syncope facility or as a more multi-faceted service, is recommended for the global assessment of the patient with syncope.
Experience and training in key components of cardiology, neurology, emergency, and geriatric medicine are pertinent.
Core equipment for the facility includes: surface ECG recording, phasic blood pressure monitoring, tilt table testing equipment, external and internal (insertable) ECG loop recorder systems, 24 hour ambulatory blood pressure monitoring, 24 hour ambulatory ECG, and autonomic function testing.
Preferential access to other tests or therapy for syncope should be guaranteed and standardized.
The majority of syncope patients should be investigated as out-patients or day cases.2
1Kenny RA, Brignole M. Organizing management of syncope in the hospital and clinic (the syncope unit). In: Benditt D, Blanc J-J, et al. eds. The Evaluation and Treatment of Syncope. Elmsford, NY: Futura;2003:55-60.
2Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope— Update 2004. Europace. 2004;6:467-537.
103. Conclusion Syncope is a common symptom with many causes
Deserves thorough investigation and appropriate treatment
A disciplined approach is essential
ESC guidelines offer current best practices
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
104. Challenges of Syncope Cost
Quality of life implications
Diagnosis and treatment
Diagnostic yield and repeatability of tests
Frequency and clustering of events
Difficulty in managing/treating/controlling future events
Appropriate risk stratification
Complex etiology
Syncope impacts patient quality of life and health care costs in important ways.
Establishing a precise diagnosis is often challenging due to the unpredictability of events and the limited positive predictive value of most available tests. The ‘gold standard’ remains the recording of the cardiac rhythm and if possible, the arterial pressure, during a spontaneous syncopal event.
Olshansky B. Syncope: Overview and approach to management. In: Grubb B and Olshansky B. eds. Syncope: Mechanisms and Management. Armonk, NY:Futura;1998:15-71.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
Syncope impacts patient quality of life and health care costs in important ways.
Establishing a precise diagnosis is often challenging due to the unpredictability of events and the limited positive predictive value of most available tests. The ‘gold standard’ remains the recording of the cardiac rhythm and if possible, the arterial pressure, during a spontaneous syncopal event.
Olshansky B. Syncope: Overview and approach to management. In: Grubb B and Olshansky B. eds. Syncope: Mechanisms and Management. Armonk, NY:Futura;1998:15-71.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update 2004. Europace. 2004;6:467-537.
105. Brief Statement Indications
9526 Reveal® Plus Insertable Loop Recorder
The Reveal Plus ILR is an implantable patient- and automatically activated monitoring system that records subcutaneous ECG and is indicated for
Patients with clinical syndromes or situations at increased risk of cardiac arrhythmias
Patients who experience transient symptoms that may suggest a cardiac arrhythmia
6191 Activator
The Model 6191 Activator is intended for use in combination with a Medtronic Model 9526 Reveal Plus Insertable Loop Recorder.
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.
6191 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.
Potential Complications
Potential complications include, but are not limited to, body tissue rejection phenomena, including local tissue reaction, infection, device migration and erosion of the device through the skin.
2090 Programmer
The Medtronic/Vitatron CareLink programmer system is comprised of prescription devices indicated for use in the interrogation and programming of implantable medical devices. Prior to use, refer to the Programmer Reference Guide as well as the appropriate programmer software and implantable device technical manuals for more information related to specific implantable device models. Programming should be attempted only by appropriately trained personnel after careful study of the technical manual for the implantable device and after careful determination of appropriate parameter values based on the patient's condition and pacing system used. The Medtronic/Vitatron CareLink programmer must be used only for programming implantable devices manufactured by Medtronic or Vitatron.
See the device manual for detailed information regarding the implant procedure, indications, contraindications, warnings, precautions, and potential complications/adverse events. For further information, please call Medtronic at 1-800-328-2518 and/or consult Medtronic’s website at www.medtronic.com. To learn more about syncope, visit www.fainting.com.
Caution: Federal law (USA) restricts this device to sale by or on the order of a physician. Indications
9526 Reveal® Plus Insertable Loop Recorder
The Reveal Plus ILR is an implantable patient- and automatically activated monitoring system that records subcutaneous ECG and is indicated for
Patients with clinical syndromes or situations at increased risk of cardiac arrhythmias
Patients who experience transient symptoms that may suggest a cardiac arrhythmia
6191 Activator
The Model 6191 Activator is intended for use in combination with a Medtronic Model 9526 Reveal Plus Insertable Loop Recorder.
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.
6191 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.
Potential Complications
Potential complications include, but are not limited to, body tissue rejection phenomena, including local tissue reaction, infection, device migration and erosion of the device through the skin.
2090 Programmer
The Medtronic/Vitatron CareLink programmer system is comprised of prescription devices indicated for use in the interrogation and programming of implantable medical devices. Prior to use, refer to the Programmer Reference Guide as well as the appropriate programmer software and implantable device technical manuals for more information related to specific implantable device models. Programming should be attempted only by appropriately trained personnel after careful study of the technical manual for the implantable device and after careful determination of appropriate parameter values based on the patient's condition and pacing system used. The Medtronic/Vitatron CareLink programmer must be used only for programming implantable devices manufactured by Medtronic or Vitatron.
See the device manual for detailed information regarding the implant procedure, indications, contraindications, warnings, precautions, and potential complications/adverse events. For further information, please call Medtronic at 1-800-328-2518 and/or consult Medtronic’s website at www.medtronic.com. To learn more about syncope, visit www.fainting.com.
Caution: Federal law (USA) restricts this device to sale by or on the order of a physician.Indications
9526 Reveal® Plus Insertable Loop Recorder
The Reveal Plus ILR is an implantable patient- and automatically activated monitoring system that records subcutaneous ECG and is indicated for
Patients with clinical syndromes or situations at increased risk of cardiac arrhythmias
Patients who experience transient symptoms that may suggest a cardiac arrhythmia
6191 Activator
The Model 6191 Activator is intended for use in combination with a Medtronic Model 9526 Reveal Plus Insertable Loop Recorder.
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.
6191 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.
Potential Complications
Potential complications include, but are not limited to, body tissue rejection phenomena, including local tissue reaction, infection, device migration and erosion of the device through the skin.
2090 Programmer
The Medtronic/Vitatron CareLink programmer system is comprised of prescription devices indicated for use in the interrogation and programming of implantable medical devices. Prior to use, refer to the Programmer Reference Guide as well as the appropriate programmer software and implantable device technical manuals for more information related to specific implantable device models. Programming should be attempted only by appropriately trained personnel after careful study of the technical manual for the implantable device and after careful determination of appropriate parameter values based on the patient's condition and pacing system used. The Medtronic/Vitatron CareLink programmer must be used only for programming implantable devices manufactured by Medtronic or Vitatron.
See the device manual for detailed information regarding the implant procedure, indications, contraindications, warnings, precautions, and potential complications/adverse events. For further information, please call Medtronic at 1-800-328-2518 and/or consult Medtronic’s website at www.medtronic.com. To learn more about syncope, visit www.fainting.com.
Caution: Federal law (USA) restricts this device to sale by or on the order of a physician.