Transcript Document 7117337

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