Transcript Hearing and Vision Impairment

DIZZINESS,
SYNCOPE AND
ATRIAL
FIBRILATION IN
THE OLDER
ADULT
OBJECTIVES
Know and understand:
• The factors that may lead to dizziness and
syncope in older adults
• The elements of evaluation (history, physical
examination, testing) of older adults with
dizziness and syncope
• The treatment options for dizziness and
syncope
Slide 2
TOPICS COVERED
• Dizziness
 Classification and Causes
 Prognosis for Older Adults with Dizziness
 Evaluation and Management
• Syncope
 Pathophysiology
 Causative Factors
 Evaluation and Management
Slide 3
IMPORTANCE AND COMPLEXITY
OF DIZZINESS
Dizziness is a common symptom in older adults
• Accounts for 7 million clinic visits/year in US
• Prevalence = 13%–38%
Challenges for clinicians
• Precise classification is difficult
• Worry about serious causes
• Specific therapy not available for many
• 50% of cases have multiple causes
Slide 4
DRUG TOXICITY  DIZZINESS
• In older adults, prescription drug toxicity is an
important contributor to dizziness
• Use of 3 medications = dizziness risk factor
• Certain drugs are more frequently implicated
– Cause orthostasis or CNS effects
– Cardiovascular or antihypertensive drugs
– Psychotropic medications
Slide 5
Oscillopsia
• seen in ototoxicity and in patients on
chemotherapy
• patients complain of blurred vision
• patients on ototoxic medications (eg,
24-hr gentamicin) should be assessed
• testing—ototoxicity possibly
developing if moving head while
looking at large printed word produces
movement or blurring of word
Slide 6
Ototoxicity
• associated with use of aminoglycosides
• Reassess need for ototoxic medication every
week
• inform patients about possible dizziness and
imbalance, and document
Slide 7
DIZZINESS: CLASSIFICATION
BY SYMPTOMS
• Vertigo — Rotational sensation
• Presyncope — Sensation of impending faint
• Disequilibrium — Loss of balance without
head sensation
• Lightheadedness — Ill-defined, not otherwise
classifiable
Slide 8
Vestibular system
• most patients with peripheral vestibular
dysfunction recover because
• 1) central nervous system (CNS) resets
incorrect information received from
ears by weighing it against information
received from eyes
• 2) proprioceptive areas in feet and
ankles maintain balance
• assess eyes
• in elderly, check vibration sense,
reflexes, and position sense in toes
Slide 9
Vertigo
• illusion of movement where none exists
• Implies asymmetry between right and left
• does not always imply peripheral vestibular
dysfunction
• 60% of patients destined for stroke may
complain of dizziness (not necessarily
vertigo)
• vertigo often prominent in cardiac
dysfunction
Slide 10
CAUSES OF VERTIGO
• Peripheral vestibular disorders
 Benign positional vertigo
 Labyrinthitis
 Ménière’s disease
• Central vestibular disorders (minority of cases)
 Transient ischemic attack (TIA)
 Vertebrobasilar ischemia
 Brain tumors
 Multiple sclerosis
Slide 11
BENIGN POSITIONAL VERTIGO (BPV)
• Episodic
• Aggravated or brought on by changes in
position (eg, turning, rolling over, bending
over)
• Spells are often brief (5–15 sec)
• Spells are often milder than in other
peripheral vestibular disorders
Slide 12
Benign paroxysmal positional
vertigo (BPPV)
• movement in the plane of semicircular canal (eg, lying back, sitting up,
or roll-ing over) results in burst of rotary nystagmus
• check for latency (ie, 1-30 sec after patient lies down); when patient
lies down, brief burst of nystagmus slows down and stops, but occurs
• (then reverses) when patient sits up again; when patient
• in patients who do not have classic rotary nystagmus, alcohol use most
common cause of positional dizziness
• lies down again, nystagmus improves or resolves
• Epley maneuver— patient sits on side of bed, lies down quickly to one
side, looks over shoulder, then sits up and lies down on other side and
looks over shoulder (should be initially performed 5 times per side
• dimenhydrinate [eg, Gravol] 30 min before exercise helpful)
• most patients with uncomplicated BPPV improve within days to weeks
• difficult for patients with cervicospinal problems (not recommended
for elderly
• associated with high recurrence of dizziness)
Slide 13
LABYRINTHITIS
• Also called vestibular neuronitis
• Occurs acutely
• Lasts several days
• Resolves spontaneously
Slide 14
Vestibular neuritis
• common; often occurs after upper
respiratory infection (URI), herpes
infection, or gastrointestinal viral infection
• patients severely ill, and always have
nystagmus
• treatment—in emergency department (ED),
give dexamethasone (eg, Decadron)
• in office, give prednisone (1 mg/kg per day)
• starting steroids early may help patients
recover sooner
• (eg, within 2 mo; most patients recover Slide 15
within 1 yr)
Exercise and physiotherapy
• initiate after vomiting resolves
• Cawthorne-Cooksey exercises
involve eye and head movements
and tilting
• balance exercises with tossing balls
• challenge brain for faster recovery
Slide 16
MÉNIÈRE’S DISEASE
• Repeated episodes of tinnitus
• Fluctuating hearing loss
• Severe vertigo
• Eventual progressive sensorineural hearing
loss
• Frequency and severity of vertigo may
improve as hearing impairment worsens
Slide 17
Endolymphatic hydrops, Meniere’s
disease
• classic episode— plugged ears; roaring tinnitus; severe vertigo
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lasts 6 to 8 hr
vomiting; ataxia; hearing decreases with each successive episode
Rare
ask about headache and visual sensitivity
Vertigo and hearing loss in elderly patient more likely ischemic problem than
true hydrops
counsel patients about decreasing caffeine, salt, and sugar intake
