Syncope A Diagnostic and Treatment Strategy David G. Benditt, M.D. Richard Sutton, DScMed University of Minnesota Medical School Royal Brompton Hospital Minneapolis, MN USA London, UK Transient Loss of Consciousness (TLOC) Classification of Transient Loss of Consciousness (TLOC) Real or Apparent TLOC Syncope Disorders Mimicking • Neurally-mediated reflex Syncope syndromes • With loss of consciousness, i.e., • Orthostatic hypotension seizure disorders, concussion • Cardiac arrhythmias • Without loss of consciousness, i.e., psychogenic “pseudo- • Structural cardiovascular syncope” disease Brignole M, et al. Europace, 2004;6:467-537. 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 Underlying mechanism is transient global cerebral hypoperfusion. Brignole M, et al. Europace, 2004;6:467-537. Presentation Overview I. Etiology, Prevalence, Impact II. Diagnosis III. Specific Conditions and Treatment IV. Special Issues Section I: Etiology, Prevalence, Impact Causes of True Syncope Structural Neurally- Cardiac Orthostatic Cardio- Mediated Arrhythmia Pulmonary 1 2 3 4 • VVS • Drug-Induced • Brady • Acute • CSS • ANS Failure SN Myocardial Dysfunction Ischemia • Situational Primary AV Block • Aortic Cough Secondary • Tachy Stenosis Post- VT • HCM Micturition SVT • Pulmonary • Long QT Hypertension Syndrome • Aortic Dissection Unexplained Causes = Approximately 1/3 DG Benditt, MD. U of M Cardiac Arrhythmia Center Syncope Mimics Acute intoxication (e.g., alcohol) Seizures Sleep disorders Somatization disorder (psychogenic pseudo-syncope) Trauma/concussion Hypoglycemia Hyperventilation Brignole M, et al. Europace, 2004;6:467-537. Impact of Syncope 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 1Kenny RA, Kapoor WN. In: Benditt D, et al. eds. The Evaluation and 3BrignoleM, et al. Europace. 2003;5:293-298. Treatment of Syncope. Futura;2003:23-27. 4Blanc J-J, et al. Eur Heart J. 2002;23:815-820. 2Kapoor W. Medicine. 1990;69:160-175. 5Campbell A, et al. Age and Ageing. 1981;10:264-270. Impact of Syncope: US Trends Inpatient Trend* Physician Office Visits** (000s) (000s) 440 1,200 420 1,100 1,000 400 900 380 800 360 700 340 600 320 500 300 400 '96 '97 '98 '99 '00 '01 '02 '96 '97 '98 '99 '00 '01 *All patients discharged with syncope and collapse **Syncope and collapse (ICD-9 Code: 780.2) (ICD-9 Code:780.2) listed among diagnoses. listed as primary reason for visit. NHDS 2003. NAMCS 2002. Impact of Syncope: US Trends Emergency Hospital Department Visits* Outpatient Visits* (000s) (000s) 900 80 70 800 60 700 50 600 40 + 500 30 '96 '97 '98 '99 '00 '01 '02 '96 '97 '98 '99 '00 '01 '02 *Syncope and collapse (ICD-9 Code:780.2) listed as + Not available primary reason for visit. NHAMCS 2002. 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, Dept. of Health, Eng. 2002-2003. Impact of Syncope: Costs Estimated hospital costs exceeded $10 billion US1 Estimated physician office expenses exceeded $470 million2 £104,285 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. In: Benditt D, et al. eds. The Evaluation and Treatment of Syncope. Futura;2003:23-27. 2OutPatientView v. 6.0. Solucient LLC, Evanston IL. 3Farwell D, et al. J Cardiovasc Electrophysiol. 2002;13(Supp):S9-S13. 4Olshansky B. In: Grubb B and Olshansky B. eds. Syncope: Mechanisms and Management. Futura. 1998:15-71. Impact of Syncope: Quality of Life 100 73%1 80 71%2 60%2 60 37%2 40 20 0 Anxiety/ Alter Daily Restricted Change Depression Activities Driving Employment 1Linzer M. J Clin Epidemiol. 1991;44:1037. 2Linzer M. J Gen Int Med. 1994;9:181. Quality of Life: UK Population Norms vs. Syncope Patients 49% 50 UK Population Norms Patients with Syncope 43% 40 37% 36% % Prevalence 30 26% 19% 20 9% 10 3% 4% 1% 0 Mobility Usual Self-Care Pain/ Anxiety/ Activities Discomfort Depression Rose M, et al. J Clin Epidemiol. 