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SYNCOPE..pptx
1) Syncope is defined as a transient loss of consciousness and postural tone due to decreased cerebral blood flow. It is a symptom with many potential causes. 2) A detailed patient history and physical exam are important for evaluating syncope. Additional testing may include ECG, cardiac monitoring, tilt table testing, electrophysiological study, and implantable loop recording. 3) The ISSUE study found that patients with isolated syncope and those with a positive tilt table test had similar outcomes when monitored with an implantable loop recorder. Bradycardic events were found in 18% of tilt-negative patients and 21% of tilt-positive patients, with asystole being a common finding.
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Syncope is a transient loss of consciousness with spontaneous recovery. It highlights the difference between syncope and sudden death.
Syncope affects various age groups, with significant mortality rates from cardiac causes. Understanding its frequency is crucial for diagnosis.
40% of individuals may experience syncope; it leads to hospital admissions, falls, and chronic conditions like anxiety.
Syncope can arise from cardiac, neurological, or external factors such as drugs. Distinguishing types is important for diagnosis.
The main goal is to identify true syncope causes to assess prognosis and initiate preventive treatment. Diagnostic plans include patient history, ECG, various monitoring methods, and specialized tests for accurate diagnosis.
Tilt testing helps identify neurocardiogenic syncope and assesses patient susceptibility, which aids in treatment planning.
Electrophysiological studies are critical in defining syncope causes in high-risk patients, despite some diagnostic limitations.
The ISSUE study analyzes the diagnostic yield of insertable loop recorders in syncope of uncertain etiology.
Vasovagal syncope involves a physiological reflex mechanism; its prevalence informs treatment strategies for affected patients.
Treatment includes patient education, dietary adjustments, and pacing strategies to reduce syncope recurrence.
Various causes of syncope necessitate different treatments ranging from pacing for bradyarrhythmias to medication adjustments for tachyarrhythmias.
Syncope, a common symptom with serious implications, requires thorough investigation and appropriate intervention.
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SYNCOPE..pptx
- 1. Syncope A Diagnostic and TreatmentStrategy DR. SURENDRA
- 2. The Significance ofSyncope The only difference between syncope and sudden death is that in one you wake up.1 1 Engel GL. Psychologic stress, vasodepressor syncope, and sudden death. Ann Intern Med 1978; 89: 403-412.
- 3. Syncope Definition: Sudden transientloss of consciousness and postural tone with subsequent spontaneous recovery. ( Greek synkope, “cessation, pause”). Transient inadequate cerebral perfusion.
- 4. Syncope: A Symptom…Nota Diagnosis Self-limited loss of consciousness and postural tone Relatively rapid onset Variable warning symptoms Spontaneous complete recovery
- 5. Individuals <18yrs Military Population 17- 40 yrs Individuals 40-59 yrs* Individuals >70 yrs* 15% 20-25% 16-19% 23% Syncope:Reported Frequency *during a 10-year period Brignole M, Alboni P, Benditt DG, et al. Eur Heart J, 2001; 22: 1256-1306.
- 6. Distribution of ageand cumulative incidence of first episode of syncope in the general population