treatment—sublingual lorazepam (eg, Ativan) for severe episodes (effective in
15-30 min
Transdermal scopolamine patch slower)
rectal dimenhydrinate
Diuretic (eg, acetazolamide [eg, Diamox]) for pressure symptoms (discuss
contraindications)
meclizine (eg, Bonine)
flunarizine (Sibelium) helpful when uncertain whether dizziness related to
migraine or peripheral vestibular problem
Meniett device decreases endolymphatic pressure (if ineffective, ablative
procedure required)
differential diagnosis—atypical migraine; ischemic disease; autoimmune
Slide
disease (consider steroid trial in patients with eg, Crohn’s disease or lupus
and18
fluctuating hearing loss)
BRAIN TUMORS
• Found in <1% of dizzy patients
• Slightly more prevalent (2%–3%) in older patients
referred to neurologists
• Acoustic neuroma
 Most common tumor associated with dizziness
 Unilateral cochlear symptoms (tinnitus and hearing
loss) predominate, not dizziness
 Bilateral cochlear symptoms in older persons
usually represent presbycusis, not tumor
Slide 19
PRESYNCOPE
• Sensation of near-fainting
• Sign of decreased cerebral perfusion
• Cardiac causes
 Electrical: tachy- or bradyarrhythmias
 Structural, esp. aortic outflow obstruction
• Vascular causes (eg, orthostatic hypotension,
vagal stimulation)
• Postural change (with or without orthostatic
hypotension)
Slide 20
DISEQUILIBRIUM
• Sensation of being unsteady when standing or,
in particular, walking
• Many factors can contribute to imbalance:
 Chronic vestibulopathies
 Visual problems
 Musculoskeletal disorders
 Somatosensory or gait deficits
Slide 21
LIGHTHEADEDNESS
• Best reserved as a description for patients who do not
experience vertigo, presyncope, or disequilibrium
• Any cause of dizziness may occasionally produce
“lightheadedness”
• The 2 most prominent considerations:
– Psychiatric causes (depression, anxiety, somatoform
disorders)
– Idiopathic causes
Slide 22
Ophthalmic migraine
• may present as visual symptoms and
dizziness without headache
• few patients have classic basilar migraine
(ie, migraine associated with dysarthria,
visual symptoms, and bilateral hearing loss)
• migraine vestibulopathy diagnosis of
exclusion
• if dizziness clearly associated with
migraine, try empiric medication (eg,
flunarizine or topiramate [Topamax]
• if patient not sleeping well, consider
nortriptyline)
Slide 23
PURPORTED CAUSES OF DIZZINESS,
ESPECIALLY IN OLDER ADULTS
• Cervical arthritis
• Visual disorders
• Carotid sinus hypersensitivity
Slide 24
Other causes of dizziness
• obstructive sleep apnea (OSA)
• Depression
• rule out nystagmus before attributing
hyperventilation dizziness to anxiety
• vestibular physiotherapy may be helpful in
anxious patients
Slide 25
Elderly
• rarely present with primary ear problem
• Sudden dizziness may be due to ischemic
cause
• perform computed tomography (CT) for
patients in ED with risk factors or >60 yr of
age
Slide 26
Trauma
• short-term memory loss, headache, and loss of sense of
smell likely due to central concussion
• slight hearing loss and dizziness with movement of head
can be due to whiplash, or central or vestibular concussion
• distinguishing central from peripheral concussion—
dizziness with head movement can be sign of either, but
dizziness without head movement more likely vestibular
• BPPV—may present later if head trauma significant
• (ask, “is this the same kind of dizziness that you had after
your
• accident?”)
• perilymph fistula—classic history includes dizziness with
straining
• patient may develop plugged ears and hearing loss,
especially after exertion (eg, weight-lifting) or head trauma
• improves in most patients if heavy lifting and straining
avoided (fistula may be repaired if hearing continues toSlide 27
drop)
PROGNOSIS FOR OLDER PERSONS
WITH DIZZINESS
• Usually resolves within days to several months
• Chronic or recurrent symptoms
 Experienced by ~25% of dizzy adults
 Commonly due to psychiatric disorders,
disequilibrium, or vestibulopathy other than BPV
or labyrinthitis
• Not associated with increased mortality,
hospitalization, or severe disability
• Associated with ↑ risk of syncope, falls, and
depression, and with worse self-rated health
Slide 28
EVALUATION OF DIZZINESS: HISTORY
• Elicit the patient’s own description of the event
without prompting
• Learn:
– Whether the dizziness is characterized by any of 3
sensations: spinning, fainting, or falling
– Whether there is a positional effect on symptoms
– What other symptoms are associated with dizziness
(specifically ask about focal neurological symptoms)
– What medications the patient is taking
Slide 29
EVALUATION OF DIZZINESS: HISTORY
• elderly have difficulty describing symptoms
• patients may not mention other symptoms when
overwhelmed by dizziness and vomiting
• ask about headache
• tingling around mouth
• Dysarthria
• Imbalance
• Severe problems usually present with nausea, vomiting,
and imbalance
• assess reduced hearing
• clinical signs more recognizable in patients with true
disability
• ask about bothersome movements
• if symptoms worsen only when patient gets up, consider
postural problem
Slide 30
EVALUATION OF DIZZINESS:
HISTORY
• true positional—occurs when patients lie down, roll to one
side, and rise (or with hyperextension of head)
• movement-induced—occurs with all types of movement
• sometimes confused with positional dizziness
• Ask whether dizziness occurs only while walking consider
cerebellar problem
• peripheral vestibular system stimulated with all
movements, even while driving
• exercise-induced— consider cardiac problem, lack of
physical conditioning, or spinocerebellar ataxia type 6
abnormality (associated with familial hemiplegia