2000;53:1209-1216. Syncope Mortality Low mortality vs. high mortality Neurally-mediated syncope vs. syncope with a cardiac cause Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med. 2002;347(12):878-885. [Framingham Study Population] Implications of Syncope for Driving a Vehicle Those who drive and have If the patient has sufficient recurrent syncope risk their warning of impending syncope lives and the lives of others – Driving may be permitted Places considerable burden on the physician Essentialto know local laws and physician responsibilities Some states – Invasion of privacy to notify motor vehicle department* • Other states – Reporting is mandatory* Olshansky B, Grubb B. In: Syncope: Mechanisms and Management. Futura. Armonk, NY. 1998. *Medtronic, Inc. Follow-up Forum. 1995/96;1(3):8-10. Challenges of Syncope Diagnosis • Complex Quality of life implications • Work • Mobility (automobiles) • Psychological Cost • Cost/year • Cost/diagnosis Section II: Diagnosis 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 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, et al. Europace, 2004;6:467-537. Diagnostic Flow Diagram for TLOC Initial Evaluation Syncope Not Syncope Certain Suspected Unexplained Diagnosis Diagnosis Syncope Cardiac Neurally-Mediated or Frequent or Severe Single/Rare Confirm with Likely Orthostatic Likely Episodes Episodes Specific Test or Specialist Consultation Cardiac Tests for Neurally- Tests for Neurally- No Further Tests Mediated Syncope Mediated Syncope Evaluation + - + - + - Re-Appraisal Re-Appraisal Treatment Treatment Treatment Treatment Brignole M, et al. Europace, 2004;6:467-537. 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 Brignole M, et al. Europace, 2004;6:467-537. 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 Brignole M, et al. Europace, 2004;6:467-537. Carotid Sinus Massage (CSM) Method1 Absolute contraindications2 • Massage, 5-10 seconds • Carotid bruit, known significant carotid arterial disease, • Don‟t occlude previous CVA, MI last 3 months • Supine and upright posture (on tilt table) Complications • Primarily neurological Outcome • Less than 0.2%3 • 3 second asystole and/or 50 mmHg fall in systolic BP • Usually transient with reproduction of symptoms = Carotid Sinus Syndrome 1Kenny RA. Heart. 2000;83:564. 2LinzerM. Ann Intern Med. 1997;126:989. 3Munro N, et al. J Am Geriatr Soc. 1994;42:1248-1251. 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) Brignole M, et al. Europace, 2004;6:467-537. Heart Monitoring Options OPTION 12-Lead 10 Seconds 2 Days Holter Monitor Event Recorders 7-30 Days (non-lead and loop) Up to 14 ILR Months 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 TIME (Months) Brignole M, et al. Europace, 2004;6:467-537. Diagnostic Assessment: Yields (N=3411 to 4332) Yield (%) Initial Evaluation History, Physical Exam, ECG, Cardiac Massage 38-40 Other Tests/Procedures Head-Up Tilt 27 External Cardiac Monitoring 5-13 Insertable Loop Recorder (ILR) 43-883-5 EP Study <2-5 Exercise Test 0.5 EEG 0.3-0.5 No data MRI available6 References Available Neurological Tests: Rarely Diagnostic for Syncope EEG, Head CT, Head MRI May help diagnose seizure Brignole M, et al. Europace. 2004;6:467-537. Head-Up Tilt Test (HUT) Protocols vary Useful as diagnostic adjunct in atypical syncope cases 60° - 80° Useful in teaching patients to recognize prodromal symptoms Not useful in assessing treatment Brignole M, et al. Europace. 2004;6:467-537. Head-up Tilt Test Click once on image to play video. Carlos Morillo, MD, FRCPC Professor, Faculty of Health Sciences McMaster University, Hamilton Ontario Head-Up Tilt Test: ECG Leads and Intra-Arterial Pressure Tracing 2 1 DG Benditt, MD. U of M Cardiac Arrhythmia Center Adenosine Triphosphate (ATP) Test Ongoing investigation Seems to identify a unique in the US mechanism of syncope found in patients with: Provokes a short and potent cardioinhibitory • Advanced age vasovagal response • More hypertension Advantages • More ECG abnormalities • Simple • Inexpensive • Correlation with pacing benefit Brignole M. Heart. 2000;83:24-28. Donateo P. J Am Coll Cardiol. 2003;41:93-98. Flammang D. Circ. 1999;99:2427-2433. 