- 7. 1 Day SC,et al. Am J of Med 1982;73:15-23. 2 Kapoor W. Medicine 1990;69:160-175. 3 Silverstein M, Sager D, Mulley A. JAMA. 1982;248:1185-1189. 4 Martin G, Adams S, Martin H. Ann Emerg Med. 1984;13:499-504. Some causes of syncope are potentially fatal Cardiac causes of syncope have the highest mortality rates(1 year) The Significance of Syncope 0% 5% 10% 15% 20% 25% Syncope Mortality Overall Due to Cardiac Causes
- 8. Outcome of syncopein SHD
- 9. Impact of Syncope 1KennyRA, Kapoor WN. In: Benditt D, et al. eds. The Evaluation and Treatment of Syncope. Futura;2003:23-27. 2Kapoor W. Medicine. 1990;69:160-175. 3Brignole M, et al. Europace. 2003;5:293-298. 4 Blanc J-J, et al. Eur Heart J. 2002;23:815-820. 5Campbell A, et al. Age and Ageing. 1981;10:264-270. 40% will experience syncope at least once in a lifetime1 1-6% of hospital admissions2 1% of emergency room visits per year3,4 10% of falls by elderly are due to syncope5 Major morbidity reported in 6%1 eg, fractures, motor vehicle accidents Minor injury in 29%1 eg, lacerations, bruises
- 10. Impact of Syncope 1Linzer,J Clin Epidemiol, 1991. 2Linzer, J Gen Int Med, 1994. 0% 20% 40% 60% 80% 100% Anxiety/ Depression Alter Daily Activities Restricted Driving Change Employment 73% 1 71% 2 60% 2 37% 2
- 11. Syncope: Etiology Orthostatic Cardiac Arrhythmia Structural Cardio- Pulmonary * 1 Vasovagal Carotid Sinus •Situational Cough Post- micturition 2 Drug Induced • ANS Failure Primary Secondary 3 Brady Sick sinus AV block • Tachy VT SVT Long QT Syndrome 4 Aortic Stenosis HOCM • Pulmonary Hypertension 5 Psychogenic • Metabolic e.g. hyper- ventilation Neurological Non- Cardio- vascular Neurally- Mediated Unknown Cause = 34% 24% 11% 14% 4% 12% DG Benditt, UM Cardiac Arrhythmia Center
- 12. Syncope-like States Migraine* Acute hypoxemia* Hyperventilation* Somatization disorder (psychogenic syncope) Acute Intoxication (e.g., alcohol) Seizures Hypoglycemia Sleep disorders * may cause ‘true’ syncope
- 13. Syncope: Diagnostic Objectives Distinguish‘True’ Syncope from other ‘Loss of Consciousness’ spells: Seizures Psychiatric disturbances Establish the cause of syncope with sufficient certainty to: Assess prognosis confidently Initiate effective preventive treatment
- 16. A Diagnostic Planis Essential Initial Examination Detailed patient history Physical exam ECG Supine and upright blood pressure Monitoring Holter Event Insertable Loop Recorder (ILR) Special Investigations Head-up tilt test Electrophysiology study Exercise test Echocardiography
- 17. Conventional Diagnostic Methods/Yield Test/ProcedureYield (based on mean time to diagnosis of 5.1 months7 History and Physical (including carotid sinus massage) 49-85% 1, 2 ECG 2-11% 2 Electrophysiology Study without SHD* 11% 3 Electrophysiology Study with SHD 49% 3 Tilt Table Test (without SHD) 11-87% 4, 5 Ambulatory ECG Monitors: • Holter 2% 7 • External Loop Recorder (2-3 weeks duration) 20% 7 • Insertable Loop Recorder (up to 14 months duration) 65-88% 6, 7 Neurological † (Head CT Scan, Carotid Doppler) 0-4% 4,5,8,9,10 * Structural Heart Disease † MRI not studied 1 Kapoor, et al N Eng J Med, 1983. 2 Kapoor, Am J Med, 1991. 3 Linzer, et al. Ann Int. Med, 1997. 4 Kapoor, Medicine, 1990. 5 Kapoor, JAMA, 1992 6 Krahn, Circulation, 1995 7 Krahn, Cardiology Clinics, 1997. 8 Eagle K,, et al. The Yale J Biol and Medicine. 1983; 56: 1-8. 9 Day S, et al. Am J Med. 1982; 73: 15-23. 10 Stetson P, et al. PACE. 1999; 22 (part II): 782.