syndromes)
• if dizziness induced by arm movement (eg, weight-lifting),
listen at base of neck for bruit (suggests subclavian steal
syndrome)
• visually-induced— common in migraineurs
• may present as new symptom in patients developing Slide 31
multiple sclerosis
EVALUATION OF DIZZINESS:
PHYSICAL EXAMINATION
• Take blood pressure and pulse while patient is
supine and after standing for 1 to 2 min
• Perform a vestibular/nystagmus exam:
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Primary position
Gaze-evoked
Head-hanging (Dix-Hallpike) test
Head shaking
• Perform cardiac examination
• Observe for balance and gait difficulties
Slide 32
Physical examination
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ask about initial episode and current symptoms
test rapid alternating movements and corneal reflex
identifying nystagmus
Enlarging patient’s eyes with high-powered reading glasses
may be helpful
dim lights and look at retina for 1 min, then look for
movement in blood vessel in other eye
peripheral vestibular nystagmus may be seen in center gaze
(accentuated by looking in direction of past component
no accentuation in central vestibular nystagmus)
Fukuda stepping test for balance—positive if patient
moves to side while stepping in place with eyes closed
hearing test—distract one ear by rubbing, and speak into
other ear, “Suzy eats tomatoes” (start at low pitch and
gradually increase)
test both ears
Slide 33
EVALUATION OF DIZZINESS:
DIAGNOSTIC TESTING (1 of 2)
• Audiometry
 May help if cochlear symptoms are present
(tinnitus, asymmetric hearing loss)
 Abnormal results may indicate Ménière’s
disease or, rarely, a tumor
• Vestibular testing
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Electronystagmography
Brain-stem auditory evoked responses
Rotatory chair
Dynamic posturography
Slide 34
EVALUATION OF DIZZINESS:
DIAGNOSTIC TESTING (2 of 2)
• Neuroimaging (CT, MRI) occasionally warranted
• Electroencephalography (EEG) and lumbar puncture
typically not useful
• Study the vertebrobasilar system if other neurologic
symptoms suggest TIA
• ECG: low yield in patients with normal cardiac exam
and no syncope
• Not useful for isolated dizziness: Holter and event
monitors, echocardiography, stress testing, tilt-table,
electrophysiologic studies
Slide 35
MANAGEMENT OF DIZZINESS (1 of 2)
Treatable Cause
Treatment
Acute vertigo of peripheral
vestibular disorders
Reassurance and behavioral
modification; meclizine
(overused), plus a benzodiazepine
only if absolutely needed, with
caution for toxicity
BPV, mild
Reassurance
BPV, severe or refractory
Home habituation exercises,
Epley’s maneuver
Ménière’s disease with
frequent attacks
Salt restriction, diuretic, or both;
occasionally refer for
consideration of surgery Slide 36
EPLEY’S MANEUVER
Slide 37
MANAGEMENT OF DIZZINESS (2 of 2)
Treatable Cause
Treatment
Orthostatic hypotension
Correct reversible causes
Disequilibrium
Prevent falls with cane or
other assistive device
Depression
Trial of an SSRI
Chronic vestibulopathy
Vestibular rehabilitation, a
type of physical therapy
Slide 38
SYNCOPE: INTRODUCTION
Sudden, transient loss of postural tone and consciousness
(not due to trauma) with spontaneous full recovery
• Accounts for:
– ~3% of emergency department visits
– 2% to 6% of hospital admissions
• 80% of those hospitalized for syncope are aged 65+
• Causes
– May be benign or life-threatening
– In older adults, may be multifactorial
– Possible causes are numerous
Slide 39
NORMAL REFLEXES THAT PREVENT
SYNCOPE
• 1/3 of blood volume pools in legs while standing
• Reflex pathways facilitate venous return and
increase cardiac output
– Baroreceptor reflex: ↑ autonomic sympathetic tone 
peripheral vasoconstriction and ↑ heart rate
– Renal nerve: ↑ renin release from juxtaglomerular
apparatus  angiotensin II (causes vasoconstriction)
and aldosterone (causes sodium retention)
– Atrial natriuretic factor: reduced upon standing,
further facilitating vasoconstriction
Slide 40
PATHOPHYSIOLOGY OF SYNCOPE: EFFECTS
OF AGING
• Reflex mechanisms are less responsive
– ↓ ability to increase heart rate in response to
sympathetic stimulation
– ↑ sensitivity to effects of dehydration and vasodilator
drugs
• Comorbidities that affect postural responses are
common (eg, diabetes mellitus)
• Drugs may further impair postural reflexes (eg,
-blockers, -blockers, tricyclic antidepressants)
Slide 41
SYNCOPE: NATURAL HISTORY
Altered systemic blood pressure or
Increased cerebral vascular resistance
Reduced cerebral perfusion
Syncope
Causes may be benign or life-threatening
Causes may be multiple
Slide 42
COMMON CAUSES OF SYNCOPE
IN ELDERLY PERSONS
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Arrhythmia
Aortic stenosis
Carotid sinus hypersensitivity
Hypoglycemia
Myocardial infarction
Orthostatic hypotension
Postprandial hypotension
Psychogenic causes
Pulmonary embolism (large)
Vasovagal faint
Slide 43
SYNCOPE: PROGNOSIS
Type of syncope
Cardiac
Noncardiac
Unknown cause
(1/3 to 1/2 of
patients)
1-yr mortality
18%–33%
6%
Intermediate,
generally
favorable
Slide 44
SYNCOPE EVALUATION:
HISTORY (1 of 2)
Precipitants?
Prodromal symptoms?
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Eating
Urinating
Coughing
Medication
Emotional stress
Physical exertion
Turning head
Chest pain
Palpitations
Dyspnea
Diaphoresis
Presyncope
Nausea
Vomiting
Slide 45
SYNCOPE EVALUATION:
HISTORY (2 of 2)
• Medications?
– How, when taken, what doses
– Relationship to meals and activities
– Recent changes
• Any witnesses?
– Duration of event
– Appearance of patient during event (flaccid tone
and motionless or increased tone and motion?)
• Comorbid conditions?