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 Symptom-Rhythm Correlation with the ILR CASE: 56 year-old woman with CASE: 65 year-old man with refractory syncope accompanied syncope accompanied by brief with seizures. retrograde amnesia. Medtronic data on file. Randomized Assessment of Syncope Trial (RAST) 60 Patients Unexplained Syncope EF > 35% 30 Patients 30 Patients Conventional Primary ILR Testing Strategy 14 6 (AECG, Tilt, EPS) + Diagnosis + – – 1 8 + + Crossover AECG, Tilt, ILR EP Study 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. 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 Benditt D. In: Topol E, ed. Textbook of Cardiovascular Medicine. Lippencott;2002:1529-1542. Lu F, et al. In: Benditt D, et al. The Evaluation and Treatment of Syncope. Futura. 2003;80-95. Brignole M, et al. Europace. 2004;6:467-537. 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 1Linzer M, et al. Ann Int Med. 1997;127:76-86. 2Lu F, et al. In: Benditt D, et al. The Evaluation and Treatment of Syncope. Futura. 2003;80-95. ISSUE International 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: 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. ISSUE Patients with Isolated Syncope and Tilt-Positive Syncope 111 Patients with Syncope No SHD, Normal ECG Tilt Test Followed by Insertable Loop Recorder 82: Tilt-Negative 29: Tilt-Positive “Isolated Syncope” Follow-Up to Recurrent Spontaneous Episode Moya A. Circulation. 2001;104:1261-1267. 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. ISSUE Patients with Heart Disease and a Negative EP Test 35 Pts with Heart Disease and Insertable Loop Recorder Syncope: 6 Pts (17%) Pre-Syncope: 13 Pts (37%) ECG-Documented: 6 Pts (17%) ECG-Documented: 8 Pts (23%) AV block + asystole: 1 Sustained VT: 1 A.Fib + asystole: 1 Parox. A.Fib/AT: 1 Sinus arrest: 1 Post tachycardia pause: 1 Sinus tachycardia: 1 No rhythm variations: 4 Rapid A.Fib: 2 Sinus tachycardia: 1 Menozzi C, et al. Circulation. 2002;105:2741-2745. ISSUE Patients 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, et al. Circulation. 2002;105:2741-2745. ISSUE Patients with Bundle Branch Block and Negative EP Test 52 Pts with BBB and Insertable Loop Recorder Syncope: Stable AVB: ILR-Detected Death: 22 Pts (42%)* 3 Pts (6%) Pre-Syncope: 1 Pt (2%) 2 Pts (4%)** ILR-Detected: 19 Not Detected: 3 AVB: 2 (4%) AVB: 12 (63%) SA: 4 (21%) Asystole-undefined: 1 (5%) NSR: 1 (5%) Sinus tachy: 1 (5%) * 5 of these also had ≥1 presyncope Brignole M., ET AL.,Circulation. 2001;104:2045-2050. ** Drop-out before primary-end point ISSUE Patients 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. Circulation. 2001;104:2045-2050. Section III: Specific Conditions and Treatment 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 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 Brignole M, et al. Europace. 2004;6:467-537. “…cardiac syncope can be a harbinger of sudden death.” Survival with and 1.0 without syncope 0.8 6-month mortality rate Probability of Survival of greater than 10% 0.6 Cardiac syncope doubled the risk 0.4 of death No Syncope Vasovagal and Includes cardiac 0.2 Other Causes Cardiac Cause arrhythmias and SHD 0.0 0 5 10 15 Follow-Up (yr) Soteriades ES, et al. N Engl J Med. 2002;347:878. Syncope Due to Structural Cardiovascular Disease: Principle Mechanisms Acute MI/Ischemia Pulmonary embolus/ pulmonary hypertension • 2° neural reflex bradycardia – Vasodilatation, arrhythmias, • Neural reflex, inadequate low output (rare) flow with exertion Hypertrophic cardiomyopathy Valvular abnormalities • Limited output during exertion • Aortic stenosis – Limited output, (increased obstruction, greater neural reflex dilation in periphery demand), arrhythmias, neural reflex • Mitral stenosis, atrial myxoma – Obstruction to adequate flow Acute aortic dissection • Neural reflex mechanism, pericardial tamponade Brignole M, et al. Europace. 2004;6:467-537. 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 Brignole M, et al. Europace. 