Approach to Syncope

VIC VYAS, MD

STAFF ELECTROPHYSIOLOGIST

SOUTH LOUISIANA MEDICAL ASSOCIATES

Disclosures

No financial disclosures to report

No off-label uses of medications or devices will be discussed

2

Definition

A transient loss of consciousness (T-LOC) due to transient cerebral

hypoperfusion characterized by:

Rapid onset

Short duration

Spontaneous complete resolution

Syncope is a symptom, not a diagnosis

Determination of etiology allows for diagnosis

Brignole et al. Europace, 2004;6:467-537

3

Impact of Syncope

1Kenny RA, Kapoor WN. In: Benditt D, et al. eds. The Evaluation and

Treatment of Syncope. Futura;2003:23-27. 2Kapoor W. Medicine. 1990;69:160-175.

3Brignole M, et al. Europace. 2003;5:293-298. 4Blanc J-J, et al. Eur Heart J. 2002;23:815-820. 5Campbell A, et al. Age and Ageing. 1981;10:264-270.

40% will experience syncope at least once in a lifetime1

Up to 6% of hospital admissions2

Up to 3% 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

4

Impact of Syncope

500,000 new syncope

patients each year 5

170,000 have recurrent

syncope 6

70,000 have recurrent,

infrequent, unexplained

syncope 1-4

1 Kapoor W, Med. 1990;69:160-175.

2 Silverstein M, et al. JAMA. 1982;248:1185-1189.

3 Martin G, et al. Ann Emerg. Med. 1984;12:499-504.

4 Kapoor W, et al. N Eng J Med. 1983;309:197-204.

5 National Disease and Therapeutic Index, IMS America, Syncope and Collapse #780.2; Jan 1997-Dec 1997.

6 Kapoor W, et al. Am J Med. 1987;83:700-708.

5

Syncope -

Reported Frequency

Individuals <18 yrs 15%

Military Population 17- 46 yrs 20-25%

Individuals 40-59 yrs* 16-19%

Individuals >70 yrs* 23% *during a 10-year period

Brignole M, Alboni P, Benditt DG, et al. Eur Heart J, 2001; 22: 1256-1306.

6

Impact of Syncope: US Trends

400

500

600

700

800

900

1,000

1,100

1,200

'96 '97 '98 '99 '00 '01

300

320

340

360

380

400

420

440

'96 '97 '98 '99 '00 '01 '02

All patients discharged with syncope and collapse

(ICD-9 Code:780.2) listed among diagnoses. NHDS 2003.

Inpatient Trend

Physician Office Visits

Syncope and collapse (ICD-9 Code: 780.2)

listed as primary reason for visit. NAMC 2002

7

Impact of Syncope: Quality of Life

1Linzer M. Journal of Clinical Epidemiology, 1991;44:1037. 2Linzer M. Journal of General Internal Medicine, 1994;9:181.

0

20

40

60

80

100

Anxiety/

Depression

Alter Daily

Activities

Restricted

Driving

Change

Employment

73%1 71%2 60%2 37%2

8

Impact of Syncope: Cost

Mean cost - $5,400 per hospitalization

Estimated total annual costs for syncope-related hospitalizations - $2.4

billion

Sun et al. American Journal of Cardiology, 2005:95;668-671

9

Syncope… or something else?

High likelihood of T-LOC due to global cerebral hypoperfusion (syncope) if:

Complete LOC

Loss of postural tone

Transient LOC with rapid onset and short duration

Spontaneous, complete recovery

10

Mimics

Consider disorders that present

without impairment of consciousness Cataplexy Drop Attacks

Falls TIA of Carotid

Origin

Pseudsyncope

11

Mimics

Consider disorders that can present

with LOC but are not due to global

cerebral hypoperfusion

Epilepsy Metabolic disorders

Intoxication Vertebrobasilar

TIA

Trauma

12

Causes of True Syncope

Orthostatic Cardiac

Arrhythmia

Structural

Cardio-

Pulmonary

• Vasovagal

• Carotid sinus syndrome

• Situational • Post-micturition

• Post-tussive

• Deglutition

• Post-exercise

• Post-prandial

• Hypovolemia

• Hypotension

• 1˚ ANS Failure •Parkinson’s

•Lewy body dementia

•Multiple system atrophy

• 2˚ ANS Failure •Diabetes

•Amyloidosis

•Spinal injury

• Bradycardia • Sinus node

dysfunction

• AV block

• SVT

• VT/VF • Structural Heart

Disease

• “Normal Heart”