Eg, coronary artery disease, diabetes mellitus
Slide 46
SYNCOPE CAUSED BY ARRHYTHMIA
• Prior to event
 Occurs in any position, <5 sec warning
 No precipitant; palpitations rare
• During event
 Flaccid tone; pulse faint or absent
 Blue, ashen skin
 Incontinence (rare)
• Recovery
 Rapid and complete
Slide 47
VASOVAGAL SYNCOPE
• Prior to event
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Aborted if person lies flat
Seconds to minutes of warning
Precipitant present; nausea/diaphoresis common
Visual changes
• During event
 Motionless; relaxed tone; slow, faint pulse
 Pale color; dilated, reactive pupils
• Recovery
 Fatigue, nausea and diaphoresis common
 No retrograde amnesia
Slide 48
SYNCOPE CAUSED BY SEIZURE
• Prior to event
 Occurs in any position
 No warning or prodrome
• During event
 Rigid tone; rapid pulse; elevated BP
 Tonic eye deviation common
 Frothing at mouth
• Recovery
 Slow, incomplete
 Disorientation; focal neurologic findings
Slide 49
SYNCOPE EVALUATION:
PHYSICAL EXAMINATION (1 of 2)
• Pulse in supine and standing positions
• Orthostatic vital signs: Measure BP in both arms, 1 min
after standing and again after standing for 3 min
• Carotid pulse examination
 Delayed upstroke and low volume may identify aortic
stenosis
 Perform carotid massage only with continuous ECG and
resuscitation equipment available
 Contraindicated with carotid bruit, CVD, recent MI
Slide 50
SYNCOPE EVALUATION:
PHYSICAL EXAMINATION (2 of 2)
• Cardiac examination for murmurs, extra
heart sounds
• Stool for occult blood
• Neurologic examination for focal deficits
Slide 51
SYNCOPE EVALUATION: TESTING
(1 of 2)
• ECG for all syncopal older adults; assess for:
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Acute or remote MI
Conduction abnormalities and pre-excitation
Sinus bradycardia
Prolonged QT interval
• Ambulatory ECG
 Among patients able and willing to operate loop
recorders, diagnostic yield is ~25%
 Implantable recorders are cost-effective for patients
with ejection fraction >35% and symptoms not
consistent with a neural cause of syncope
Slide 52
SYNCOPE EVALUATION: TESTING
(2 of 2)
• Echocardiography
• Tilt-table testing
• Electrophysiologic (EP) studies
• Neurologic testing (MRI and CT, plus EEG)
if focal neurologic signs or symptoms are
present, or if the history suggests seizure
Slide 53
TREATMENT OF SYNCOPE (1 of 3)
• Focus on treating the underlying disorder
• In older patients, treatment of multiple
possible causes is often necessary
• Discontinuation of medications that increase
the risk of syncope is always an early step
Slide 54
TREATMENT OF SYNCOPE (2 of 3)
Cause
Myocardial ischemia
Valvular heart disease
(esp. aortic stenosis)
Symptomatic SVT
Treatment
Revascularization or aggressive
medical therapy
Usually surgery, avoid preload
reduction
Significant ventricular
tachyarrhythmia
Medical therapy or
electrophysiology ablation
Implanted defibrillator or medical
therapy
Bradyarrhythmia
Usually pacemaker
Slide 55
TREATMENT OF SYNCOPE (3 of 3)
Cause
Treatment
Orthostatic
hypotension
Vasovagal syncope
Adjust medications, ensure adequate
volume, other conservative measures
Avoidance of triggers; medical therapy
is somewhat controversial (-blockers,
clonidine, paroxetine, midodrine)
Carotid sinus
hypersensitivity
Avoid stimulating factors (tight collars or
rapid neck movements); pacemaker
Postprandial
hypotension
Avoid alcohol and high-carbohydrate
meals; remain recumbent after meals
Slide 56
RECURRENT SYNCOPE
WITHOUT IDENTIFIABLE CAUSE
• Help patients avoid harm to themselves or others
• Consider recommending against driving for
several months and resuming if patient remains
recurrence-free (American Heart Association
guidelines)
• Many states have laws against driving with a
history of syncope
Slide 57
Complications of A Fib
• Complications associated with
permanent atrial fibrillation (AF)
• increased risk for stroke
• systemic thromboembolism,
• Death
• mortality is a function of underlying
structural heart disease or other
comorbidities (survival in patients with
lone AF same as that in otherwise
healthy age-matched controls)
Slide 58
Evaluation
• history—control of hypertension
important
• OSA
• look for reversible causes (eg,
hyperthyroidism, pneumonia)
• medical history
• 12-lead electrocardiography (ECG)
required
• echocardiography recommended
Slide 59
Patterns of AF
• second episode of AF may occur years after
first
• important when considering long-term or
temporary antiarrhythmic drug therapy
• management of persistent AF
• may differ from that of paroxysmal AF
Slide 60
Rhythm control vs rate control
• AFFIRM trial found rhythm control not
• superior to rate control for reducing mortality (survival
curves similar
• in Atrial Fibrillation Follow-up Investigation of
• Rhythm Management (AFFIRM) trial, lower survival rates
seen in patients randomized to rhythm control
• no difference in incidence of stroke over time between
patients randomized to rate control vs rhythm control
• Canadian Cardiovascular Society guidelines—rate or
rhythm control acceptable
• Management must be based on symptoms, patient’s
preference, and risk factors
• (rhythm control might be favorable in high-risk groups)
• factors that may favor rate control include persistent AF,
frequent recurrent AF, less symptomatology, older age, and
hypertension
• according to Atrial Fibrillation and Congestive Heart
Failure (AF-CHF) study, rhythm control appears moreSlide 61
beneficial than rate control in HF
Treatment of newly diagnosed AF
• paroxysmal AF— consider anticoagulation
• treat if symptomatic, or if ventricular rate
uncontrolled
• persistent AF—restore sinus rhythm with electrical
or pharmacologic cardioversion
• temporary use of antiarrhythmic drugs (consider
maintenance and long-term use)
• permanent AF—anticoagulation and rate control
drugs as required
• rhythm control—may need to consider
cardioversion
• reevaluate therapy over time (as AF evolves,
antiarrhythmic drugs may no longer maintain
Slide 62
sinus rhythm)
Infrequent episodes of paroxysmal
AF
• “pill in the pocket” approach—give loading
dose of propafenone (450 or 600 mg)
• then wait 30 min for conversion
• usually prescribed with rate control drugs
• shown highly effective
Slide 63
Medications
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Beta-blockers
calcium channel blockers; dose
based on symptoms
digoxin alone usually not effective in controlling
heart rate during AF, but may be synergistic with
other drugs
flecainide, propafenone, sotalol, and amiodarone
