Download AHA/ACC Scientific Statement on the Evaluation of Syncope

Current Trends in the Evaluation
of Syncope
John D. Hummel, M.D
Professor of Clinical Internal Medicine
Director of Electrophysiology Research
Ohio State University
Definition
• a syndrome in which loss of
consciousness is:
– relatively sudden
– temporary
– self-terminating
– usually rapid recovery
• due to inadequate cerebral
perfusion
• most often triggered by a fall in
systemic arterial pressure
Syncope: High Incidence and
Likely to Increase
• 7814 participants followed for
an average of 17 years, 822
reported syncope
• Estimated 10-year cumulative
incidence of syncope was 6%
• The incidence rates increased
with age, with a sharp rise at
70 years
• 22% of the study participants
with syncope had a
recurrence
Soteriades et al. NEJM 2002; 347: 878
Syncope
Annual U.S. Emergency Dept. Visits
• ~40% of the population will
have at least one syncopal
event in their lifetime
1,200,000
1
• 10% of falls by elderly are
believed due to syncope
2
1,000,000
• Major morbidity reported in 6%
1
(e.g., fractures, motor vehicle accident)
• Minor injury reported in 29%
1
800,000
(e.g., lacerations, bruises)
600,000
2001 2002 2003 2004 2005 2006
1Kenny
RA, et al. eds. The Evaluation and Treatment of Syncope. Futura;2003:23-27.
2Kapoor
W. Medicine. 1990;69:160-175.
Syncope
QOL Impact
100%
Percent of Patients
1
73%
2
71%
75%
2
60%
50%
2
37%
25%
0%
Anxiety/
Depression
Alter Daily
Activities
1Linzer
2Linzer
Restricted
Driving
M. J Clin Epidemiol, 1991;44:1037-1043.
M. J Gen Int Med, 1994;9:181-186.
Change
Employment
Syncope
• In one-third of participants, a
cause for syncope could not be
assigned
• Risk of death was increased by
31% among all participants with
syncope
• Risk of death was doubled
among participants with cardiac
syncope
• Neurologic syncope (CVA, TIA,
seizure) also associated with
three-fold risk of stroke
Soteriades et al. NEJM 2002; 347: 878
Causes of True Syncope
NeurallyMediated
Reflex
1
• VVS
• CSS
• Situational
Cough
Postmicturition
60%
Orthostatic
2
• Drug-Induced
• ANS Failure
Primary
Secondary
15%
Cardiac
Arrhythmia
3
• Bradycardia
Sinus
pause/arrest
AV block
• Tachycardia
VT
SVT
• LongQT Synd
10%
Unexplained Causes = Approximately 10%
Structural
CardioPulmonary
4
• Aortic Stenosis
• HCM
• Pulmonary
Hypertension
• Aortic
Dissection
5%
Goals
• Determine whether the patient is at increased risk for death.
•
- patients with underlying heart disease
•
- myocardial ischemia
•
- Wolff-Parkinson-White syndrome
•
- life-threatening genetic diseases (LQTS, Brugada)
•
Once excluded, the goal becomes identification of the cause of
syncope in an attempt to:
•
- improve the quality of the patient’s life
•
- to prevent injury to the patient or others.
AHA/ACCF Scientific Statement on the Evaluation of Syncope
Circulation, February 2006
The Initial Evaluation:
4 Key Questions
Did the patient suffer ‘true’ Transient Loss of Consciousness (TLOC)?
Was TLOC due to syncope or some other cause?
Is heart disease present?
Does the medical history (including observations by witnesses)
suggest a specific diagnosis?
