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SYNCOPE Nora Goldschlager, M.D. MACP, FACC, FAHA, FHRS Cardiology – San Francisco General Hospital UCSF Disclosures: None SCOPE OF THE PROBLEM • Cumulative lifetime incidence in general population up to 35% • 1% of all hospital admissions • 3% of all ER visits; up to 65% are vasovagal • 6% incidence in institutionalized elderly • Prevalence: 7 - 47% in young, healthy subjects; unknown in elderly • Up to 30% of patients may have no diagnosis established at hospital discharge • 6% annual mortality if no cause established • 12 - 25% recurrence Mortality % 50 40 Cardiac 30 Noncardiac 20 10 Unknown 0 Yr. of FU: 0 No. at risk: 433 Kapoor 1 380 Medicine 69:1990 2 349 N = 433 3 295 4 179 Sudden death: 37% 5 44 Probability of survival SURVIVAL IN SYNCOPAL PATIENTS No syncope Vasovagal & other causes (OH, med Rx) Unknown cause Neurologic cause Cardiac cause 1.0 .8 .6 .4 .2 0 0 Soteriades et al 5 10 15 Follow-up (yr) NEJM 2002;347:878 20 25 (Framingham) N = 822/7814 Prevalence (%) PREVALENCE OF SYNCOPE BY AGE 50 Males Females 40 30 20 10 0 0 Ganzeboom et al 7 14 Age (yrs) AJC 4.15.03 21 YOUNGER ADULTS OH, situational, seizures, drugs 1° arrhythmia 15% 30% 15% 40% ELDERLY OH, CSS, situational, seizures, drugs 1° arrhythmia, LV obstruction 30% 30% 25% 15% Vasovagal Cardiogenic Undetermined Other causes ETIOLOGY OF FIRST SYNCOPE IN PATIENTS > 65 YEARS % • Reflex-mediated (VVS, CSS, situational) • Orthostatic • Cardiac Arrhythmic Nonarrhythmic • Drug-induced • CNS • Unexplained 13-30% 12 8 3 8 6 49 Roussanov et al, Am J Geriatric Cardiol 2007;16:249 N=304 (VA patients) FEATURES OF UNEXPLAINED SYNCOPE IN OLDER PATIENTS • High incidence of comorbid conditions • 24% recurrence rate • Concurrent BP and HF Rx increases susceptibility to + HUT • Only 9% had an etiology established during follow-up • Lower diagnostic yield of history and tests compared in younger patients Roussanov et al, Am J Geriatric Cardiol 2007;16:249 N=304 (VA patients) Proportion of pts alive PROGNOSIS IN UNEXPLAINED SYNCOPE IN PATIENTS > 65 1.0 Control .75 Syncope .50 .25 0 0 1 2 3 Yrs FU Roussanov et al Am J Geriatric Cardiol 2007; 16:249 N = 304 VA pts EVALUATION OF SYNCOPE: PERTINENT HISTORY • Precipitating factors - Posture changes (orthostatic hypotension) - Cough, swallowing, micturition, defecation (“situational” syncope) - Exercise (consider aortic stenosis, HOCM, VT) - Head turning, Valsalva (suggests carotid sinus syndrome) • Prodromal symptoms • Speed of onset and recovery (prolonged recovery suggests vasovagal syncope) • Aura (suggests seizure) • Hx heart disease (predicts cardiac syncope: 95% specificity <50%>) NATURAL HISTORY OF AORTIC STENOSIS Onset of Sx % Survival 100 75 With AVR Asx stage Without AVR 50 25 CHF Syncope 0 10 20 Years Angina 30 EVALUATION OF SYNCOPE: PERTINENT HISTORY • Drugs - Diuretics ( hypokalemia, hypomagnesemia) - Digitalis (AVB, VT-classically bidirectional) - Antihypertensives - Antiarrhythmic agents ( proarrhythmia) - Ophthalmic -blockers - Antianginal medications (preload and afterload reduction) - QT prolonging drugs (www.torsades.org) - OTC drugs - Herbs - Illicit drugs, alcohol - β-blockers • Family history of sudden death (congenital long QT syndrome, hypertrophic obstructive cardiomyopathy) • Known rhythm abnormality (e.g., WPW) Exercise-induced RVOT VT Tussive bradycardia Deglutition bradycardia Continuous strips CONGENITAL LQTS • 1:10,000 is a gene carrier • 3-4,000 