used in patients with no underlying structural heart
disease
dronedarone—amiodarone analogue with fewer
associated side effects (eg, no corneal deposits,
lower frequency
of hyper- or hypothyroidism, no pulmonary
toxicity)
Slide 64
shown superior to placebo
Stroke and systemic
thromboembolism
• moderate-risk group—>75 yr of age with
hypertension, some left ventricular
dysfunction, HF, or diabetes
• high-risk group— history of stroke,
transient ischemic attack (TIA), or valvular
heart disease
• aspirin shown to slightly reduce risk for
stroke in high-risk group, and warfarin
significantly reduced risk for stroke
(warfarin appears superior to aspirin in all
risk groups
• but less beneficial because relative risk for
Slide 65
stroke in low-risk group “very low”)
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CHADS2 score
1 point assigned for history of CHF
hypertension
older age
Diabetes
2 points assigned for history of stroke or TIA
paroxysmal AF, persistent AF, and atrial flutter
assigned same number of points
recommendations—
treat with aspirin (or no medication) with score of
0
Treat with aspirin or warfarin (based on patient’s
preference) with score of 1
treat with warfarin and maintain international
normalized ratio (INR) at 2 to 3 with score 2 or
more
Slide 66
CHADS2 score and risk for stroke may vary
Other risk factors for stroke
• Other risk factors
• risk for stroke associated with paroxysmal
AF appears lower in recent clinical trials
than in earlier studies
• patients who have episodes of AF lasting
>24 hr have higher risk for
thromboembolism than those with episodes
lasting <24 hr
Slide 67
Warfarin use in AFFIRM trial
• Warfarin use in AFFIRM trial
• warfarin stopped in patients prescribed
antiarrhythmic drug therapy in mistaken belief
patients would remain in sinus rhythm
• risk for ischemic stroke slightly higher in patients
treated with rhythm control who discontinued
warfarin
• maintain INR of 2 to 3
• (>3 increases risk for significant hemorrhage)
Slide 68
Risk for intracranial bleeding
• predictors—
in
elderly
• inadequate education about use of oral
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anticoagulants
Polypharmacy
INR outside of therapeutic range
study did not see association between cognitive,
visual, or hearing impairment and increased risk of
bleeding
careful use of anticoagulation can be successful
warfarin more effective than aspirin at preventing
thromboembolism in elderly patients with AF, but
associated with increased risk of bleeding
substantial risk in first year after initiation of
anticoagulation (intense monitoring required)
risk higher in patients with higher CHADS2 Slide 69
scores
Cardioversion
• associated with increased risk for stroke
• Anticoagulation recommended for 3 to 4 wk
before initiating and for 1 mo after
cardioversion
• if AF has persisted for >48 hr, perform
transesophageal echocardiography to rule
out clotting in atrium, then proceed with
cardioversion
Slide 70
ACTIVE studies
• Atrial fibrillation Clopidogrel Trial with
Irbesartan for prevention of Vascular Events
(ACTIVE) studies
• ACTIVE W—warfarin superior to clopidogrel and
aspirin in preventing stroke (risk of bleeding
similar)
• patients naïve to warfarin at time of randomization
and treated with either clopidogrel and aspirin had
increased risk of bleeding, compared to patients
who were not naive to warfarin before
randomization (suggests that patients with history
of bleeding on warfarin had been weeded out of
group)
• ACTIVE result a minor benefit in stroke reduction
with aspirin and clopidogrel (compared to aspirin
alone)
Slide 71
Principles
•
•
•
•
Principles of antithrombotic therapy
individualize therapy
reassess risk factors over time
risk stratify when deciding to use aspirin or
warfarin
Slide 72
RE-LY trial
• Randomized Evaluation of Long-term
anticoagulation therapY (RE-LY) trial
• prevention of stroke or thromboembolism—
low-dose dabigatran equivalent to warfarin
• high-dose dabigatran superior to warfarin
• risk of bleeding—lower with low-dose
dabigatran than with warfarin
• equivalent in high-dose dabigatran and
warfarin
Slide 73
Who to refer
• most patients with AF
• patients <35 yr of age with
symptomatic AF or atrial flutter should
be evaluated for supraventricular or
atrial tachycardia (can be cured with
catheter ablation)
• patients who remain highly
symptomatic despite trials of
antiarrhythmic drug therapy
• patients intolerant of therapies
Slide 74
Volume 360:668-678 February 12, 2009 Number 7
Effect of Dronedarone on Cardiovascular Events in Atrial Fibrillation
Stefan H. Hohnloser, M.D., Harry J.G.M. Crijns, M.D., Martin van
Eickels, M.D., Christophe Gaudin, M.D., Richard L. Page, M.D.,
Christian Torp-Pedersen, M.D., Stuart J. Connolly, M.D., for the ATHENA
Investigators
•
•
•
•
•
•
ABSTRACT
Background Dronedarone is a new antiarrhythmic drug that is being developed for the treatment of
patients with atrial fibrillation.
Methods We conducted a multicenter trial to evaluate the use of dronedarone in 4628 patients with
atrial fibrillation who had additional risk factors for death. Patients were randomly assigned to
receive dronedarone, 400 mg twice a day, or placebo. The primary outcome was the first
hospitalization due to cardiovascular events or death. Secondary outcomes were death from any
cause, death from cardiovascular causes, and hospitalization due to cardiovascular events.
Results The mean follow-up period was 21±5 months, with the study drug discontinued prematurely
in 696 of the 2301 patients (30.2%) receiving dronedarone and in 716 of the 2327 patients (30.8%)
receiving placebo, mostly because of adverse events. The primary outcome occurred in 734 patients
(31.9%) in the dronedarone group and in 917 patients (39.4%) in the placebo group, with a hazard
ratio for dronedarone of 0.76 (95% confidenceinterval [CI], 0.69 to 0.84; P<0.001). There were 116
deaths (5.0%) in the dronedarone group and 139 (6.0%) in the placebo group (hazard ratio, 0.84; 95%
CI, 0.66 to 1.08; P=0.18). There were 63 deaths from cardiovascular causes (2.7%) in the
dronedarone group and 90 (3.9%) in the placebo group (hazard ratio, 0.71; 95% CI, 0.51 to 0.98;
P=0.03), largely due to a reduction in the rate of death from arrhythmia with dronedarone. The
dronedaronegroup had higher rates of bradycardia, QT-interval prolongation, nausea, diarrhea, rash,
and an increased serum creatinine level than the placebo group. Rates of thyroid- and pulmonaryrelated adverse events were not significantly different between thetwo groups.