- 18. Initial Exam: DetailedPatient 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
- 19. Clinical Features SuggestingSpecific Cause of Syncope Neurally-Mediated Syncope Absence of cardiac disease Long history of syncope After sudden unexpected, unpleasant sensation Prolonged standing in crowded, hot places Nausea vomiting associated with syncope During or after a meal With head rotation or pressure on carotid sinus After exertion
- 20. Clinical Features SuggestingSpecific Cause of Syncope Syncope due to orthostatic hypotension After standing up Temporal relationship to taking a medication that can cause hypotension Prolonged standing Presence of autonomic neuropathy After exertion
- 21. Clinical Features SuggestionCause of Syncope Cardiac Syncope Presence of structural heart disease With exertion or supine Preceded by palpitations Family history of sudden death
- 22. 12-Lead ECG Normalor Abnormal? Acute MI Severe Sinus Bradycardia/pause AV Block Tachyarrhythmia (SVT, VT) Preexcitation (WPW), Long QT, Brugada Short sampling window (approx. 12 sec)
- 23. Carotid Sinus Massage Site: Carotid arterial pulse just below thyroid cartilage Method: Right followed by left, pause between Massage, NOT occlusion Duration: 5-10 sec Posture – supine & erect
- 24. Carotid Sinus Massage Outcome: 3 sec asystole and/or 50 mmHg fall in systolic blood pressure with reproduction of symptoms = Carotid Sinus Syndrome (CSS) Contraindications Carotid bruit, known significant carotid arterial disease, previous CVA, stroke last 3 months Risks 1 in 5000 massages complicated by TIA
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- 26. Head-up Tilt Test(HUT) Unmasks VVS susceptibility Reproduces symptoms Patient learns VVS warning symptoms Physician is better able to give prognostic / treatment advice
- 28. Tilt Table Diagnosis Neurocardiogenic-seen in 50% of patients with heart disease and 75% of patients without heart disease who present with syncope Type 1 mixed: bp falls before heart rate and the heart rate does not get <40 and no pauses >3 secs and heart rate falls at the time of syncope Type 2a: cardioinhibitory without asystole-bp falls before the heart rate and heart rate gets below 40 but no asystole > 3 secs Type 2b: cardioinhibitory with asystole-heart rate falls below 40 for > 10secs and asystole is present >3 secs Type 3: pure vasodepressor-bp falls but heart rate does not fall >10% from peak heart rate .
- 29. Tilt testing -outcomes
- 30. Head-Up Tilt Test(HUT) DG Benditt, UM Cardiac Arrhythmia Center
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- 34. Method Comments Holter (24-48hours) Useful for frequent events Event Recorder •Useful for infrequent events •Limited value in sudden LOC Loop Recorder •Useful for infrequent events •Implantable type more convenient (ILR) Wireless (internet) Event Monitoring In development Ambulatory ECG
- 35. Investigation of syncope: ambulatoryECG (holter) monitoring AV block
- 36. Investigation of syncope: eventrecorder
- 37. Investigation of syncope: implantableloop recorder
- 38. Patient Activator Reveal® PlusILR 9790 Programmer Reveal® Plus Insertable Loop Recorder
- 39. Insertable Loop Recorder (ILR) TypicalLocation of the Reveal® Plus ILR
- 40. Value of Event Recorder in Syncope LinzerM. Am J Cardiol. 1990;66:214-219. *Asterisk denotes event marker
- 41. ILR Recordings* 56 yowoman with syncope accompanied with seizures. Infra-Hisian AV Block: Dual chamber pacemaker 65 yo man with syncope accompanied with brief retrograde amnesia. VT and VF: ICD and meds *Medtronic data on file
- 42.
- 43. Classification of ECGrecordings obtained with ILR, with their probable-related mechanism (adapted from ISSUE classification)
- 44. Randomized Assessment of SyncopeTrial (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 1Krahn AD, et al. Circ. 2001;104:46-51. 2Krahn AD, et al. JACC. 2003;42:495-501. Unexplained Syncope EF > 35% 60 Patients AECG, Tilt, EP Study Diagnosis ILR + – + – ILR Conventional Testing (AECG, Tilt, EPS) 30 Patients 30 Patients Primary Strategy Crossover 14 6 1 8 + +
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- 48. Syncope: The Role ofElectrophysiologic Testing Most important diagnostic tool is the history High risk historical elements Syncope resulting in injury Syncope resulting in motor vehicle accident Syncope in the setting of structural heart disease Syncope preceded by palpitations Syncope while supine Abnormal ECG Lack of “low risk” elements
- 49. Conventional EP Testingin Syncope Limited utility in syncope evaluation Most useful in patients with structural heart disease Heart disease……..50-80% No Heart disease…18-50% Relatively ineffective for assessing bradyarrhythmias Brignole M, Alboni P, Benditt DG, et al. Eur Heart Journal 2001; 22: 1256-1306.
- 50. Diagnostic Limitations ofEPS 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
- 51. Guidelines for EPTesting in Syncope Class I: General agreement Patients with structural heart disease and unexplained syncope Class II: Less certain, but accepted Patients with recurrent unexplained syncope without structural heart disease and a negative tilt test Class III: Not indicated Patients with known cause of syncope in whom treatment will not be guided by EP testing
- 52.
- 55. ISSUE International Study ofSyncope 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: 1) Isolated syncope: No SHD, Normal ECG1 Negative tilt Positive tilt 2) Patients with heart disease and negative EP test2 3) Patients with bundle branch block and negative EP test3 1Moya A. Circulation. 2001; 104:1261-1267. 2Menozzi C, et al. Circulation. 2002;105:2741-2745. 3Brignole M, et al. Circulation. 2001;104:2045-2050.