Syncope vs. Non-Syncopal Events
Task Force members, et al. Eur Heart J 2004 25:2054-2072
Flow chart for the diagnostic approach to the patient with syncope
Strickberger, S. A. et al. Circulation 2006;113:316-327
History and Physical: The Most Valuable
Part of the Initial Evaluation
H&P yields a diagnosis prior to confirmatory studies in 45% of
patients in 7 population based studies (n=1607)
History:
Prodome/Residua
Activity/Posture
Palpitations
Seizure Activity
Medications
Prior Episodes
Family History: Syncope,
Sudden Death,
Cardiac Disease
Physical Exam
Orthostatic BP
Murmurs, Bruits, Pulses, Differential BP’s
ECG
Abnormal in 50% of patients. Identifies potential cause in 2-11%
• Pre-excitation
• Conduction Delays
• MI
• LVH/RVH (Hypertrophic CM, Aortic Stenosis, Pulmonary HTN)
• QT Interval (QTc=460) should raise suspicion
• Brugada Abnormalities
• Epsilon Waves (ARVD)
ECG changes in the Brugada syndrome
Strickberger, S. A. et al. Circulation 2006;113:316-327
Long QT syndrome-Triggers
LQT1
• Swimming- LQT1
• Auditory/emotional
trigger- LQT2
• Inactivity- LQT3
LQT2
LQT3
LQT2
Different patterns of QT prolongation in LQTS
Strickberger, S. A. et al. Circulation 2006;113:316-327
Twelve-lead ECG in normal sinus rhythm with epsilon wave
Kenigsberg, D. N. et al. Circulation 2007;115:e538-e539
High-resolution delayed enhanced magnetic resonance image
Kenigsberg, D. N. et al. Circulation 2007;115:e538-e539
Neurally Mediated Syncopal Syndromes
The Most Common Cause of Syncope
•Vasodepressor Syndrome
(Common Faint)
• Micturition/Cough/Sneeze Syncope
• Carotid Hypersensitivity
Reflex Arcs in Neurally Mediated Syncope
Upright Posture: 15-20% Decrease in Plasma Volume With Decrease in C.O.
Baroreceptors
Mechanoreceptors
Higher Centers
(Cortex)
Cranial Nerves
V, VII, VIII
GI/GU
Mechanoreceptors
Vagus
Medullary
Vasodepressor
Region
Skeletal Muscle
& Resp. Pump
Reflex Activation
Central Sympathetic Outflow
Vasodepressor Syncope
Clinical Syndrome Characterized By:
1.
Settings:
- young patients, no SHD
- Frightening/stressful situation
- hunger, fatigue, dehydration, hot room
- standing position, sitting occasional
2. Premonitory Signs:
- nausea, blurred vision
- warmth, diaphoresis
- pallor, yawning
3. Syncopal Event:
- white, pale
- no injury
- may be aborted by becoming supine
4. Recovery:
- nausea, diaphoresis
- fatigue
Tilt Test
1.
2.
3.
4.
Supine 5 min, 20 min with I.V. pretest
Tilt 60-70 degrees
Passive 20-45 minutes
Isuprel or SL NTG 400 ug spray in neg
for 15-20 minutes
5. Endpoint: Syncope or Full Duration
Complete
Rapid Protocols:
1. 10 min baseline, Return to supine
and infuse isuprel with HUTT for
20min after 20-25% increase in HR
2. Clomipramine I.V. 5mg (1mg/min)
during the first 5 min of 20 min.
TTT (spec.93%, sens. 64-83%
Carotid Sinus Massage
• Classification: Cardioihibitory, VDP, Mixed
• Abnormal:
– Ventricular pause > 3 seconds or fall in SBP > 50mmHg
with symptoms
• Technique:
– Recommend continuous ECG and BP monitoring
– Assess VDS response with repeat massage after 1 mg of
atropine
– Perform CSM with TTT if negative CSM supine: Only
positive in HUTT in 49%
• Complications: Neuro in 0.17-0.45%
• Contraindicated: Sig. carotid disease
• Treatment: PPM for CI, PPM±VDS meds mixed
68 y/o man with a history of CAD, s/p, IMI, EF = 45%
Presented with 2 recent syncopal episodes which
occurred while sitting without prodrome.