Conclusions Dronedarone reduced the incidence of hospitalization due to cardiovascular events or
death in patients with atrial fibrillation. (ClinicalTrials.gov number,
Slide 75
NCT00174785 [ClinicalTrials.gov] .)
•
•
•
Safely switch from amiodarone to
dronedarone in two days, suggests
analysis
MARCH 15, 2010 | Steve Stiles
Atlanta, GA - Patients on amiodarone for maintenance of sinus rhythm after cardioversion of atrial
fibrillation (AF) who are looking to switch to dronedarone (Multaq, Sanofi-Aventis) in most cases
can safely begin taking the newer antiarrhythmic agent within two days of stopping the older one,
according to a post hoc analysis of two randomized trials [1].
The rate of serious adverse events associated with initiating dronedarone in the combined population
of >1200 patients was low and varied little by whether patients had stopped taking amiodarone <48
or >48 hours previously or hadn't been on amiodarone at all.
The patients were part of the European Trial in Atrial Fibrillation or Flutter Patients Receiving
Dronedarone for the Maintenance of Sinus Rhythm (EURIDIS) and American-AustralianAfrican Trial with Dronedarone in Atrial Fibrillation or Flutter Patients for the Maintenance of
Sinus Rhythm (ADONIS), which together saw dronedarone reduce the risk of AF recurrence by
25% (p=0.022) over one year compared with placebo [2].
•
The most effective and most toxic drug for AF
•
•
•
•
The finding that a switch can be made fairly safely and rapidly may help allay concerns over possibly
severe increased risk if a patient starts dronedarone too soon after withdrawing from a drug with an
unusually long half life and a notorious adverse-effect profile.
"Amiodarone is the most effective drug we have for atrial fibrillation, and it's also the most toxic
drug we have for atrial fibrillation," observed Dr Peter R Kowey (Main Line Health System,
Wynnewood, PA) for heartwire. Its multiorgan toxicities are cumulative, he noted, so a transition to
the demonstrably safer dronedarone might be wise for younger patients. "With amiodarone, the fear
is that if you continue to use it over the long term, then eventually the toxicity will emerge."
Others on amiodarone who might switch to the newer drug, he said, are those who aren't tolerating it
and those who still have AF recurrences despite it.
Slide 76
Kowey, who cautioned that the post hoc analysis is based on a fairly small population and can be
only hypothesis-generating, was to present it here today at the American College of
•
•
•
•
•
•
•
•
Rapid transition preserves
efficacy
Of the 1237 patients with AF or atrial flutter in EURIDIS and ADONIS combined, who
were randomized to dronedarone (400 mg twice daily) or placebo after cardioversion to
sinus rhythm, 98 had started dronedarone within 48 hours of stopping amiodarone. Their
rate of recurrence fell by 36% (p=0.022) compared with 56 placebo recipients with the
same amiodarone history. But the two groups' rates of serious adverse events, including
bradyarrhythmia, were similar, at 15.3% and 14.3%, respectively.
For the 35 patients who started dronedarone longer than 48 hours after stopping
amiodarone, the rate of serious adverse events was 17.1%, compared with 11.8% for
their 17 corresponding placebo recipients.
In the much-larger group with no history of receiving amiodarone, the rates were 13.7%
for the 680 dronedarone patients and 16.2% for the 334 that had been assigned to
placebo, Kowey reported.
The rate of adverse events leading to drug discontinuation—especially
bradyarrhythmia—was generally higher for dronedarone compared with placebo
regardless of time since amiodarone withdrawal. It was 8.2% vs 3.6% for the group
starting the new treatment within 48 hours and 20% vs 11.8% when the wait was longer
than 48 hours.
There were no instances of torsades de pointes, but QT-interval prolongation was more
likely with dronedarone regardless of amiodarone status.
Kowey says there may be some concern about adding dronedarone soon after
amiodarone withdrawal in patients with a slow heart rate. In such cases, he said, "it's
probably a good idea to wait a bit longer [than 48 hours]."
And for patients with a long QT interval when taking amiodarone, "it's probably better
to wait until the QT comes down."
Slide 77
Otherwise, he said, "there doesn't seem to be any major liability" involved in starting
dronedarone within 48 hours of stopping the older drug.
Brits Not NICE to Dronedarone
• Monday January 11, 2010
• The British National Institute for Clinical Excellence
(NICE) has made a preliminary determination NOT to
cover the new antiarrhythmic drug dronedarone (Multaq,
Sanofi-Aventis) for British patients with atrial
fibrillation (AF). Instead, NICE implies, patients should
continue receiving amiodarone (Cordarone, Pacerone),
which is more effective and cheaper.
• Amiodarone is the most effective antiarrhythmic drug
(drug that is supposed to stabilize the heart rhythm)
available, but it unfortunately produces a bizarre array of
side effects that are common, often dangerous or disabling,
and difficult to treat. A suitable "replacement" for
amiodarone has long been sought.
• Amiodarone: A Uniquely Toxic Drug
• Amiodarone's Strange History
• For a long time, it was hoped that dronedarone (a
compound related to amiodarone) would be that perfect
replacement. It is not. While it appears to have much less
Slide 78
toxicity than amiodarone, it is not as effective in treating
Dronedarone Drug Information
•
•
•
•
•
•
And indeed, this was the very logic used by NICE to deny approval for dronedarone -- it
is not as effective as amiodarone, and it is much more expensive. So it will not be made
available for British patients.
