dr sajeer k t senior resident dept. of cardiology mch, kozhikode 1
TRANSCRIPT
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Dr Sajeer K TSenior ResidentDept. of Cardiology MCH, Kozhikode
Syncope- initial approach, diagnosis and management of neurocardiogenic
syncope
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Definition: Syncope is a transient loss of consciousness due to transient global cerebral hypo perfusion characterized by rapid onset, short duration, and spontaneous complete recovery - ESC 2009
Mechanism: Transient global cerebral
hypoperfusion.
Brignole et al. Europace. 6:467-537;2004
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Impact of Syncope 40% will experience syncope
at least once in a lifetime
Major morbidity reported in 6%(e g: fractures, motor vehicle accidents)
Minor injury in 29%(e g: lacerations, bruises)
common medical problem ≈ 3% of ER visits ≈1-6 % of hospital admissions
Brignole M, et al. Europace. 2003;5:293-298
Impact of Syncope
1Linzer, J Clin Epidemiol, 1991.2Linzer, J Gen Int Med, 1994.
0%
20%
40%
60%
80%
100%
Anxiety/Depression
Alter DailyActivities
RestrictedDriving
ChangeEmployment
73% 171% 2
60% 2
37% 2
Pro
port
ion
of P
atie
nts
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Syncope – A Symptom, Not a Diagnosis
Self-limited loss of consciousness and postural tone Relatively rapid onset Variable warning symptoms Spontaneous, complete, and usually prompt recovery
without medical or surgical intervention
Brignole M, et al. Europace, 2004;6:467-537.
Complete loss of consciousness in vasovagal syncope is usually no longer than 20 s in duration
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Pre-syncope or near-syncope indicate symptoms and signs that occur before
unconsciousness in syncope
- Patients feels syncope is imminent
- Symptoms associated with pre-syncope may be non-specific (e.g. dizziness)
- tend to overlap the premonitory phase of true syncope ( light-headedness, nausea, sweating, weakness, and visual disturbances)
- True Syncope should be differentiated from Nonsyncopal
events a/w real or apparent transient LOCCauses of non-syncopal attacks (commonly misdiagnosed as syncope)
European Heart Journal (2009) 30, 2631–2671
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Syncope Evaluation
- Two main reasons to evaluate patients with syncope: 1. To determine the etiology of syncope
2. To stratify the risk of future adverse outcomes
ESC
syncope
Neurally mediated
Orthostatic
Cardiac arrhythmia related
Structural heart disease related
Cerebrovascular syncopeBrignole et al. Europace. 6:467-537;2004
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Classification and Etiology of Syncope
Orthostatic (11%)
CardiacArrhythmia
(14%)
StructuralCardio-
Pulmonary (4%
1• VVS• CSS• Situational
CoughPost- Micturition
2• Drug-Induced• Vol. Depletion• ANS FailurePrimarySecondary
3• Brady
SN Dysfunction
AV Block
• TachyVTSVT
• L QT S• Brugada
Neurally-Mediated
(24%)
Unexplained Causes = Approximately 1/3 (34%)
Cerebro- Vascular
(12%)
5 • Vascular steal synd.