Holter = NSVT EPS=Normal
Right CSM
• History and Physical
–
–
–
–
–
–
Presence of definite structural heart disease
Syncope during exertion or when supine
Syncope preceded by palpitations
Family history of SCA
Malignant Syncope
Hx of CADz
• EKG
–
–
–
–
–
Bifasicular block or QRS>120 msec
Mobitz I, second degree AV block (off meds)
Asymptomatic Sinus Brady, pause > 3 sec
Long QT, WPW, Brugada, Neg precordial T’s/epsilon
Q waves
Echo, Stress Testing
EVM, Loop
EPS
Echocardiogram
• Excellent for detecting associated cardiac
disease
- Left atrial myxoma
- HOCM
- Early cardiomyopathy
- Valvular disease
- Amyloid
- Ischemic heart disease
- RV abnormalities (+/-)
• Provides key data affecting prognosis and
further evaluation
Exercise Testing
• Should be performed in the patient with unexplained
syncope, especially if the episode was exercise related.
• Exercise testing
– in patients less than 40 years of age, a drop in blood pressure or
failure of blood pressure to rise with exercise raises the question
of hypertrophic obstructive cardiomyopathy or left main coronary
artery disease.
– In the elderly patient, it may be a manifestation of autonomic
failure.
• Exercise testing also screens for catecholaminergic
polymorphic ventricular tachycardia and chronotropic
incompetence (failure to achieve 100 bpm or 75%
MPHR)
• Exercise testing with a functional study can exclude
ischemia as a potential cause of syncope
EPS: Indications for Syncope Evaluation
Syncope:
Class I:
Structural Heart Dz, Unexplained after initial eval.
Palpitations preceding syncope
Palps, Rapid pulse by medical
personnel
Class II:
Recurrent Unexplained syncope, nl heart and neg TTT
Palps, Inability to obtain recording
Class III:
Known cause of syncope, EPS will not guide Rx
EPS: Catheter Insertion and Targets
After IV Procainamide
Induction of SMVT – Rate = 250bpm, SBP <
60
WPW: Atrial Fibrillation, Ventricular
Fibrillation
Combined Use of EP and Tilt Table Testing
for Syncope
Unexplained Syncope (86pts.)
+EPS, 29 (34%) pts.
Tachyarrhythmia
VT, 21
(73%) pts.
SVT, 5
(18%) pts.
-EPS, 57 (66%) pts.
Bradyarrhythmia
SND, 1
(3%) pts.
+HUT 34
(60%) pts.
-HUT 23
(40%) pts.
AV Block, 2
(6%) pts.
70% of patients were diagnosed with the combined use of EP and Tilt Testing
Sra et al, 1993
Outcome in pts with Unexplained
Syncope and Nondiagnostic EPS
1) the incidence of sudden death is low
(<2%)
2) the remission rate of syncope is high
(80%)
3) the EPS falsely negative in greater
than or equal to 20% of patients who
continue to have syncope (AV block,
SN dysfunction)
Flow chart for the diagnostic approach to the patient with syncope
Strickberger, S. A. et al. Circulation 2006;113:316-327
Types of External Arrhythmia Monitors
•
•
Electrocardiogram: snapshot in time
Holter monitor : 24 to 48 hours of continuous outpatient electrocardiographic
(ECG) recording
–
–
•
Event recorder: stores 1 to 2 minutes of ECG as soon as the patient activates
–
–
•
Enables much longer period of monitoring
Misses asymptomatic arrhythmias and some symptomatic arrhythmias when pt fails
to activate
Automatic-trigger loop monitors: Records in continuous loop and
automatically captures certain arrhythmias or can be manually activated during
symptoms
–
–
•
Shortcoming: repeated monitoring if an arrhythmia not occur 24-48 hours
Processing can delay action on malignant arrhythmias
Devices can capture detect several types of arrhythmias.
Typically worn for up to 30 days.
Real-time cardiac surveillance: continuous outpatient ECG monitoring for
periods ranging up to several weeks, if necessary.