DrRich Comments:
The dronedarone/NICE story illustrates how panels of "clinical excellence" (like NICE,
or like the panels apparently being established in the United States under pending
healthcare reforms), even when they strictly follow the results of randomized clinical
trials, can make decisions that seem reasonable on the surface but ultimately are harmful
to patients.
Consider that while the effectiveness of dronedarone in treating AF (effective in
approximately 30% to 40% of patients) is substantially less than for amiodarone (which
is effective in approximately 50% to 60%), this still means that a substantial minority of
patients could potentially be treated effectively with dronedarone. So, for instance, if
patients with AF were given a trial of dronedarone, potentially up to 40% of them could
be spared exposure to the extravagant toxicity of amiodarone.
But because randomized trials tell us that, in a large population of patients,
the averageresponse to dronedarone is significantly lower than the average response to
amiodarone, no patients (in Britain, at least) will have the opportunity to try
dronedarone.
To my mind, this example succinctly illustrates a key problem with how our bureaucrats
propose to use panels of experts. Such panels can be of immense help in providing
guidance to clinicians. But when bureaucrats insist on converting such recommendations
into strict, "up or down" coverage decisions, individual patients will lose their
opportunity to receive the kind of individualized care most of us value -- care given by
our chosen doctors, who judiciously apply expert-generated clinical guidelines, while
Slide 79
still taking our individual circumstances into account.
Dronedarone
•
•
•
•
•
Dronedarone is the latest antiarrhythmic drug to be developed for atrial fibrillation. In
their search for a safe and effective drug for atrial fibrillation, pharmaceutical companies
have long imagined their "Holy Grail:" A drug that is as effective as amiodarone, but
without its unique toxicity profile. Dronedarone (Multaq) was developed by Sanofi (the
makers of amiodarone) specifically in the hopes of creating that holy grail.
Dronedarone is indeed a derivative of amiodarone -- the most effective, but the most
toxic, antiarrhythmic drug yet developed. Unlike amiodarone, dronedarone does not
contain idodine atoms, and the iodine within amiodarone has been postulated to produce
some of the drug's striking toxic effects, especially the thyroid toxicity seen with the
drug, and perhaps the lung toxicity. Encouragingly, during the clinical trials with
dronedarone, amiodarone-like toxicity so far has not been seen.
Several clinical trials with dronedarone have been reported. Two of these trials (the
EURIDIS and ADONIS trials) assessed the effectiveness of dronedarone for treating
atrial fibrillation. In these trials, 64% of patients treated with dronedarone had recurrent
atrial fibrillation during the first year after beginning treatment, as compared with 75%
of patients treated with placebo. This improvement is statistically significant, but is by
no means striking -- and indeed is little better than the reduction in atrial fibrillation
seen with many other antiarrhythmic drugs.
More recently, however, the ATHENA trial reported that patients treated with
dronedarone for atrial fibrillation for 21 months had a signficantly reduced risk of death
or cardiac hospitalization, compared to patients treated with placebo. This study is the
first clinical study to suggest that treating patients who have atrial fibrillation
with any antiarrhythmic drug can improve survival or reduce hospitalizations.
While the results of the ATHENA trial have caused quite a stir, the mechanism for
reduced mortality with dronedarone is unclear. Since dronedarone may not be
remarkably effective in reducing recurrences of atrial fibrillation, perhaps the drug may
have some other, undefined, benefit aside from actually preventing atrial fibrillation.
Slide 80
•
•
•
•
•
•
•
Dronedarone
Keep in mind that in 2003, Sanofi had to prematurely halt a clinical trial using
dronedarone in patients with significant heart failure and atrial fibrillation, at
the urging of the independent Data Safety and Monitorning Board, because
those treated with dronedarone appeared to have an increased risk of death.
Notably, patients enrolled in the ATHENA trial were significantly healthier
than in that earlier, more alarming, study.
Side effects with dronedarone so far appear to be relatively benign. The most
common reported side effects are diarrhea or nausea, slow heart rate, and rash.
The unique side effects seen with amiodarone (such as lung toxicity, thyroid
disorders, visual disturbances, or neurological disorders) have not been seen
with dronedarone. However, it should be noted that none of the clinical trials
with dronedarone have lasted for more than two years -- and some of the
unusual toxicities seen with amiodarone may not appear until the drug has
been taken for for several years. So, while dronedarone at this point looks
reasonably safe, its true safety profile will not be known until it has been in
use for a substantial period of time.
The FDA approved the use of dronedarone for the treatment of atrial
fibrillation in the summer of 2009. The FDA specified that dronedarone should
be limited to patients who (like those enrolled in the ATHENA trial) do not
have significant heart failure.
Sources:
Hohnloser SH, Crijns HJGM, van Eickels M, et al. Effect of dronedarone on
cardiovascular events in atrial fibrillation. N Engl J Med 2009; 360:668-678.
Singh BN, Connolly SJ, Crijns HJGM, et al. Dronedarone for maintenance of
sinus rhythm in atrial fibrillation or flutter. N Engl J Med 2007; 357:987-99.
Ezekowitz MD. Maintaining sinus rhythm—making treatment better thanSlide
the 81
disease. N Engl J Med 2007; 357:1039.
Dabigatran
• Atrial fibrillation increases the risks of stroke and death. Vitamin K
antagonists, such as warfarin, reduce the risks of stroke and death but
increase the risk of hemorrhage as compared with control
therapy.1 Therefore, warfarin is recommended for patients who have
atrial fibrillation and are at risk for stroke.2Vitamin K antagonists are
cumbersome to use, because of their multiple interactions with food
and drugs, and they require frequent laboratory monitoring. Therefore,
they are often not used, and when they are, rates of discontinuation are
high.3,4 Many patients receiving warfarin still have inadequate
anticoagulation.5Thus, there is a need for new anticoagulant agents
that are effective, safe, and convenient to use.