• VBA disease
• Carotid .A disease
4 • Acute
Myocardial Ischemia
• Aortic Stenosis
• HCM• Pulmonary
Hypertension• Aortic
Dissection
Brignole et al. Europace. 6:467-537;2004
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Classification of Syncope According to Etiology (Modified by ESC Guidelines )Versus Classification According to Mechanism (Modified by ISSUE Classification
J Am Coll Cardiol 2012;59:1583–91
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Causes of syncope & Prevalence
Linzer et al. Ann Intern Med 1997;126:989-96
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Frequency of the causes of syncope in general population, Emergency Department and specialized clinical settings from some recent studies
European Heart Journal (2009) 30, 2631–2671
14 BMJ 2010;340:c880
Causes of syncope by age
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Frequency of the causes of syncope according to age
European Heart Journal (2009) 30, 2631–2671
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Clinical Features Suggestive of Specific Causes of Syncope
Episodes occur after sudden unexpected pain, fear, or unpleasant sight, sound, or smell Episodes occur after prolonged standing at attention
Episodes occur in a well-trained athlete without heart disease after exertion
Vasovagal attack
Kapoor. NEJM, 1857 -1862; 2000
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Episodes occur during or immediately after micturition, cough, swallowing,or defecation - Situational syncope
Episodes occur with head rotation or pressure on carotid sinus (due to tumors, shaving, or tight collars) - Carotid-sinus syncope
Episodes occur immediately on standing - Orthostatic hypotension
Patient takes medications that may lead to a long QT interval or orthostasisand bradycardia - Drug-induced syncope
Patient is confused after episode, or loss of consciousness lasts >5 minutes - Seizure
Patient has a brief loss of consciousness with no prodrome and has heart disease - Arrhythmias
Syncope occurs with exertion - AS, Pul.HTN, MS,HCM CADPatient has frequent syncope with somatic symptoms but no heart disease - Psychiatric illness
Kapoor. NEJM, 1857 -1862; 2000
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Reflex syncope (neurally mediated syncope)Neurocardiogenic, Vasodepressor, Vasovagal syncope ,Fainting
Cardiovascular reflexes controlling the circulation become intermittently inappropriate
(In response to a trigger)
Resulting in vasodilatation and/ or bradycardia
Fall in arterial BP and global cerebral perfusion
Brignole et al. Europace. 6:467-537;2004
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Reflex syncope (neurally mediated syncope)Neurocardiogenic, Vasodepressor, Vasovagal syncope ,Fainting
- Common abnormality of blood pressure regulation characterized by the abrupt onset of hypotension with or without bradycardia
- Triggers: - orthostatic stress ( prolonged standing )- hot shower- emotional stress ( sight of blood)
- Neurally mediated syncope results from a paradoxical reflex - initiated when ventricular preload is reduced by venous pooling
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Venous pooling→ reduced ventricular preload
↓ in COP and BP sensed by arterial baroreceptors
↑catecholamine levels Vigorously contracting vol-depleted ventricle
Mechanoreceptors or C fibers (atria, ventricles, pulmonary artery)
Afferent C fibers → dorsal vagal nucleus of the medulla
Paradoxical withdrawal of peripheral sympathetic tone Increase in vagal toneVasodilatation bradycardia
syncope or presyncope
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Vasodepressor type
Reflex syncope-3 types ( based on efferent pathway) sympathetic or parasympathetic
Cardioinhibitory type Mixed type
Vasodilatation (↓BP)
hypotension
Bradycardia(↓HR)
or
Asystole( predominate)
Vasodilatation (↓BP)
+ Bradycardia (↓HR)
- ESC 2009
Etiology of CSS
Sensory nerve endings in the carotid sinus walls respond to deformation
“Deafferentation” of neck muscles may contribute
Increased afferent signals tobrain stem
Reflex increase in efferent vagal activity and diminution of sympathetic tone results in bradycardia and vasodilatation
Carotid Sinus
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Orthostatic hypotension and orthostaticintolerance syndromes
OH is defined as an abnormal decrease in systolic BP upon standing.
1.Classical OH : - a decrease in systolic BP ≥ 20 mmHg and in diastolic BP ≥10
mmHg within 3 min of standing
- in patients with pure ANF, hypovolemia, or other forms of ANF
2.Initial OH: - Characterized by a BP decrease immediately on standing of
> 40 mmHg, BP then spontaneously and rapidly returns to normal
- period of hypotension and symptoms is short (< 30 s)J Neurol Sci 1996;144:218–219
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J Neurol Sci 1996;144:218–219
(L) panel - healthy 17-year-old teenager with complaints of severe transient light headedness upon active standing, a pronounced initial fall in BP is observed. The nadir is at 7–10 s and followed by recovery of BP.
(R) panel- 47-year-old male with pure ANF : BP starts to fall immediately after standing to very low levels after 1 min upright with little increase in HR despite the hypotension.
Initial orthostatic hypotension ( L)
V/S
Classical orthostatic
hypotension (R).
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3.Delayed (progressive) OH : - slow progressive decrease in systolic blood pressure on standing
- absence of a bradycardiac reflex (vagal) differentiates delayed OH from reflex syncope
Reflex syncope (mixed form) induced by tilt testing : 1. 31-year-old patient (upper panel)
And
2. 69-year-old patient (lower panel).
Note the typical age differences with a much steeper fall in BP in the younger subject compared with the older subject
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Syndromes of orthostatic intolerance which may cause syncope
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Initial evaluation- Careful history- Physical examination (including orthostatic BP measurements)- ECG
Initial evaluation should answer three key questions (1) Is it a syncopal episode or not?(2) Has the etiological diagnosis been determined?