• Acquired

• Acute MI

• Aortic stenosis

• HCM

• Intracardiac mass

• Tamponade

• Acute aortic dissection

• PH/VTE

Neurally-

Mediated

Adapted from Benditt et al. Cardiology Clinics, 2013;31:9-25

Distribution of Causes

13%

20%

9% 31%

27%

Men

Cardiac

Vasovagal

Orthostatic

Unknown

Other*

Soteriades et al. New England Journal of Medicine, 2002;347:878-885

7%

22%

10%

40%

21%

Women

Cardiac

Vasovagal

Orthostatic

Unknown

Other*

* Includes situational syncope

14

SURVIVAL IN SYNCOPAL PATIENTS

Follow-up (yrs)

Soteriades et al. New England Journal of Medicine, 2002;347:878-885

0 5 10 15 20 25

Pro

bab

ilit

y o

f s

urv

ival

1.0

.8

.6

.4

.2

0

No syncope

Vasovagal &

OH

Unknown

Neurologic

Cardiac cause

PROGNOSIS IN UNEXPLAINED SYNCOPE IN PATIENTS > 65

Pro

po

rtio

n o

f p

ts a

live

1.0

.75

.50

.25

0 0 1 2 3

Follow up (yrs) Roussanov et al. American Journal of Geriatric Cardiology, 2007;16:249-255

Control

Syncope

Determining Etiology

Step 1: Detailed History

Number, frequency and duration of episodes

Episodes scattered over many years tend to be benign

Frequent episodes over short period of time suggests a more ominous etiology (i.e. intermittent AVB or paroxysmal tachyarrhythmias)

Onset

An extended prodrome suggests vasovagal process whereas abrupt LOC without prodrome is more common in cardiac syncope

Body position

Supine erect positional change preceding event suggests orthostatic process

Reflex syncope usually occurs in upright position

Syncope while supine is worrisome for arrhythmia

17

Determining Etiology

Step 1: Detailed History (cont.)

Provocative factors

During/immediately after exercise,

During/immediately after urination, coughing, defecation or swallowing

While standing in warm/crowded place

During prolonged standing

In association with emotional stress, fear or intense pain

Immediately after turning neck

Associated symptoms preceding the event

Nausea, vomiting, feeling cold/clammy

Palpitations

Chest pain

Dyspnea

18

Determining Etiology

Step 1: Detailed History (cont.)

Associated symptoms following the event

Persistent nausea, diaphoresis or pallor suggests vasovagal process

Profound resultant fatigue is also characteristic of a vasovagal process

Significant neurological changes or confusion during the recovery period suggests a primary CNS process (CVA, seizure)

Bystander report

Abrupt loss of postural tone?

Total duration of LOC

Physical signs (tonic/clonic movements, tongue biting)? Before or after collapse?

19

Determining Etiology

Step 1: Detailed History (cont.)

Past Medical History

CAD or structural heart disease?

Risk factors for ASCVD or structural heart disease?

Seizure disorder or other neurological conditions?

Social History

Use of intoxicants?

20

Determining Etiology

Step 1: Detailed History (cont.)

Family History

Sudden cardiac death in family members <40

Any known hereditary disorders that would predispose to SCD?

Familial cardiomyopathy (HCM, ARVC)

Familial channelopathy (Brugada, LQTS, CPVT)

Medications

Diuretics hypovolemia, electrolyte derangements predisposing to arrhythmia

Antihypertensives hypotension

Acquired LQTs www.crediblemeds.org

21

Determining Etiology

Step 2: Physical Exam

Orthostatic vital signs

Supine, seated, standing

3-5 minutes in each position with serial VS measurements throughout

Real time telemetry monitoring preferred

Non-invasive BP monitoring (i.e. “beat to beat”

measurement) is ideal but not universally available

22

Determining Etiology

23

Determining Etiology

Step 2: Physical Exam (cont.)

Comprehensive cardiovascular exam

Evidence of acute cardiopulmonary process?

Evidence of structural heart disease?

Neuro exam

Focal deficits?

Stigmata of Parkinson’s?

24

Determining Etiology

Step 3: Telemetry & ECG

Indicated in ALL patients with syncope

Limited yield but diagnostic if any of the

following are present:

Persistent sinus bradycardia (<40bpm) while

awake

Repetitive SA pauses >3 secs while awake

Mobitz II AVB

3rd degree AVB

Alternating LBBB/RBBB

Sustained tachyarrhythmia

Ischemic changes, particularly ST elevation

25

26

27

28

Determining Etiology

Step 3: ECG (cont.)