–
–
–
Cardiac activity detected by 3 electrodes attached to a ~2 ounce pager-sized sensor
or telephone transmitter
Continuously analyzes the heart rhythm data. If an arrhythmia detected, the monitor
automatically transmits data to a central monitoring station for analysis/action
Any symptoms recorded by the patient are also transmitted.
Cumulative number of patients who sent an electrocardiogram from an event
recorder by the number of days needed to record an electrocardiogram during
palpitations
Prospective, randomized
crossover comparison 48
hour holter to 30 day EVM
Twice as many symptomatic
recordings from EVM as
holter
19% of events recorded on
EVM required intervention,
none from the holter
Kinlay, S. et. al. Ann Intern Med 1996;124:16-20
MCOT Study
• Multicenter randomized controlled trial
• 266 pts with palpitations, presyncope,
syncope and nondiagnostic Holter
• Randomized to 30 days of MCOT
(Cardionet) or external loop (Loop Group).
• Results
– Clinically significant arrhythmias
• 55 (41%) pts in the MCOT Group
• 19 (14%) patients in the Loop Group (p< 0.001).
Rothman SA, Laughlin JC, Seltzer J, et al. J Cardiovasc Electrophysiol. 2007;18(3):241-247
RAST study
Randomized Assessment of Syncope Trial
• Results:
– Primary strategy: diagnostic yield is 47% vs.
20%
– Diagnosis overall: 19 vs. 55% (p=0.0014) 39
A. Krahn. Circulation 2001; 104: 46-51
ISSUE Study Implications
• HUT outcome was not predictive of
vasodepressor vs. cardioinhibitory response
– Bradycardia is common in spontaneous VVS independent of HUT outcome
• Bradycardia is more prevalent in spontaneous
events vs. HUT induced VVS
• Clinical Implication: Consider a strategy of ILR
guided evaluation in positive TTT patients
unresponsive to medication
Moya A. Circulation. 2001; 104:1261-1267
ISSUE 2
Methods:
Syncopal Episodes per Patient per Year
• 392 patients with suspected neurallymediated syncope were enrolled
0.83
• 103 pts. had an ECG documented
syncope, leading to therapy and a
follow-up observational period
Results:
• A 92% relative reduction in syncope
burden and 80% relative reduction in
one-year recurrence rate with pacing
and antiarrhythmic therapies guided
by ILR findings
0.07
0.05
Brignole M. Eur Heart J. 2006;27:1085-1092 (ISSUE 2).
Non-Specific
Therapy
ILR-Based
Pacemaker
Therapy
(all patients receiving
antiarrhythmic therapy
Only
or pacemaker therapy)
Diagnostic Methods & Yield
Test/Procedure
Yield
based on mean time to diagnosis of 5.1
months7
History and Physical (including carotid sinus
49-85% 1, 2
massage)
ECG
Electrophysiology Study without SHD*
Electrophysiology Study with SHD
Tilt Table Test (without SHD)
Ambulatory ECG Monitors:
- Holter
- External Loop Recorder (2-3 weeks duration)
-Insertable Loop Recorder (up to 18 months
2-11% 2
11% 3
49% 3
11-87% 4, 5
2% 7
20% 7
65-88% 6, 7
duration)
Neurological † (Head CT Scan, Carotid Doppler)
1
Kapoor, et al N Eng J Med, 1983.
6
Krahn, Circulation, 1995
2
Kapoor, Am J Med, 1991.
7
Krahn, Cardiology Clinics, 1997.
3
Linzer, et al. Ann Int. Med, 1997.
8 Eagle
4
Kapoor, Medicine, 1990.
9
5
Kapoor, JAMA, 1992
10
0-4%
4,5,8,9,10
K,, et al. The Yale J Biol and Medicine. 1983; 56: 1-8.
*
Structural Heart Disease
†
MRI not studied
Day S, et al. Am J Med. 1982; 73: 15-23.
Stetson P, et al. PACE. 1999; 22 (part II): 782.
