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SYNCOPE Nora Goldschlager, M.D.

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

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SYNCOPE Nora Goldschlager, M.D.

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  1. SYNCOPE Nora Goldschlager, M.D. MACP, FACC, FAHA, FHRSCardiology – San Francisco General HospitalUCSF Disclosures: None

  2. 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

  3. 50 40 30 20 10 0 Cardiac Mortality % Noncardiac Unknown Yr. of FU: 0 1 2 3 4 5 No. at risk: 433 380 349 295 179 44 Kapoor Medicine 69:1990 N = 433 Sudden death: 37%

  4. 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 Probability of survival 0 5 10 15 20 25 Follow-up (yr) Soteriades et al NEJM 2002;347:878 (Framingham) N = 822/7814

  5. Males Females Prevalence (%) 0 7 14 21 Age (yrs) PREVALENCE OF SYNCOPE BY AGE 50 40 30 20 10 0 Ganzeboom et al AJC 4.15.03

  6. 15% 15% 25% 30% 30% 15% 40% 30% YOUNGER ADULTS ELDERLY OH, CSS, situational, seizures, drugs 1° arrhythmia, LV obstruction OH, situational,seizures, drugs 1° arrhythmia Vasovagal Undetermined Cardiogenic Other causes

  7. ETIOLOGY OF FIRST SYNCOPE IN PATIENTS > 65 YEARS % • Reflex-mediated (VVS, CSS, situational) 13-30% • Orthostatic 12 • Cardiac Arrhythmic 8 Nonarrhythmic 3 • Drug-induced 8 • CNS 6 • Unexplained 49 Roussanov et al, Am J Geriatric Cardiol 2007;16:249 N=304 (VA patients)

  8. 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)

  9. PROGNOSIS IN UNEXPLAINED SYNCOPE IN PATIENTS > 65 1.0 .75 .50 .25 0 Control Syncope Proportion of pts alive 0 1 2 3 Yrs FU Roussanov et al Am J Geriatric Cardiol 2007; 16:249 N = 304 VA pts

  10. 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%>)

  11. NATURAL HISTORY OF AORTIC STENOSIS Onset of Sx With AVR 100 75 50 25 0 Asx stage Without AVR % Survival CHF Angina Syncope 10 20 30 Years

  12. • 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 historyof sudden death (congenital long QT syndrome, hypertrophic obstructive cardiomyopathy) • Known rhythm abnormality (e.g., WPW) EVALUATION OF SYNCOPE: PERTINENT HISTORY

  13. Exercise-induced RVOT VT

  14. Tussive bradycardia

  15. Deglutition bradycardia Continuous strips

  16. 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

  17. 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

  18. 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

  19. 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)

  20. Epsilon wave of RV dysplasia V1 V2 V3 Marcus, Fontaine PACE 6.95

  21. 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)

  22. RV dysplasia

  23. BRUGADA SYNDROME

  24. BRUGADA SYNDROME

  25. OUTCOME IN PTS WITH BRUGADA ECG 1.0 .8 .6 .4 .2 0 Asymptomatic (57%) Free of events (SD, VF) Syncope (22%) Sudden death (21%) p = 0.00001 0 100 200 300 Mos Brugada et al Circulation 2002; 105:73 N = 334, all EPS 63% of syncopal pts had VT induced

  26. PROGNOSIS OF SYNCOPE IN BRUGADA SYNDROME 1.0 .8 .6 .4 .2 0 Asymptomatic Syncope Free of Appropriate ICD Rx Sudden death 0 12 24 36 48 60 Follow-up (mos) Antzelevitch et al Circulation 2005; 111:659 N=258 (Registry)

  27. • 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 ROLE OF ECHOCARDIOGRAPHY IN SYNCOPE

  28. 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

  29. Syncope in aortic stenosis Recorded during syncopal spell. BP unobtainable.

  30. Syncope in aortic stenosis Lead III: During syncopal spell

  31. 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

  32. 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

  33. 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 SVR • Decreased cerebral perfusion

  34. 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

  35. 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

  36. 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

  37. VV (%) Arrhythmic (%) VASOVAGAL vs ARRHYTHMIC* SYNCOPE P Male < .001 Age > 54 < .001 Supine NS Upright NS Precipitant < .001 No presyncope NS Warning NS Diaphoresis < .001 0 20 40 60 80 100 *VT + AVB Calkins et alAJM 98:1995

  38. VV (%) Arrhythmic (%) VASOVAGAL vs ARRHYTHMIC* SYNCOPE P Fatigue Post < .001 Confusion NS Palpitations NS Incontinence .02 Injury NS Major Injury NS Recovery > 0” < .001 0 20 40 60 80 100 *VT + AVB Calkins et alAJM 98:1995

  39. HEAD UP TILT NEUROCARDIOGENIC SYNCOPE  LV volume  Venous return  LV contractility Peripheral venous pooling Mechanoreceptor stimulation (myocardial C fibers)  Vagal tone Peripheral vasodilation Vasomotor center  adrenergic tone Hypotension Bradycardia or asytole

  40. VVS: PHARMACOLOGIC THERAPY • Anticholinergic agents - Disopyramide* (effect vs placebo is controversial) - Scopolamine • Negative inotropic agents - Disopyramide* • Fludrocortisone • Vasopressin • Alpha-adrenergic agonists - Ephedrine - Etilephrine - Theophylline - Dexedrine - Midodrine • Serotonin reuptake inhibitors * Watch for urinary retention, torsades de pointes VT

  41. 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 VVS: PACEMAKER THERAPY

  42. VVS: PACING vs -BLOCKADE (SYDIT) 1.0 0.9 0.8 0.7 0.6 Pacemaker % syncope free pts P = 0.0031 Atenolol 0 200 400 600 800 1000 Days Ammirati et al Circulation 2001; 104:52 N = 93

  43. “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

  44. 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

  45. ISOMETRIC ARM EXERCISE TO ABORT VASOVAGAL SYNCOPE Control 2 min handgrip HR 112 90 68 45 BP 178 156 133 111 89 67 44 Asx 11% Syncope 47% Asx 63% Syncope 5% Brignole et al JACC 2002;40:2053 N = 19

  46. 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

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