Suggestive of CV pathology (EP consultation recommended):

Bifascular block

LBBB or IVCD with QRSd >120ms

LVH

Q waves

Sinus bradycardia >40bpm

Ventricular pre-excitation

Long/short QT interval

Brugada pattern

Epsilon waves suggesting ARVC

29

LBBB

30

LVH

31

Ventricular Pre-excitation

32

Spears et al. Application of Clinical Genetics. 2014;8:215-233

Domingo et al. Rev Esp Cardiol. 2007;60:739-52

Long QT

33

Woosley et al. www.crediblemeds.org (QTdrugs List), [Accessed 2/12/17]

34

Woosley et al. www.crediblemeds.org (QTdrugs List), [Accessed 2/12/17]

35

Nielson et al. Frontiers in Physiology. 2013;4:179

Brugada et al. JACC. 1992;20:1391–1396

Brugada

36

ARVC

Lang et al. Encyclopedia of Molecular Mechanisms of Disease; 2009:155

37

Determining Etiology

Step 4: Echocardiography

IF structural heart disease is evident or suggested by history,

exam or ECG.

Usually normal

Can reveal:

HFrEF

HCM

Valvulopathy

Intracardiac mass

Pericardial effusion

Acute right heart failure

38

50%

30%

20%

Outcome after initial

evaluation

Certain

Diagnosis

Suspected

diagnosis

Unexplained

Brignole et al. JACC. 2012;59:1583-1591

Inpt Consult

Outpt Consult

39

Moya et al. European Heart Journal, 2009;30:2631–2671

Who is high risk?

Structural Abnormalities

• Low LVEF

• Decompensated heart failure

• Prior myocardial infarction

Clinical Clues

• Syncope duration exertion

• Syncope while supine

• Preceding chest pain or palpitations

• Family history of SCD

• ECG/Telemetry abnormalities:

• NSVT

• Bifascicular block

• QRSd>120ms

• Bradycardia

• Pre-excitation

• Abnormal QTc

• Brugada pattern

• Suspected ARVC

Comorbid Conditions

Severe Anemia

Severe electrolyte derangements

Moya et al. European Heart Journal, 2009;30:2631–2671

40

Testing Performed By The Consultant

Carotid Sinus Massage

Exercise Test

Ambulatory ECG

Holter monitoring

Event recorder

Implantable Loop Recorder

Head-Up Tilt

Electrophysiology Study (EPS)

Brignole M, et al. Europace, 2004;6:467-537.

41

Diagnostic Assessment: Yields

1Alboni et al. JACC. 2001;37:1921-1928. 2Kapoor W. Medicine. 1990;69:160-175. 3Krahn et al. Circulation. 1999;99;406-410.

Yield (%)

Initial Evaluation

History, Physical Exam, ECG, CSM

38-40

Other Tests/Procedures

Head-Up Tilt 27

External Cardiac Monitoring 5-13

Insertable Loop Recorder (ILR) 43-88

EP Study 2-5

Exercise Test 0.5

EEG 0.3-0.5

4Krahn et al. Circulation. 2001;104:46-51. 5Krahn et al. American Heart Journal. 1999;137:870-877. 6Moya et al. European Heart Journal, 2009;30:2631–2671.

42

Carotid Sinus Massage

Indications:

Age >40 with syncope of unknown etiology

after initial evaluation or when CSS is

suspected

Stimulates carotid baroreceptor reflex

(vagally-mediated bradycardia/asystole)

1Kenny RA. Heart. 2000;83:564

43

Carotid Sinus

Method1

Usually performed in conjunction with

tilt (supine and upright)

Massage, 5-10 seconds

Don’t occlude!

Outcome

3 second asystole and/or 50 mmHg fall

in systolic BP with reproduction of

symptoms = Carotid Sinus Syndrome

Absolute contraindications2

Carotid bruit, known significant carotid

arterial disease, previous CVA, MI last 3

months

Complications

Primarily neurological

Less than 0.2%3

Usually transient

1Kenny RA. Heart. 2000;83:564. 2Linzer M. Annnals of Internal Medicine. 1997;126:989. 3Munro N, et al. Journal American Geriatric Society. 1994;42:1248-1251.

44

Exercise Treadmill Testing

Indications:

Patients who experience syncope during or

immediately after exercise

Low Yield but can demonstrate:

Abnormal BP response to exercise

Chronotropic incompetence

Exercise-induced tachyarrhythmia

Exercise-induced high grade AV block

Moya et al. European Heart Journal, 2009;30:2631–2671.