3) Are there data s/o of a high risk CVS events or death?
Diagnosis of syncope
The following questions should be answered:1. Was LOC complete?2. Was LOC transient with rapid onset and short duration?3. Did the patient recover spontaneously, completely and without sequelae?4. Did the patient lose postural tone?
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Risk stratification
When cause of syncope remains uncertain after
initial evaluation
Assess the risk of major CVS
events or SCD.
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Risk stratification at initial evaluation in prospective population studies
Table shows several different studies that have analysed the impact of different clinical data on the follow-up of patients presenting with syncope. ( presence of abnormal ECG, increased age, or data suggestive of heart disease imply a worse prognosis at 1–2 year follow-up)
CHESS acronym Patients with syncope are at 25% risk for serious outcomes if they present with one of these five clinical conditions:
1. Congestive heart failure (CHF), 2.Hematocrit <30%3. ECG abnormalities4. Shortness of breath5. Systolic blood pressure <90 mm Hg
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Diagnostic Tests
Ambulatory ECGHolter monitoringEvent recorder
○ Intermittent vs. Loop○ Implantable Loop Recorder (ILR)
Head-Up Tilt (HUT)Includes drug provocation (NTG, isoproterenol)Carotid Sinus Massage (CSM)
Adenosine Triphosphate Test (ATP)
Brignole M, et al. Europace, 2004;6:467-537.
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Diagnostic tests
1. Carotid sinus massage
- Pressure at CCA bifurcation site produces a reflex slowing in heart rate and fall in blood pressure
- Carotid sinus hypersensitivity (CSH): - a ventricular pause lasting > 3 s
and/or - a fall in systolic BP of >50 mmHg
- When CSH associated with spontaneous syncope → CSS.
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Afferent limb arising from the mechanoreceptors of the carotid. A
Carotid sinus reflex arc
Midbrain centres ( vagal nucleus and the vasomotor centre)
Efferent limb is via the vagal nerve and the parasympathetic ganglia to the sinus and atrioventricular nodes
via the sympathetic nervous system to the heart and the blood vessels
Carotid Sinus Massage (CSM)
MethodMassage, 5-10 secondsDon’t occludeSupine and upright
posture (on tilt table)
Outcome>3 second asystole
and/or > 50 mmHg fall in systolic BP with reproduction of symptoms = Carotid Sinus Syndrome
Absolute contraindicationsCarotid bruit, known
significant carotid arterial disease, previous CVA( last 3 months )
Complications Primarily neurologicalLess than 0.2%Usually transient
Kenny RA. Heart. 2000;83:564.Linzer M. Ann Intern Med. 1997;126:989.
Munro N, et al. J Am Geriatr Soc. 1994;42:1248-1251.
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Tests for orthostatic challenge
Changing from supine to upright position →displacement of blood from the thorax to the lower limbs → ↓ in venous return and CO
In the absence of compensatory mechanisms→ a fall in BP may lead to syncope
2 methods: 1. Active standing: (in which patients arise actively from
supine to erect) 2. Tilt table test :
Brignole et al. Europace. 6:467-537;2004
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Recommendations: active standing
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Head-up tilt test (HUTT)
Kenny et al (1986) : reported usefulness of HUTT in the investigation of patients with vasovagal syncope
Protocols: - Patients should be fasted for 4 h prior to the test- Passive phase (20 min) + Sensitization phase (20 min)
1. low-dose intravenous isoproterenol test : incremental doses in order to increase average HR by 20–25% over baseline (usually ≤3 µg/min)2. Sublingual nitro-glycerine protocol 300–400 µg of NTG after a 20 min unmedicated phase.
- Both protocols have a similar rate of positive responses (61– 69%)- Specificity (92–94%)
Arq Bras Cardiol 2011;96(3):246-254
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Brignole M, et al. Europace, 2004;6:467-537.
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HUTT-Class I recommendation1. Young patients without obvious or suspected heart disease with recurrent syncope of unexplained origin, in which the history is not typical enough for the diagnosis NMS.
2. In cases of a single episode of unexplained syncope, which occurred in situation where there is high risk of physical injury
or with occupational implications
HUTT- Class II recommendation1. In the differentiation between convulsive syncope and epilepsy.2. In diagnosis to differentiate between reflex syncope and OH3. For the evaluation of patients unexplained recurrent falls.4. When dealing with patients with presyncope or recurrent dizziness.5. In the evaluation of patients with recurrent syncope and psychiatric illnesses.