- 56. ISSUE Patients with IsolatedSyncope and Tilt-Positive Syncope Moya A. Circulation. 2001;104:1261-1267. Follow-Up to Recurrent Spontaneous Episode 111 Patients with Syncope No SHD, Normal ECG 29: Tilt-Positive 82: Tilt-Negative “Isolated Syncope” Tilt Test Followed by Insertable Loop Recorder
- 57. ISSUE Isolated 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%) as tilt-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 Moya A. Circulation. 2001;104:1261-1267.
- 58. ISSUE Patients with HeartDisease and a Negative EP Test Menozzi C, et al. Circulation. 2002;105:2741-2745. 35 Pts with Heart Disease and Insertable Loop Recorder Syncope: 6 Pts (17%) ECG-Documented: 6 Pts (17%) Pre-Syncope: 13 Pts (37%) ECG-Documented: 8 Pts (23%) AV block + asystole: 1 A.Fib + asystole: 1 Sinus arrest: 1 Sinus tachycardia: 1 Rapid A.Fib: 2 Sustained VT: 1 Parox. A.Fib/AT: 1 Post tachycardia pause: 1 No rhythm variations: 4 Sinus tachycardia: 1
- 59. ISSUE Patients with HeartDisease 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, et al. Circulation. 2002;105:2741-2745.
- 60. ISSUE Patients with BundleBranch Block and Negative EP Test Brignole M., ET AL.,Circulation. 2001;104:2045-2050. * 5 of these also had ≥1 presyncope ** Drop-out before primary-end point 52 Pts with BBB and Insertable Loop Recorder Syncope: 22 Pts (42%)* ILR-Detected: 19 AVB: 12 (63%) SA: 4 (21%) Asystole-undefined: 1 (5%) NSR: 1 (5%) Sinus tachy: 1 (5%) Not Detected: 3 Stable AVB: 3 Pts (6%) ILR-Detected Pre-Syncope: 2 Pts (4%)** Death: 1 Pt (2%) AVB: 2 (4%)
- 61. ISSUE Patients with BundleBranch 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. Circulation. 2001;104:2045-2050.
- 62. Typical Cardiovascular DiagnosticPathway Adapted from: Linzer M, et al. Annals of Int Med, 1997. 127:76-86. Syncope: Mechanisms and Management. Grubb B, Olshansky B (eds) Futura Publishing 1999 Zimetbaum P, Josephson M. Annals of Int Med, 1999. 130:848-856. Krahn A et al. ACC Current Journal Review,1999. Jan/Feb:80-84. History and Physical, ECG Syncope Known SHD No SHD Echo EPS + Treat > 30 days; > 2 Events Tilt ILR Tilt Holter/ ELR ILR Tilt/ILR < 30 days -
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- 67. Neurally-Mediated Reflex Syncope(NM Vasovagal syncope (VVS) Carotid sinus syndrome (CSS) Situational syncope post-micturition cough swallow defecation blood drawing etc.
- 68. NM Reflex Syncope:Pathophysiology Multiple triggers Variable contribution of vasodilatation and bradycardia
- 69. NMS – BasicPathophysiology Cerebral Cortex Vascular Bed Bradycardia/ Hypotension Baro- receptors Heart Feedback via Carotid Baroreceptors Other Mechanoreceptors Parasympathetic (+) sympathetic (+) ) ¯ Heart Rate ¯ AV Conduction _ Vasodilatation Benditt DG, Lurie KG, Adler SW, et al. Pathophysiology of vasovagal syncope. In: Neurally mediated syncope: Pathophysiology, investigations and treatment. Blanc JJ, Benditt D, Sutton R. Bakken Research Center Series, v. 10. Armonk, NY: Futura, 1996
- 70. Neurological basis of“vasovagal syndrome”
- 71. Neurally MediatedPhysiologic Reflex Mechanism with two Components: Cardioinhibitory ( HR ) Vasodepressor ( BP ) Both components are usually present VVS: Clinical Pathophysiology
- 72. Prevalence of VVS Prevalence is poorly known Various studies report 8% to 37% (mean 18%) of cases of syncope (Linzer 1997) In general: VVS patients younger than CSS patients Ages range from adolescence to elderly (median 43 years) Pallor, nausea, sweating, palpitations are common Amnesia for warning symptoms in older patients
- 73. DG Benditt, UMCardiac Arrhythmia Center 16.3 sec Continuous Tracing 1 sec Spontaneous VVS
- 74.