45

Head-Up Tilt Test

Indications:

Syncope in patient exposed to high risk

settings

Recurrent episodes of syncope without

organic heart disease

Recurrent episodes of syncope with organic

heart disease and cardiac etiology of

syncope has been ruled out

Moya et al. European Heart Journal, 2009;30:2631–2671.

46

Head-Up Tilt Test

Method

Continuous BP and ECG monitoring

Supine phase 5-20 min

Tilt angle 60-70%

20-45 min passive tilt phase

+/- SL NTG or isoproterenol IV

Outcome

Responses:

Cardioinhibitory

Vasodepressor

Mixed

Reproduction of symptoms

Moya et al. European Heart Journal, 2009;30:2631–2671.

47

Ambulatory Monitoring Options

ILR

Event Recorders (non-lead and loop)

Holter Monitor

12-Lead

2 Days

7-30 Days

10 Seconds

TIME (Months)

0 1 2 3 4 5 6 7 8 9 10 11 12

Brignole M, et al. Europace, 2004;6:467-537.

Up to 3 Years

Brignole et al. JACC. 2012;59:1583-1591

48

Ambulatory Monitoring

Indications

Patients who have clinical or ECG features suggesting arrhythmic syncope

Type of testing

Inpatient telemetry – high risk patients

Holter monitor – low risk, very frequent symptoms

Event monitor – low risk, expected to have symptoms within 4 weeks

Remote telemetry – emerging technology

ILR

Late implant – high risk patients with negative comprehensive evaluation thus far

Early implant – recurrent syncope, unknown cause, no events during external monitoring

Moya et al. European Heart Journal, 2009;30:2631–2671.

49

Insertable Loop Recorder

50

Electrophysiological Study (EPS)

Indications for evaluation of syncope:

Ischemic heart disease without standard indication for ICD

Presence of BBB; negative non-invasive testing

Syncope preceded by palpitations; negative non-invasive testing

High risk occupations (every effort to exclude arrhythmic etiology is warranted)

Generally not indicated in patients with normal ECG, normal echo & no

history of palpitations

51

EPS Outcomes

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 > 525 ms

Inducible SVT with hypotension

HV interval ≥ 70 ms

Pacing induced infra-nodal block

PMVT/VF in Brugada, ARVC (?)

Benditt D. Textbook of Cardiovascular Medicine. Lippencott;2002:1529-1542.

Lu et al. The Evaluation and Treatment of Syncope. Futura. 2003;80-95.

Brignole M, et al. Europace. 2004;6:467-537.

52

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. Annals of Internal Medicine. 1997;127:76-86. 2Lu F, et al. In: Benditt D, et al. The Evaluation and Treatment of Syncope. Futura. 2003;80-95.

53

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Questions?

v-vvyas@ochsner.org

(225)610-0993

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.

56

ISSUE - Patients with Isolated Syncope and Tilt-Positive

Syncope

Moya A. Circulation. 2001;104:1261-1267.

Follow-Up to Recurrent

Spontaneous Episode

111 Patients with Syncope

No SHD, Normal ECG

29: Tilt-Positive 82: Tilt-Negative

“Isolated Syncope”

Tilt Test Followed by

Insertable Loop Recorder

57

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.

58

ISSUE - Patients with Heart Disease and a Negative EPS

Menozzi C, et al. Circulation. 2002;105:2741-2745.

35 Pts with Heart Disease

and Insertable Loop Recorder

Syncope: 6 Pts (17%)

ECG-Documented: 6 Pts (17%)

Pre-Syncope: 13 Pts (37%)

ECG-Documented: 8 Pts (23%)

AV block + asystole: 1

A.Fib + asystole: 1

Sinus arrest: 1

Sinus tachycardia: 1

Rapid A.Fib: 2

Sustained VT: 1

Parox. A.Fib/AT: 1

Post tachycardia pause: 1

No rhythm variations: 4

Sinus tachycardia: 1

59

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.

60

ISSUE - Patients with Bundle Branch Block and Negative

EP Test

Brignole M., ET AL.,Circulation. 2001;104:2045-2050.

* 5 of these also had ≥1 presyncope

** Drop-out before primary-end point

52 Pts with BBB

and Insertable Loop Recorder

Syncope:

22 Pts (42%)*

ILR-Detected: 19

AVB: 12 (63%)

SA: 4 (21%)

Asystole-undefined: 1 (5%)

NSR: 1 (5%)

Sinus tachy: 1 (5%)

Not Detected: 3

Stable AVB:

3 Pts (6%) ILR-Detected

Pre-Syncope:

2 Pts (4%)**

Death:

1 Pt (2%)

AVB: 2 (4%)

61

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.

62