2004;6:467-537. ILR Recordings CASE: 83 year-old woman with CASE: 28 year-old man presents syncope due to bradycardia: to ER multiple times after falls Pacemaker implanted. resulting in trauma. VT: Ablated and medicated. Reveal ® ILR recordings; Medtronic data on file. Cardiac Rhythms During Unexplained Syncope Composite: N=133 to 7109 Bradycardia 16% No Recurrence (11-21%) 36% (31-48%) Arrhythmia 22% (13-32%) Tachycardia 6% (2-11%) Other 11% Normal Sinus Rhythm 31% (17-44%) Seidl K. Europace. 2000;2(3):256-262. Krahn AD. PACE. 2002;25:37-41. Medtronic ILR Replacement Data. FY03, 04. On file. 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. Syncope: Torsade de Pointes From the files of DG Benditt, MD. U of M Cardiac Arrhythmia Center Long QT Syndromes: 12-Lead ECG From the files of DG Benditt, MD. U of M Cardiac Arrhythmia Center Drug-Induced QT Prolongation (List is continuously being updated) Antiarrhythmics Antibiotics • Class IA ...Quinidine, • Erythromycin, Pentamidine, Procainamide, Disopyramide Fluconazole, Ciprofloxacin and its relatives • Class III…Sotalol, Ibutilide, Dofetilide, Amiodarone, NAPA* Nonsedating antihistamines Antianginal Agents • Terfenadine*, Astemizole • Bepridil* Others Psychoactive Agents • Cisapride*, Droperidol, Haloperidol • Phenothiazines, Amitriptyline, Imipramine, Ziprasidone *Removed from U.S. Market Brignole M, et al. Europace, 2004;6:467-537. 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, Priori S. In: Zipes D and Jalife J, eds. Cardiac Electrophysiology. Saunders;2004:651-659. Treatment of Syncope Due to Bradyarrhythmia Class I indication for 0.4 nV 0.2 pacing using dual 08:23:21 0.0 chamber system -0.2 -0.4 wherever possible :21 :22 :23 :24 :25 :26 :27 :28 :29 0.4 0.2 Ventricular pacing in 8:23:29 0.0 -0.2 atrial fibrillation with -0.4 slow ventricular :29 :30 :31 :32 :33 :34 :35 :36 :37 0.4 0.2 response 08:23:37 0.0 -0.2 -0.4 :37 :38 :39 :40 :41 :42 :43 :44 :45 ACC/AHA/NASPE 2002 Guideline Update. Circ. 2002;106:2145-2161. 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 Brignole M, et al. Europace. 2004;6:467-537. Neurally-Mediated Reflex Syncope Vasovagal Syncope (VVS) Carotid Sinus Syndrome (CSS) Situational syncope • Post-micturition • Cough • Swallow • Defecation • Blood drawing, etc. Brignole M, et al. Europace, 2004;6:467-537. Pathophysiology Autonomic Nervous System Benditt D, et al. Neurally mediated syncope: Pathophysiology, investigations and treatment. Blanc JJ, et al. eds. Futura. 1996. VVS Clinical 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 1 2 Wieling W, et al. In: Benditt D, et al. The Evaluation and Treatment of Syncope. Futura. 2003;11-22. VVS Incidence 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 Linzer M, et al. Ann Intern Med. 1997;126:989. VVS vs. CSS In general: • VVS patients younger than CSS patients • Ages range from adolescence to older adults (median 43 years) Linzer M, et al. Ann Intern Med. 1997;126:989. VVS Recurrences 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 > 75% 800 Total Number of Syncopal Episodes Two Year Risk 100 50 25 50-75% 8 4 25-50% 2 1 < 25% 1 2 3 6 24 84 480 Months Since Symptoms Began 1Savage D, et al. STROKE. 1985;16:626-29. 2Sheldon R, et al. Circulation. 1996;93:973-81. VVS Spontaneous 16 year-old male, healthy, athletic, monitored for fainting. 16.3 sec Continuous Tracing 1 sec From the files of DG Benditt, MD. U of M Cardiac Arrhythmia Center VVS Diagnosis History and physical exam, ECG and BP Head-Up Tilt (HUT) – Protocol: 60° - 80° • 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 Benditt D, et al. JACC. 1996;28:263-275. Brignole M, et al. Europace, 2004;6:467-537. VVS General Treatment Measures Optimal treatment Long-term prevention strategies for VVS are • Tilt training a source of debate • Education Treatment goals • Diet, fluids, salt • Acute intervention • Support hose − Physical maneuvers, eg, crossing legs or tugging arms • Drug therapy − Lowering head • Pacing − Lying down Brignole M, et al. Europace, 2004;6:467-537. 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, et al. PACE. 2000;23(4 Pt. 1):493-498. 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. 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. 