sudden deaths/yr, mostly young patients • 10% sudden deaths in untreated patients • 30% of sudden or aborted sudden deaths occur as 1st event • Female gender • About 10% have normal QTC; about 30% have borderline QTC CLUES TO ETIOLOGY OF SYNCOPE FROM PHYSICAL EXAMINATION • Left ventricular impulse abnormalities suggesting past myocardial infarction • Ventricular hypertrophy (need for AV synchrony) • Ventricular gallops • Murmurs (aortic stenosis, hypertrophic obstructive cardiomyopathy) • Pulmonary hypertension • Mitral valve prolapse (PSVT, VT, autonomic dysfunction) • Carotid sinus massage indicating CSH CAROTID SINUS MASSAGE • Generally accepted contraindications - Carotid bruits - Prior endarterectomy - Prior TIA or CVA - Known cerebrovascular disease • Responses to CSM - Bradycardia / asystole usually abrupt - Hypotension often not abrupt, and outlasts the CSM - Complications (< 1%): TIA, transient paresis, visual disturbances CLUES TO ETIOLOGY OF SYNCOPE FROM 12-LEAD ECG • Long QT interval • Prior MI (substrate for VT) • Epsilon wave, anterior (V1-3) T inversion, QRS duration V1-3 / V4-6 > 1.2, suggesting RV dysplasia • Brugada pattern • Short QT interval (with tall symmetric T waves) • Ectopy • Bradycardia • AV conduction delay / block • Bifascicular block • Ventricular hypertrophy (need for AV synchrony) Epsilon wave of RV dysplasia V1 V2 V3 Marcus, Fontaine PACE 6.95 RV DYSPLASIA • Young pt • Can present as syncope or aborted sudden death • ECG: - Anterior T inversion V1-3 - Prominent anterior forces - RIVCD - Delayed S wave V1-2 • MRI is usually (but not always) diagnostic (fat replacement) RV dysplasia BRUGADA SYNDROME BRUGADA SYNDROME OUTCOME IN PTS WITH BRUGADA ECG Free of events (SD, VF) 1.0 .8 Asymptomatic (57%) .6 Syncope (22%) .4 Sudden death (21%) .2 p = 0.00001 0 0 100 Mos 200 Brugada et al Circulation 2002; 105:73 N = 334, all EPS 63% of syncopal pts had VT induced 300 Free of Appropriate ICD Rx PROGNOSIS OF SYNCOPE IN BRUGADA SYNDROME 1.0 Asymptomatic .8 .6 Syncope .4 Sudden death .2 0 0 12 24 36 48 Follow-up (mos) Antzelevitch et al Circulation 2005; 111:659 N=258 (Registry) 60 ROLE OF ECHOCARDIOGRAPHY IN SYNCOPE • Aortic stenosis • Hypertrophic cardiomyopathy (especially obstructive) • Regional wall-motion disorders (substrate for VT) • Right ventricular dysplasia • Calcified mitral / aortic annulus ( AV block incidence) • Intracardiac tumor • Mitral valve prolapse • Repaired congenital heart disease • Normal echo NONARRHYTHMIC CARDIAC SYNCOPE: OBSTRUCTION TO FLOW • Aortic stenosis - LV baroceptor stimulation with reflex peripheral vasodilation - Ventricular arrhythmias - Transmural ischemic injury with LV dysfunction • Hypertrophic obstructive cardiomyopathy • Tumor • Primary pulmonary hypertension, pulmonic stenosis • Pulmonary embolism Syncope in aortic stenosis Recorded during syncopal spell. BP unobtainable. Syncope in aortic stenosis Lead III: During syncopal spell SYNCOPE IN HYPERTROPHIC CARDIOMYOPATHY - 1 • Causes - SVT (especially AF) - VT - LV outflow tract gradient - Abnormal baroreceptor reflexes - Ischemia • EP studies unreliable • -blockers, disopyramide and Ca++ channel blockers do not reduce incidence of SD SYNCOPE IN HYPERTROPHIC CARDIOMYOPATHY - 2 • ICD indicated for high risk patients - Family hx syncope/sudden death LVH > 3 cm Aborted sudden death Nonsustained VT on Holter SYNCOPE IN PULMONARY HYPERTENSION • Usually exertional or immediately post-exercise • “Fixed” right