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- Table tilted at an angle of 70 degrees, with footrest and rest for the upper limb in which the BP will be measured. - The Velcro straps allow securing the patient in case of loss of postural tone. - The necessary equipment:
- Device for non-invasive monitoring of BP (beat to beat)- BP curve - ECG monitoring devices Arq Bras Cardiol 2011;96(3):246-254
Head-up tilt test (HUTT)
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A modified classification of VASIS (Vasovagal Syncope International Study)
Arq Bras Cardiol 2011;96(3):246-254
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A modified classification of VASIS (Vasovagal Syncope International Study)
Arq Bras Cardiol 2011;96(3):246-254
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A modified classification of VASIS (Vasovagal Syncope International Study)
Arq Bras Cardiol 2011;96(3):246-254
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Complications and contraindications
- Tilt testing is safe- life-threatening ventricular arrhythmias with isoproterenol in the presence of IHD or sick sinus syndrome
-No complications have been published with the use of NTG
- Minor side effects are common- - Palpitations with isoproterenol - Headache with nitro glycerine
Contraindications to the administration of isoproterenol : - IHD
- uncontrolled HTN-left ventricular outflow tract obstruction- significant aortic stenosis
Method CommentsHolter (24-48 hours) Not Useful for infrequent events
Event Recorder Useful for infrequent eventsLimited value in sudden LOC
Loop Recorder Useful for infrequent eventsImplantable type more convenient (ILR)
Ambulatory ECG
The recording device is worn by the patient using a shoulder strap or belt loop, attaching to 3-5 skin electrodes for continuous monitoring.
An event button (not shown) at the top of the housing of the device is pressed in the event of symptoms to mark the recording
Holter Monitor
Continuous ECG monitoring ispossible for a maximum of 48 hours
Current Cardiology Reviews, 2008, 4, 41-48
Patient Activator Reveal® Plus ILR 9790 Programmer
Reveal
Plus Insertable Loop Recorder
World J Cardiol 2010 ; 26 : 2(10): 308-315
Am J Cardiol, 1998;82:117-119.
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Time-Dependent Cumulative Diagnostic Yield of ILRJ Am Coll Cardiol 2012;59:1583–91
Diagnostic Assessment: Yields (N=341)
Yield (%)
Initial Evaluation
History, Physical Exam, ECG 38-40
Other Tests/Procedures
Head-Up Tilt 27
External Cardiac Monitoring 5-13
Insertable Loop Recorder (ILR) 43-88
EP Study <2-5
J Am Coll Cardiol. 2001;37:1921-1928. Circulation. 2001;104:46-51
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Treatment of Neurocardiogenic syncope
Management Strategies for VVS
Optimal management strategies for VVS are a source of debatePatient education, reassurance, instructionFluids, saltsTilt Training
Drug therapies
Pacing Class IIb indication for VVS patients with positive HUT
and cardioinhibitory or mixed reflex
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Goals of treatment: - Prevention of symptom recurrence and associated injuries - improved quality of life
General principles of treatment of syncope:
Initial treatment:
1.Education regarding avoidance of triggering events(hot crowded environments, volume depletion, effects of
cough, tight collars) 2. Recognition of premonitory symptoms
3. Manoeuvres to abort the episode (e.g. supine posture, physical Counter pressure manoeuvres (PCMs))4.Careful avoidance of agents lowering BP:
: alpha-blockers, diuretics, alcohol
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Additional treatment may be necessary in high risk or high frequency settings when:
syncope is very frequent (e.g. alters the quality of life )
syncope is recurrent and unpredictable (absence of premonitory symptoms) and exposes patients at high risk of trauma
syncope occurs during the prosecution of a high risk activity(e.g., driving, machine operator, flying, competitive athletics).
Treatment is not necessary in patients who have sustained a single syncope and are not having syncope in a high risk setting.
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Physical counter pressure manoeuvres
Isometric PCMs - induce a significant increase in BP- leg crossing- hand grip and arm tensing
- Mediated largely by sympathetic nerve discharge - Vascular resistance increase during manoeuvres - Mechanical compression of the venous vascular bed in the legs and abdomen
J Am Coll Cardiol 2006;48:1652–7
VVS - Tilt Training Protocol Objectives
Enhance orthostatic toleranceDiminish excessive autonomic
reflex activityReduce syncope
susceptibility/recurrences Technique
Prescribed periods of upright posture against a wall
Start with 3-5 min BIDIncrease by 5 min each
week until a duration of 30 min is achieved
Reybrouck T, et al. PACE. 2000;23:493-498.