Symptom-Rhythm Correlation
Auto Activation
Point
Patient
Activation
Point
Syncope Diagnosis: Role of an ILR
AHA/ACC Scientific
Statement on the
Evaluation of
Syncope:
“This approach (ILRs) is
more likely to identify
the mechanism of
syncope than is a
conventional approach
that uses Holter or
event monitors and EP
testing and is costeffective.”
A. Strickberger et al. Circulation 2006; 113: 316-327
Ideal System for Long Term
Cardiac Monitoring
• Subcutaneous placement, simple and fast to implant,
excellent safety profile.
• Reliably provides information that can aid selection and
titration of therapies
– High sensitivity detector in ILR
– Signal processing software to remove false positives and extract
information at monitoring center
– Human over-read at service center to assure information delivered
to physician is clinically relevant
• Simple for the patient – requires little or no compliance
– Long-range telemetry for automated data transfer
• Simple for the physician – maximizes practice efficiency,
follow up requires minimal work load
– Data download tailored to institution/practice
Sub-Q ILR’s: Evolution
Reveal
1998
Reveal Plus
2000
Reveal is developed to help diagnose unexplained
syncope
Automatic detection added
Transoma
Sleuth
Transoma: the first wireless
and automated monitoring system
Reveal DX
Longevity and ECG memory increased (to 3 yrs., 49.5
minutes), with episode logs, ICD sensing technology,
MRI labeling, and remote monitoring added
2007
Reveal XT,
Sleuth AT
Confirm
2009
AF detection and long-term trended diagnostics (the
Cardiac Compass and AF Summary Reports) added
Competing ILR’s
Transoma
‘Sleuth AT”
Medtronic
‘Reveal XT’
St. Jude
‘Confirm’
Asystole
Any single pause >3.0 sec.
>1.5, >3.0, >4.5 sec
>1.5, >3.0, >4.5 sec
Bradycardia
Detection
Settings
30, 40, 50 bpm
30, 40, 60 bpm
30, 40, 50 bpm
Tachycardia
Detection
Settings
120 to 220 bpm, Off
4/4, 6/8, 8/8, 16/16, 32/32 beats
VT = 250 to 520 ms
(115 to 240 bpm)
FVT = 240 to 400 ms
(150 to 250 bpm)
VT = 250 to 520 ms
(115 to 240 bpm)
FVT = 240 to 400 ms
(150 to 250 bpm
AF Detection
20 sec. ECG strips sent to
Monitoring Center every 7.5
min.
Analysis of ECG data and
arrhythmia classification, by
Certified Cardiac Techs at
Monitoring Center
On board detection algorithm
based on R to R variability
On board detection
algorithm based on R to R
variability but can’t turn on
until clinical study is
completed and approved by
FDA for AF detection
Memory for
ECG Data
673 min. between automatic,
wireless transmission to the
Monitoring Center
ILR: 43 min.
PDM: 630 min.
49.5 minutes total between
scheduled office visits
Memory available on ILR only
Download to Carelink
48 minutes total between
scheduled office visits
Memory available on ILR
only
Download to TTM
18 to 30 months
36 months
36months
ILR Battery Life
RUP Study: Importance of Wireless Download
Automatic detection mode in the REVEAL was activated, but no significant arrhythmias were recorded:
because ILR memory “was always saturated by inappropriate activations.”
1.Franco Giada et al.. J Am Coll Cardiol 2007;49:1951–6
Importance of an Antenna
Loss of tissue contact from
shape/form factor
Krahn et al, PACE 2004; 27: 657
Medicomp Arrhythmia Access
Patient
Activated
Report
Page
Arrhythmia Access-Sleuth Patient Summary Report
The Value of Advanced Diagnostics
• Daily AF burden
• V-rate during AF
• Avg. day/night HR
• Patient activity
• Heart rate
variability (HRV)
Note: All clinic, physician, and patient names and data in this document are fictitious
Value of Advanced Diagnostics
What is the
AF burden?
How long do
the episodes
last?
When did the
episodes start?