- 75. VVS: Recurrences 1Savage D,et al. STROKE. 1985;16:626-29. 2Sheldon R, et al. Circulation. 1996;93:973-81. 35% of patients report syncope recurrence during follow-up ≤3 years1 Positive HUT with >6 lifetime syncope episodes: recurrence risk >50% over 2 years2 1000 800 50 100 25 8 4 2 1 1 2 3 6 24 84 480 Months Since Symptoms Began Two Year Risk Total Number of Syncopal Episodes > 75% 50-75% 25-50% < 25%
- 76. Carotid Sinus Syndrome(CSS) Syncope clearly associated with carotid sinus stimulation is rare (≤1% of syncope) CSS may be an important cause of unexplained syncope / falls in older individuals
- 77. Etiology of CSS Sensory nerve endings in the carotid sinus walls respond to deformation “Deafferentation” of neck muscles may contribute Increased afferent signals to brain stem Reflex increase in efferent vagal activity and diminution of sympathetic tone results in bradycardia and vasodilation Carotid Sinus
- 78. Carotid Sinus Hypersensitivity(CSH) Abnormalresponse to CSM Absence of symptoms attributable to CSS CSH reported frequent in ‘fallers’ (Kenny) CSH CSS
- 79. Management Strategies forVVS Optimal management strategies for VVS are a source of debate Patient education, reassurance, instruction Fluids, salt, diet Tilt Training Support hose Drug therapies Pacing Class IIa indication for VVS patients with positive HUT and cardioinhibitory or mixed reflex
- 80. VVS Tilt TrainingProtocol 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, et al. PACE. 2000;23(4 Pt. 1):493-498.
- 81. 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 T, et al. PACE. 2000;23:493-498.
- 82. 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, et al. Europace. 2004;6:199-204.
- 84. Status of Pacingin VVS Perception of pacing for VVS changing: VVS with +HUT and cardioinhibitory response a Class Iia indication1 Recent clinical studies demonstrated benefits of pacing in select VVS patients: VPS I VASIS SYDIT VPS II –Phase I ROME VVS Trial 1Gregoratos G, et al. ACC/AHA Guidelines for Implantation of Cardiac Pacemakers and Antiarrhythmic Devices. Circulation. 1998; 97: 1325-1335.
- 85. VPS-I Vasovagal Pacemaker StudyI Connolly S, et al. J Am Coll Cardiol 1999; 33: 16-20. Study Design: – 54 patients randomized, prospective, single center 27 DDD pacemaker with rate drop response (RDR) 27 no pacemaker Patient Inclusion Criteria: – 6 syncopal events ever – +HUT – Relative bradycardia* *a trough heart rate <60/min if no isoproterenol used, <70/min if up to 2 mcg/min isoproterenol used, or <80/min if over 2 mcg/min isoproterenol used
- 86. VPS- I Connolly S,et al. J Am Coll Cardiol 1999; 33: 16-20. Cumulative Risk (%) 100 90 80 70 60 50 40 30 20 10 0 15 12 9 6 3 0 Control (No Pacemaker) 2P=0.000022 Pacemaker Time in Months Number At Risk C 27 9 4 2 1 0 P 27 21 17 12 11 8
- 87. VASIS Vasovagal Syncope InternationalStudy Sutton, R, et al. Circulation. 2000; 102:294-299. Study Design: – 42 patients, randomized, prospective, multicenter 19 DDI pacemaker (80 bpm) with rate hysteresis (45 bpm) 23 no pacemaker Patient Inclusion Criteria: – > 3 syncopal events in 2 years and last event occurring within 6 months of enrollment and, – Positive VASIS type 2A or 2B cardioinhibitory response to HUT and, – Age > 40 years or drug refractory if < 40 years
- 88. VASIS Pacemaker No-Pacemaker p=0.0004 Years % syncope-free 100 80 60 40 20 0 2 34 5 6 7 12 14 15 23 31 40 # of pts Sutton, R, et al. Circulation. 2000; 102:294-299.
- 89. 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 Ammirati F. Circulation. 2001;104:52-57.