VVS: Pharmacologic treatment
Salt /VolumeSalt tablets fludrocortisone
Beta-adrenergic blockers
Disopyramide
SSRIs Paroxetine
Vasoconstrictors Midodrine
Etilephrine
The Role of Pacing as Therapy for Syncope
VVS with +HUT and Cardioinhibitory response: - Class IIb indication for
pacing Three randomized, prospective trials reported benefits
of pacing in select VVS patients:VPS IVASISSYDIT
Subsequent study results less clearVPS IISynpace
Connolly SJ. J Am Coll Cardiol. 1999;33:16-20.Sutton R. Circulation. 2000;102:294-299.
Ammirati F. Circ. 2001;104:52-57.
VPS I (North American Vasovagal Pacemaker Study)
Objective: To evaluate pacemaker therapy for severe recurrent vasovagal
syncope Randomized, prospective, single center N=54 patients
27: DDD pacemaker with rate drop response 27: No pacemaker
Inclusion: ≥ 6 lifetime episodes of syncope & +ve HUT Primary outcome: First recurrence of syncope
Connolly SJ. J Am Coll Cardiol. 1999;33:16-20.
100
90
80
70
60
50
40
30
20
10
0
0 3 6 9 12 15Time in Months
No Pacemaker (PM)
2P=0.000022
PacemakerCu
mu
lati
ve R
isk
(%)
Connolly SJ. J Am Coll Cardiol. 1999;33:16-20.
Results: 6/27 (22%) with PM had recurrence vs. 19/27 (70%) without PM 84% RRR (2p=0.000022)
VPS I (North American Vasovagal Pacemaker Study)
VASIS (VAsovagal Syncope International Study)
Objective: To evaluate pacemaker therapy for severe cardioinhibitory tilt-
positive neurally mediated syncope Randomized, prospective, multi-center N=42 patients
19: Dual chamber pacemaker with rate hysteresis23: No pacemaker
Inclusion: Positive cardioinhibitory response Primary outcome: First recurrence of syncope
Sutton R. Circulation. 2000;102:294-299.
Sutton R. Circulation. 2000;102:294-299.
Pacemaker (PM)
No Pacemaker
p=0.0004
Years
% S
ynco
pe-
Fre
e
100
80
60
40
20
0 2 3 4 5 6
Results: 1/19(5%) with PM had recurrence vs. 14/23 (61%) without PM
VASIS (VAsovagal Syncope International Study)
SYDIT (SYncope Diagnosis and Treatment)
Objective: To compare the effects of cardiac pacing with
pharmacological therapy in patients with recurrent vasovagal syncope
Randomized, prospective, multi-center N=93 patients
46: DDD pacemaker with rate drop response47: Atenolol 100 mg/d
Inclusion: Positive HUT with relative bradycardia Primary outcome: First recurrence of syncope
Ammirati F. Circulation. 2001;104:52-57.
SYDIT (SYncope DIagnosis and Treatment)
Ammirati F. Circulation. 2001;104:52-57.
0.6
0.7
0.8
0.9
1.0
0 100 200 300 400 500 600 700 800 900 1000
Drug
Pacemaker (PM)
Time (Days)
% S
ynco
pe-
Fre
e
p=0.0032
Results: 2/46 (4%) with PM had syncope recurrence vs. 12/47 (26%) without PM
VPS II (Vasovagal Pacemaker Study II)
Objective: To determine if pacing therapy reduces the risk of syncope
in patients with vasovagal syncope Randomized, double-blind, prospective, multi-center N=100 patients
52: Only sensing without pacing48: DDD pacemaker with rate drop response
Inclusion: Positive HUT with (HR x BP) < 6000/min x mm Hg Primary outcome: First recurrence of syncope
Connolly S. JAMA. 2003;289:2224-2229.
Dual Chamber Pacing (DDD)
Only Sensing Without Pacing (ODO)
1.0
0.8
0.6
0.4
0.2
0
Months Since Randomization
Cu
mu
lati
ve R
isk
6543210
Connolly S. JAMA. 2003;289:2224–2229.