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 1BrignoleM, et al. Europace, 2004;6:467-537. 2Di 4Ward C, et al. Heart. 1998;79:45-49. Girolamo E, et al. JACC. 1999;33:1227-1230. 3Raviele A, et al. Circ. 1999;99:1452-1457. 5Perez-Lugones A, et al. J Cardiovasc Electrophysiol. 2001;12(8):935-938. Midodrine for VVS 100 80 Symptom-Free Interval 60 Midodrine Fluid 40 20 p < 0.001 0 0 20 40 60 80 100 120 140 160 180 Months Perez-Lugones A, Schweikert R, Pavia S, et al. J Cardiovasc Electrophysiol. 2001;12(8):935-938. 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 1Connolly 4Connolly S. JAMA. 2003;289:2224-2229. SJ. J Am Coll Cardiol. 1999;33:16-20. 2Sutton R. Circulation. 2000;102:294-299. 5GiadaF. PACE . 2003;26:1016 (abstract). 3Ammirati F. Circ. 2001;104:52-57. 6Occhetta E, et al. Europace. 2004;6:538-547. 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 1Kapoor W. JAMA. 2003;289:2272-2275. 2Brignole M, et al.. Europace. 2004;6:467-537. CSS Carotid 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 Kenny RA, et al. J Am Coll Cardiol. 2001;38:1491-1496. Brignole M, et al. Europace. 2004;6:467-537. Sutton R. In: Neurally Mediated Syncope: Pathophysiology, Investigation and Treatment. Blanc JJ, et al. eds. Armonk, NY: Futura;1996:138. CSS Etiology 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 Carotid Sinus activity and diminution of sympathetic tone results in bradycardia and vasodilatation Falls: Incidence, Recurrence, CSH* 75 50% 1 50 30% 1 23% 2 25 0 Incidence Recurrence CSH* Present > Age 65 in Fallers > Age 50 Presenting at ER *Carotid Sinus Hypersensitivity 1J Am Geriatr Soc. 1995. 2 Richardson D, et al. PACE. 1997;20:820. CSS Role of Pacing – Syncope Recurrence Rate Class I indication for pacing 75 (AHA and BPEG) 57% Limit pacing to CSS that is: 50 • Cardioinhibitory • Mixed 25 DDD/DDI superior to VVI %6 • Mean follow-up = 6 months 0 No Pacing Pacing Brignole M, et al. Eur JCPE. 1992;4:247-254. SAFE PACE Syncope And Falls in the Elderly – Pacing And Carotid Sinus Evaluation Objective Results • Determine whether cardiac • More than 1/3 of adults over pacing reduces falls in 50 years presented to the older adults with carotid Emergency Department sinus hypersensitivity because of a fall Randomized controlled • With pacing, falls 70% trial (N=175) • Syncopal events 53% • Adults > 50 years, • Injurious events 70% non-accidental fall, positive CSM • Pacing (n=87) vs. No Pacing (n=88) Kenny RA. J Am Coll Cardiol. 2001;38:1491-1496. 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, J Am Coll Cardiol. 2001; 38:1491-1496. Orthostatic Hypotension Etiology Secondary autonomic failure Drug-induced (very common) • Diabetes • Diuretics • Alcohol • Vasodilators • Amyloid Primary autonomic failure • Multiple system atrophy • Parkinson‟s Disease • Postural Orthostatic Tachycardia Syndrome (POTS) Brignole M, et al. Europace, 2004;6:467-537. 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, et al. Europace, 2004;6:467-537. Section IV: Special Issues 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, et al. Europace. 2004;6:467-537. SEEDS: Syncope Evaluation in the Emergency Department Study Long-Term Clinical Outcomes Survival Free from Death Survival Free from Recurrence 100% 100% 90% 90% Syncope Unit Group Syncope Unit Group 80% Standard Care Group 80% Standard Care Group P=0.30 P=0.72 70% 70% 0 1 2 0 1 2 Years Years Results: Syncope unit improved diagnostic yield in the ED and reduced hospital admission and length of stay Shen W, et al. Circ. 2004;110(24):3636-3645. 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 1Kenny RA, Brignole M. In: Benditt D, et al. eds. The Evaluation and Treatment of Syncope. Futura;2003:55-60. 2Brignole M, et al. Europace, 2004;6:467-537. 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, et al. Europace, 2004;6:467-537. 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 Olshansky B. In: Grubb B and Olshansky B. eds. Syncope: Mechanisms and Management. Futura. 1998:15-71. Brignole M, et al. Europace, 2004;6:467-537. 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.