sided obstruction due to high pulmonary vascular resistance • Inability to increase CO in response to • Decreased cerebral perfusion SVR SYNCOPE IN SYSTOLIC HEART FAILURE • In patients with syncope, heart failure is an independent predictor of mortality • Syncopal patients with ICDs have appropriate therapies delivered • SCD-HeFT: - Predictors of syncope: QRSd > 120 ms, NYHA III, no beta blocker - Not predictors: EF, NSVT, AF, other HF Rx - 16% with ICD had syncope; 41% had appropriate shock (vs 12% with no syncope) - Syncope was predictor of total and CV mortality, but not sudden death and did not differ among ICD, amio, or placebo pts - ICDs did not reduce mortality in syncope patients NEUROCARDIOGENIC (VASOVAGAL) SYNCOPE • Occurs at all ages • 17 - 35% suffer significant injury • 5 - 7% have fractures • Up to 4% of pts diagnosed with VVS may have cardiac syncope FEATURES OF HISTORY IN VVS • Usually occurs in upright position • Rare during exercise • 3 phases: prodrome, loss of consciousness, postsyncopal period • May have specific triggers: pain, trauma, stress, “situational” (swallow, micturition, defecation) • Peri-event amnesia common • Association with chronic fatigue syndrome, depression, somatic disorders • May run in families • frequency around menses VASOVAGAL vs ARRHYTHMIC* SYNCOPE Male Age > 54 Supine Upright Precipitant No presyncope Warning Diaphoresis *VT + AVB Calkins et al AJM 98:1995 P < .001 < .001 NS NS < .001 NS NS < .001 0 20 VV (%) 40 60 80 100 Arrhythmic (%) VASOVAGAL vs ARRHYTHMIC* SYNCOPE Fatigue Post Confusion Palpitations Incontinence Injury Major Injury Recovery > 0” *VT + AVB Calkins et al AJM 98:1995 0 P < .001 NS NS .02 NS NS < .001 20 40 VV (%) 60 80 100 Arrhythmic (%) NEUROCARDIOGENIC SYNCOPE LV volume Venous return HEAD UP TILT Peripheral venous pooling Mechanoreceptor stimulation (myocardial C fibers) Peripheral vasodilation Hypotension LV contractility Vasomotor center adrenergic tone Vagal tone Bradycardia or asytole VVS: PHARMACOLOGIC THERAPY • Anticholinergic agents • Alpha-adrenergic - Disopyramide* agonists (effect vs placebo - Ephedrine is controversial) - Etilephrine - Scopolamine - Theophylline • Negative inotropic agents - Dexedrine - Disopyramide* - Midodrine • Fludrocortisone • Serotonin reuptake • Vasopressin inhibitors * Watch for urinary retention, torsades de pointes VT VVS: PACEMAKER THERAPY Effect vs placebo is controversial and not supported in RCTs - Dual chamber - Rate-drop response or other algorithm which detects heart rate, then tachypaces while periodically searching for spontaneous rhythm % syncope free pts VVS: PACING vs -BLOCKADE (SYDIT) 1.0 Pacemaker 0.9 P = 0.0031 0.8 0.7 Atenolol 0.6 0 200 Ammirati et al 400 600 Days 800 1000 Circulation 2001; 104:52 N = 93 “ORTHOSTATIC TRAINING” FOR REFRACTORY NEUROCARDIOGENIC SYNCOPE N = 47, mean age 16 5 in hospital training sessions 40 min BID standing against wall at home Results: (FU 18 ± 5 mos) 96% had – HUT (Control 26%) 0% had syncope (Control 57%) Girolamo et al Circulation 1999;100:1798 LEG CROSSING AND MUSCLE TENSING TO ABORT / MITIGATE VASOVAGAL SYNCOPE • N = 21 • At onset of sx, leg crossing with tensing of abdominal, leg and buttock muscles • BP and HR stabilized in all pts in 3 - 6" • 5 / 20 aborted syncope • 15 / 20 had delayed onset of syncope by 0.5 - 11' • At 10 mo FU, 16 / 19 benefited from maneuver • Similar benefit for cardiac pacing Krediet at al, Circulation 2002;106:1684 ISOMETRIC ARM EXERCISE