Results: 16/48 (33% ) with pacing had recurrence vs. 22/52(42% ) with only sensing
(not statistically significant)
VPS II (Vasovagal Pacemaker Study II)
SYNPACE (Vasovagal SYNcope and PACing)
Objective: To determine if pacing therapy will reduce syncope
relapses in patients with recurrent vasovagal syncope, compared to those with a pacemaker programmed to OFF
Randomized, double-blind, prospective, multi-center, placebo-controlled
N=29 patients16: DDD PM with rate drop response programmed ON13: PM programmed OFF (OOO mode)
Inclusion: Recurrent VVS and +HUT with asystolic or mixed response
Primary outcome: First recurrence of syncope
Raviele A, et al. Eur Heart J. 2004;25:1741-1748.
SYNPACE (Vasovagal SYNcope and PACing)
Results: 8/16(50%) with pacing ON had recurrence vs. 5/13 (38%) with pacing OFF
(not statistically significant)
0.6
0.7
0.8
0.9
1.0
0 200 400 600 800 1000
Pacemaker OFF
% S
ynco
pe-
Fre
e
p=0.58
0.5
0.4
0.3
0.2
0.1
0.0
Pacemaker ON
Days Since Randomization
Raviele A, et al. Eur Heart J. 2004;25:1741-1748.
Role of Pacing as Therapy for Syncope: Summary
Pacemaker implantation may modulate reflex syncope and autonomic responses
Study results may differ based on pre-implant selection criteria and tilt-testing techniques
Pacing therapy is effective in some but not all (cardioinhibition vs. vasodepression)
In five pacing studies, syncope recurred in 33/156 (21%) of paced patients, 72/162 (44%) in non-paced patients (p<0.000)
Kapoor W. JAMA. 2003;289:2272-2275.
CSS : Role of Pacing – Syncope Recurrence Rate
Class I indication for pacing (AHA and HRS)
Limit pacing to CSS that is:CardioinhibitoryMixed
DDD/DDI superior to VVI
If the diagnosis of CSH is based on a >3-second pause with carotid sinus massage without clear, provocative events, pacemaker implantation is less strongly recommended (Class IIa).
VVS Pacing Trials Conclusions
DDD pacing reduces the risk of syncope in patientswith recurrent, refractory, highly-symptomatic,
cardioinhibitory vasovagal syncope.
SAFE PACESyncope And Falls in the Elderly – Pacing And Carotid Sinus Evaluation
ObjectiveDetermine whether
cardiac pacing reduces falls in older adults with carotid sinus hypersensitivity
Randomized controlled trial (N=175)Adults > 50 years,
non-accidental fall, positive CSM
Pacing (n=87) vs. No Pacing (n=88)
ResultsMore than 1/3 of adults
over 50 years presented to the ER because of a fall
With pacing, falls 70%Syncopal events 53%Injurious events 70%
Kenny RA. J Am Coll Cardiol. 2001;38:1491-1496.
SAFE PACE
ConclusionsStrong association between non-accidental falls and
cardioinhibitory CSHCardiac pacing significantly reduced subsequent fallsCSH should be considered in all older adults who have
non-accidental falls
Kenny RA, J Am Coll Cardiol. 2001; 38:1491-1496.
Conclusion
Syncope is a common symptom with many causes Deserves thorough investigation and appropriate
treatment A disciplined approach is essential ESC guidelines offer current best practices
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1. Guidelines for the diagnosis and management of syncope (version 2009)- The Task Force for the Diagnosis and Management of Syncope of the European Society of Cardiology (ESC)-European Heart Journal (2009) 30, 2631–26712. Guidelines on Management (Diagnosis and Treatment) of Syncope Update 2004 Europace (2004) 6,
467e5373. Kapoor- Syncope Review article New Eng J Med 2000, 12; 1856-18674. Steve W Parry, Maw Pin Tan- clinical review- An approach to the evaluation and management of
syncope in adults BMJ 2010;340:c8805. Paula Gonçalves Macedo Tilt Test - from the Necessary to the Indispensable. Arq Bras Cardiol
2011;96(3):246-2546. Rajesh Subbiah Syncope: Review of Monitoring Modalities Current Cardiology Reviews 2008, 4, 41-487. Michele Brignole, New Concepts in the Assessment of Syncope J Am Coll Cardiol 2012;59:1583–918. Kapoor- Current evaluation of syncope Circulation. 2002;106:1606-16099. Paolo Alboni Diagnostic Value of History in Patients With Syncope With or Without Heart Disease J Am Coll Cardiol 2001;37:1921–8 10. Nynke van DijkEffectiveness of Physical Counterpressure Maneuvers in Preventing Vasovagal Syncope The Physical Counterpressure Manoeuvres Trial (PC-Trial) J Am Coll Cardiol 2006;48:1652–711. Nevin T Wijesekera, Arvinder S Kurbaan Pacing for Vasovagal Syncope. Indian Pacing and Electr.