Note: All clinic, physician, and patient names and data in this document are fictitious
Summary: Current Trends in
Arrhythmia Monitoring
• Greater use of external continuous
auto-trigger wireless loop recorders
• Greater Use of Implantable Loop
Recorders:
– Diagnosis of Syncope
– Management of Atrial Fibrillation
– Evaluation of Cyptogenic Stroke
Reference
• AHA/ACCF Scientific Statement on the
Evaluation of Syncope: From the American
Heart Association Councils on Clinical
Cardiology, Cardiovascular Nursing,
Cardiovascualr Disease in the Young, and
Stroke, and the Quality of Care and
Outcomes Research Interdisciplinary
Working Group; and the American College of
Cardiology Foundation in Collaboration With
the Heart Rhythm Society. S. Adam
Strickberger, et al. JACC. 2006; 47; 473-484
Other References
• Soteriades et al. NEJM 2002; 347: 878
• Rothman SA, et al. J Cardiovasc
Electrophysiol. 2007;18(3):241-247
• Franco Giada et al.. J Am Coll Cardiol
2007;49:1951–6
• A. Krahn, et. Al. Circulation 2001; 104: 4651
• Moya A, et Al. Circulation. 2001; 104:12611267
• Brignole M., et. AL. Eur Heart J.
2006;27:1085-1092
ACC/AHA Guidelines for Pacing
With Syncope
•
Class I
–
–
–
–
–
•
Class II
–
–
–
–
–
–
–
–
–
–
•
Third degree AV block with or without Sx’s
Advanced 2nd deg. AV block
Documented sinus brady causing syncope
Sustained Pause dependent VT eliminated by pacing
CSM causing syncope, pauses > 3 seconds min CSM in absence of culprit meds
Sinus brady less than 40 bpm or pauses > 3 seconds awake without symptoms
Abnormal Sinus node function on EPS
Neuromuscular diseases (Kearns-Sayre, Erb’s dystrophy, Peroneal Muscular Atrophy) with any
degree AV block (including first degree)
Bifasicular, Trifasicular block (other causes excluded)
SVT resolved only by ATP (RFA and meds failed or not elected)
High risk congenital LQTS patients
Prevention of recurrent drug refractory AF in pts with coexisting SN disease
ASx CSM with > 3 second pause
Significantly symptomatic, recurrent VDS associated with bradycardia
Brady-Tachy syndrome requiring therapy
Class III
–
–
–
Reversible Causes (drug toxicity, Lyme, non-essential drug Rx causative)
Documentation of syncope in absence of bradycardia
Situational syncope with bradycardia when avoidance effective
ACC/AHA Guidelines for Pacing
With Syncope
• Class I
– Third degree AV block with or without Sx’s
– Advanced 2nd deg. AV block
– Documented sinus brady causing
syncope
– Sustained Pause dependent VT
eliminated by pacing
– CSM causing syncope, pauses > 3
seconds CSM in absence of culprit meds
with sx’s
ACC/AHA Guidelines for Pacing
With Syncope
• Class II
– Sinus brady less than 40 bpm or pauses > 3 seconds awake
without symptoms
– Abnormal Sinus node function on EPS
– Neuromuscular diseases (Kearns-Sayre, Myotonic dystrophy,
Peroneal Muscular Atrophy) with any degree AV block (including
first degree)
– Bifasicular, Trifasicular block (other causes excluded)
– SVT resolved only by ATP (RFA and meds failed or not elected)
– High risk congenital LQTS patients
– Prevention of recurrent drug refractory AF in pts with coexisting
SN disease
– ASx CSM with > 3 second pause
– Significantly symptomatic, recurrent VDS associated with
bradycardia
– Brady-Tachy syndrome requiring therapy
ACC/AHA Guidelines for Pacing
With Syncope
• Class III
– Reversible Causes (drug toxicity, Lyme,
non-essential drug Rx causative)
– Documentation of syncope in absence of
bradycardia
– Situational syncope with bradycardia
when avoidance effective