- 90. SYDIT (SYncope DIagnosis andTreatment) Ammirati F. Circulation. 2001;104:52-57. 0.6 0.7 0.8 0.9 1.0 0 100 200 300 400 500 600 700 800 900 1000 Drug Pacemaker (PM) Time (Days) % Syncope-Free p=0.0032 Results: 2 (4%) with PM had syncope recurrence vs. 12 (26%) without PM
- 91. VVS Pacing TrialsConclusions DDD pacing reduces the risk of syncope in patients with recurrent, refractory, highly-symptomatic, cardioinhibitory vasovagal syncope.
- 92. Principal Causes ofOrthostatic Syncope Drug-induced (very common) diuretics vasodilators Primary autonomic failure multiple system atrophy Parkinsonism Secondary autonomic failure diabetes alcohol amyloid Alcohol orthostatic intolerance apart from neuropathy
- 94. Syncope Due toArrhythmia or Structural CV Disease: General Rules Often life-threatening and/or exposes patient to high risk of injury May be warning of critical CV disease Aortic stenosis, Myocardial ischemia, Pulmonary hypertension Assess culprit arrhythmia / structural abnormality aggressively Initiate treatment promptly
- 95. Principal Causes ofSyncope due to Structural Cardiovascular Disease Acute MI / Ischemia Acquired coronary artery disease Congenital coronary artery anomalies HCM Acute aortic dissection Pericardial disease / tamponade Pulmonary embolus / pulmonary hypertension Valvular abnormalities Aortic stenosis, Atrial myxoma
- 96. Syncope Due toCardiac Arrhythmias Bradyarrhythmias Sinus arrest, exit block High grade or acute complete AV block Tachyarrhythmias Atrial fibrillation / flutter with rapid ventricular rate (e.g. WPW syndrome) Paroxysmal SVT or VT Torsades de pointes
- 97. Rhythms During Recurrent Syncope KrahnA, et al. Circulation. 1999; 99: 406-410 Normal Sinus Rhythm 58% Sinus Rhythm 58% Bradycardia 36% Tachyarrhythmia 6%
- 98. AECG: 74 yrMale, Syncope From the files of DG Benditt, UM Cardiac Arrhythmia Center
- 99. Syncope: Torsades From thefiles of DG Benditt, UM Cardiac Arrhythmia Center
- 100. 83 yo woman Bradycardia:Pacemaker implanted 28 yo man in the ER multiple times after falls resulting in trauma VT: ablated and medicated Reveal ® ILR recordings; Medtronic data on file.
- 101. Infra-His Block From thefiles of DG Benditt, UM Cardiac Arrhythmia Center
- 102. 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, Priori S. In: Zipes D and Jalife J, eds. Cardiac Electrophysiology. Saunders;2004:651-659.
- 103. Drug-Induced QT Prolongation Antiarrhythmics Class IA ...Quinidine, Procainamide, Disopyramide Class III…Sotalol, Ibutilide, Dofetilide, Amiodarone, (NAPA) Antianginal Agents (Bepridil) Psychoactive Agents Phenothiazines, Amitriptyline, Imipramine, Ziprasidone Antibiotics Erythromycin, Pentamidine, Fluconazole Nonsedating antihistamines (Terfenadine), Astemizole Others (Cisapride), Droperidol
- 104. Treatment of LongQT 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
- 105. Treatment of SyncopeDue to Bradyarrhythmia Class I indication for pacing using dual- chamber system wherever adequate atrial rhythm is available Ventricular pacing in atrial fibrillation with slow ventricular response
- 106. Treatment of SyncopeDue to Tachyarrhythmia Atrial Tachyarrhythmias; AVRT due to accessory pathway – ablate pathway AVNRT – ablate AV nodal slow pathway Atrial fib– Pacing, linear / focal ablation, ICD selected pts Atrial flutter – Ablation of reentrant circuit Ventricular Tachyarrhythmias; Ventricular tachycardia – ICD or ablation where appropriate Torsades de Pointes – withdraw offending Rx or ICD (long-QT/Brugada) Drug therapy may be an alternative in many cases
- 107. Syncope and Driving:Medical Legal Concerns Examples of syncopal conditions that would prohibit driving Untreated syncope in patients with heart disease Undiagnosed recurrent syncope which occurs without prodrome and can occur while sitting
- 109. Conclusion Syncope is acommon symptom, often with dramatic consequences, which deserves thorough investigation and appropriate treatment of its cause.
- 110.