Journal 2002 2(4): 114-11912. Blair P. Grubb, M.D Neurocardiogenic Syncope N Engl J Med 2005;352:1004-10.
REFERENCES
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13. Joanne L.Evaluation and Management of Syncope Clinical Scholars Review, Vol. 2, No. 2, 2009 14. Attilio Del Rosso Relation of Clinical Presentation of Syncope to the Age of Patients Am J Cardiol 2005;96:1431–143515. Chad Kessler The Emergency Department Approach to Syncope: Evidence-based Guidelines and Prediction Emerg Med Clin N Am 28 (2010) 487–5016. STUART J. The North American Vasovagal Pacemaker Study (VPS) A Randomized Trial of Permanent Cardiac Pacing for the Prevention of Vasovagal Syncope J Am Coll Cardiol 1999;33:16–2017. Richard Sutton et al .Dual-Chamber Pacing in the Treatment of Neurally Mediated Tilt-Positive Cardioinhibitory Syncope Pacemaker Versus No Therapy: A Multicenter Randomized Study Circulation. 2000;102:294-29918. Fabrizio Ammirati et al. Permanent Cardiac Pacing Versus Medical Treatment for the Prevention of Recurrent Vasovagal Circulation. 2001;104:52-5719. Rose Anne M. Kenny Carotid Sinus Syndrome: A Modifiable Risk Factor for Non accidental Falls in Older Adults (SAFE PACE) J Am Coll Cardiol 2001;38:1491– 6 20. Ward .Midodrine: a role in the management of neurocardiogenic syncope. Heart 1998;79:45–4921. Peter et al. Fludrocortisone in neurally mediated hypotension chronic fatigue syndrome JAMA 2001; 285: 52-59. 22. Antonio Raviele et al . Effect of Etilefrine in Preventing Syncopal Recurrence in Patients With Vasovagal Syncope -A Double-Blind, Randomized, Placebo-Controlled Trial Circulation. 1999;99:1452-1457. 23. Enrico Di Girolamo et al. Effects of Paroxetine Hydrochloride : A Selective Serotonin Reuptake Inhibitor, on Refractory Vasovagal Syncope: A Randomized, Double-blind, Placebo-controlled Study J Am Coll Cardiol 1999;33:1227–30.
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THANK YOU
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MCQs
1. Drugs proven to be useful in VVS except
A) Midodrine B) Etilefrine C) Fludrocortisone D) Paroxetine E) Atenolol
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2). Carotid sinus hypersensitivity (CSH) : incorrect ?
A) a ventricular pause lasting > 3 s B) a fall in systolic BP of >50 mmHg C) A & B D) BP < 100 mm Hg
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3). Investigation with highest diagnostic yield in evaluation of syncope?
A) Holter B) EP study C) ILR D) TMT
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4) True about HUTT A) Passive phase 40 min+ sensitization
phase 40 min B) isoproterenol contraindicated in IHD C) done in all cases of syncope
evaluation D) gold standard for NMS evaluation
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5) Contraindications to the administration of isoproterenol except? :
a) - IHD b) - hypotension c) -left ventricular outflow tract obstruction -d) significant aortic stenosis
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6. trials showing benefit of pacing in VVS except? VPS IVASISSYDITSynpace
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7. All are CHESS acronym in SFS score except?
1. Congestive heart failure (CHF) 2.Hematocrit <30% 3. ECG abnormalities 4. Angina 5. Systolic blood pressure <90 mm Hg
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8) True about CSS except? a) Sensory nerve endings in the carotid sinus walls
respond to deformation
B) “Deafferentation” of neck muscles may contribute
C) Increased afferent signals to brain stem
Reflex decrease in efferent vagal activity and diminution of sympathetic tone results in bradycardia and vasodilatation
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9. True about pacing in NMS except? A) class I recommendation in CSS B) Calss II b recommendation In VVS C) DDD with rate drop response is
preferred D) none
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10. All are trials in VVS except? A) VPS 1 B) Issue 3 C) VASIS D) SAFE pace trial