TO ABORT VASOVAGAL SYNCOPE HR Control 2 min handgrip Asx 11% Syncope 47% Asx 63% Syncope 5% 112 90 68 45 BP 178 156 133 111 89 67 44 Brignole et al JACC 2002;40:2053 N = 19 FALLS: SCOPE OF THE PROBLEM • 30% of pts > 65 fall / yr • 60% of pts in long-term care facilities fall / yr • 10 - 20% result in injury • 2 - 6% result in fractures • Usually unwitnessed • 30% have LOC with CSM; 80% had amnesia Kenny et al SAFEPACE JACC 2001;38 N = 175 SAFE-PACE TRIAL* *Syncope and Falls in the Elderly Pacing and Carotid Sinus Evaluation • Prospective randomized, controlled trial of 175 patients > 50 y.o. with cardioinhibitory carotid sinus hypersensitivity and unexplained falls • Randomized to pacing (with rate-drop response) vs. no pacing • Follow-up one year • Odds-ratio of falls in nonpaced patients 4:1, 0. 35 in paced patients Kenny et al JACC 2001;38 DDD PACING FOR CAROTID SINUS SYNDROME WITH FALLS, DIZZINESS AND SYNCOPE 100 Before After 80 60 40 20 0 Syncope Crilley et al Falls Dizziness Postgrad Med J 73:1997 N = 42 SYNCOPE WORKUP • • • • • ECG Holter (overall yield 2-35%) Event Monitor (patient cannot be syncopal) Head-up tilt table testing Electrophysiologic study (predictive value variable) • Implantable loop recorder TILT-TABLE TESTING FOR EVALUATION OF SYNCOPE: SUMMARY OF PRINCIPAL INDICATIONS Tilt-table testing warranted • Recurrent syncope or single syncopal episode in a high risk patient, whether or not the medical history is suggestive of neurally mediated (vasovagal) origin and: 1. No evidence of structural cardiovascular disease, or 2. Structural cardiovascular disease is present, but other causes of syncope have been excluded by appropriate testing Benditt et al JACC July 1996 Tilt-table testing warranted • Further evaluation of patients in whom an apparent cause has been established (e.g., asystole, atrioventricular block), but in whom demonstration of susceptibility to neurally mediated syncope would affect treatment plans • Part of the evaluation of exercise-induced or exercise-associated syncope Reasonable differences of opinion exist regarding utility of tilt-table testing • Differentiating convulsive syncope from seizures • Evaluating patients (especially the elderly) with recurrent unexplained falls • Assessing recurrent dizziness or presyncope • Evaluating unexplained syncope in the setting of peripheral neuropathies or dysautonomias • Follow-up evaluation to assess therapy of neurally mediated syncope Tilt-table testing not warranted • Single syncopal episode, without injury and not in a high risk setting, with clear-cut vasovagal features • Syncope in which an alternative specific cause has been established and in which additional demonstration of a neurally mediated susceptibility would not alter Rx DIAGNOSTIC YIELD OF AMBULATORY ELECTROCARDIOGRAPHIC MONITORING (AECG) IN SYMPTOMATIC PATIENTS Sx w/o AECG arrhythmia (%) No Sx with AECG arrhythmia (%) No. + – + – Zeldis 37 Clark 98 Jonas 358 Kala 108 Gibson 1,512 Boudoulas 119 Diamond 85 TOTAL 2,651 Overall yield 2% 13 3 4 7 2 26 44 34 39 0 7 15 13 20 21 30 41 16 16 10 27 4 23 17 80 69 79 34 33 48 DiMarco and Philbrick, Ann Intern Med 6/90 PATIENT PRESENTING WITH SYNCOPE AND SEIZURE ADVANTAGES AND LIMITATIONS OF IMPLANTABLE LOOP RECORDERS Advantages • Prolonged ECG recording capability (to 2 yrs) • Memory - allows activation after syncopal event • Automatic recording, allowing automatic acquisition of ECG events which fall outside programmable boundaries • Elimination of technical factors which impair good quality surface ECG recording during sx • High sx-ECG correlation yield: Dx made in 25-50% of pts, and suggested in an additional 15-25% Benditt et al ADVANTAGES AND LIMITATIONS OF IMPLANTABLE LOOP RECORDERS Limitations • Surgical implantation • Does not record other potentially important parameters (e.g., BP) • Sx - ECG correlation not available when automatic recordings are obtained • Does not distinguish vasovagal episodes from conduction system disease Benditt et al RECOMMENDATIONS FOR IMPLANTABLE CARDIOVERTER DEFIBRILLATORS IN SYNCOPAL PATIENTS Class I Syncope of undetermined origin with clinically relevant, hemodynamically significant sustained VT or VF induced at EPS Class IIa Reasonable for patients with unexplained syncope, significant LV dysfunction, and nonischemic dilated cardiomyopathy Reasonable for patients with Brugada syndrome who have had syncope. ACC/AHA/HRS Guidelines 2008 ACC/AHA/ESC 2006 Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death EP Testing in Patients with Syncope Class I Patients with syncope of unknown cause with impaired LV function or structural heart disease Class IIa Can be useful in patients with syncope when brady- or tachyarrhythmias are suspected, and in whom noninvasive diagnostic studies are not conclusive. RECOMMENDATIONS FOR ICDS IN SYNCOPAL PATIENTS Class IIb May be consideered in patients with syncope and advanced structural heart disease in whom thorough invasive and noninvasive investigations have failed to define a cause. Class III Syncope of undetermined cause in a patient without inducible ventricular tachyarrhythmias and without structural heart disease. ACC/AHA/HRS Guidelines 2008 ESC GUIDELINES ON SYNCOPE Hospital Admission for Syncope Management For Dx: Strongly recommended • Suspected or known significant heart disease • ECG abnormalities suggestive of arrhythmic syncope • Syncope during exercise • Syncope causing severe injury • Strong family history of sudden death Europace 2004;6: 467-537 ESC GUIDELINES ON SYNCOPE May need to be admitted • Patients with or without heart disease but with: Sudden palpitations shortly before syncope Syncope in supine position Worrisome family history Significant physical injury • Patients with minimal or mild heart disease when there is high suspicion for cardiac syncope • Suspected pacemaker or ICD problem Europace 2004;6: 467-537 ESC GUIDELINES ON SYNCOPE Hospital Admission for Syncope Management For Rx: • Cardiac arrhythmias as cause • Syncope due to cardiac ischemia • Syncope due to structural cardiac or pulmonary disease • Stroke or focal neurologic disorders • Cardioinhibitory neurally mediated syncope when pacemaker implant is planned Europace 2004;6: 467 - 537 INDICATIONS TO REFER SYNCOPAL PT TO ELECTROPHYSIOLOGIST • Neurocardiogenic syncope, especially if refractory to avoidance of triggers and drug Rx, or associated with prolonged pauses in cardiac rhythm • Arrhythmia identified during evaluation: - VT due to any cause - Bradyarrhythmia caused by Rx that cannot be withheld or changed - Supraventricular tachycardia, esp. with WPW conduction INDICATIONS TO REFER SYNCOPAL PT TO ELECTROPHYSIOLOGIST • Congenital long QT syndrome • Brugada syndrome • Structural heart disease • Syncope in athletes • Syncope during exercise • Short QT syndrome • Origin of syncope remains unknown and prolonged arrhythmia monitoring by implantable loop recorder is being considered