• Dabigatran etexilate is an oral prodrug that is rapidly converted by a
serum esterase to dabigatran, a potent, direct, competitive inhibitor of
thrombin. It has an absolute bioavailability of 6.5%, 80% of the given
dose is excreted by the kidneys, its serum half-life is 12 to 17 hours,
and it does not require regular monitoring.6Dabigatran has been
evaluated in a pilot trial involving patients with atrial fibrillation and in
a study for the prevention of venous thromboembolism, in which doses
of 150 mg twice daily and 220 mg once daily, respectively,
were promising.7,8 We performed a large, randomized trial
comparing the use of dabigatran, at doses of 110 mg twice daily and
150 mg twice daily, with warfarin.
Slide 82
Volume 361:1139-1151 September 17, 2009 Number 12
Dabigatran versus Warfarin in Patients with Atrial Fibrillation
Stuart J. Connolly, M.D., Michael D. Ezekowitz, M.B., Ch.B., D.Phil., Salim Yusuf,
F.R.C.P.C., D.Phil., John Eikelboom, M.D., Jonas Oldgren, M.D., Ph.D., Amit Parekh, M.D.,
Janice Pogue, M.Sc., Paul A. Reilly, Ph.D., Ellison Themeles, B.A., Jeanne Varrone, M.D.,
Susan Wang, Ph.D., Marco Alings, M.D., Ph.D., Denis Xavier, M.D., Jun Zhu, M.D., Rafael
Diaz, M.D., Basil S. Lewis, M.D., Harald Darius, M.D., Hans-Christoph Diener, M.D.,
Ph.D., Campbell D. Joyner, M.D., Lars Wallentin, M.D., Ph.D., and the RE-LY Steering
Committee and Investigators
•
•
•
•
•
ABSTRACT
Background Warfarin reduces the risk of stroke in patients with atrial fibrillation but increases the
risk of hemorrhage and is difficult to use. Dabigatran is a new oral direct thrombin inhibitor.
Methods In this noninferiority trial, we randomly assigned 18,113 patients who had atrial fibrillation
and a risk of stroke to receive, in a blinded fashion, fixed doses of dabigatran — 110 mg or 150 mg
twice daily — or, in an unblinded fashion, adjusted-dose warfarin. The median duration of the
follow-up period was 2.0 years. The primary outcome was stroke or systemic embolism.
Results Rates of the primary outcome were 1.69% per year in the warfarin group, as compared with
1.53% per year in the group that received 110 mg of dabigatran (relative risk with dabigatran, 0.91;
95% confidence interval [CI], 0.74 to 1.11; P<0.001 for noninferiority) and 1.11% per year in the
group that received 150 mg of dabigatran (relative risk, 0.66; 95% CI, 0.53 to 0.82; P<0.001 for
superiority). The rate of major bleeding was 3.36% per year in the warfarin group, as compared with
2.71% per year in the group receiving 110 mg of dabigatran (P=0.003)and 3.11% per year in the
group receiving 150 mg of dabigatran (P=0.31). The rate of hemorrhagic stroke was 0.38% per
year in the warfarin group, as compared with 0.12% per year with 110 mg of dabigatran (P<0.001)
and 0.10% per year with 150 mg of dabigatran (P<0.001). The mortality rate was 4.13% per year in
the warfarin group, as compared with 3.75% per year with 110 mg of dabigatran (P=0.13) and 3.64%
per year with 150 mg of dabigatran (P=0.051).
Conclusions In patients with atrial fibrillation, dabigatran given at a dose of 110 mg was associated
with rates of stroke and systemic embolism that were similar to those associated with warfarin, as
well as lower rates of major hemorrhage. Dabigatran administered at a dose of 150 mg, as compared
with warfarin, was associated with lower rates of stroke and systemic embolism but similar rates of
Slide 83
major hemorrhage. (ClinicalTrials.gov number, NCT00262600 [ClinicalTrials.gov] .)
Dabigatran
•
•
•
•
•
•
•
•
We compared two fixed-dose regimens of dabigatran (110 mg twice daily and 150 mg twice daily), administered in a blinded fashion, with
adjusted-dose warfarin, administered in an unblinded fashion, in patients who had atrial fibrillation and were at risk for stroke. Both
dabigatran doses were noninferior to warfarin withrespect to the primary efficacy outcome of stroke or systemic embolism. In addition, the
150-mg dose of dabigatran was superior to warfarin with respect to stroke or systemic embolism, and the 110-mg dose was superior to
warfarin with respect to major bleeding.
Previous studies seeking to identify a safe and effective alternative to warfarin for patients with atrial fibrillation have all had specific
limitations. The combination of clopidogrel and aspirin was more effective than aspirin alone13 but less effective
than warfarin.14 Subcutaneous idraparinux was more effective than warfarin but was associated with a substantially higher risk of
bleeding.15 Ximelagatran, an earlier direct thrombin inhibitor, appeared to be similar to warfarin with respect to efficacy and safety but was
found to be hepatotoxic.16 In our serial measurement of liver function, we did not find evidence of hepatotoxicity with dabigatran.
The rate of myocardial infarction was higher with both doses of dabigatran than with warfarin. An explanation might be that warfarin
provides better protection against coronary ischemic events than dabigatran, and warfarin is known to reduce the risk of myocardial
infarction.17 However, rates of myocardial infarction were similar between patients with atrial fibrillation who were receiving warfarin and
those who were receiving ximelagatran, another direct thrombin inhibitor.16The explanation for this finding is therefore uncertain.
The most devastating complication of warfarin therapy is intracranial hemorrhage, especially hemorrhagic stroke. As compared with aspirin,
warfarin doubles the risk of intracranial hemorrhage.1 Thus, our finding that the rate of this complication with both doses of dabigatran was
less than one third the rate with warfarin,without a reduction in the efficacy against ischemic stroke, suggests an important advantage of
dabigatran. The rate of major bleeding with warfarin was higher in our study than in some previous trials.11,13,14 This is partly explained by
the more inclusive definition of major bleeding in our study. There was an increase in the rate of gastrointestinal bleeding with the higher
dabigatran dose, despite the overall lower rates of bleeding at other sites. To enhance absorption of dabigatran, a low pH is required.
Therefore, dabigatran capsules contain dabigatran-coated pellets with a tartaric acid core. This acidity may partly explain the increased
incidence of dyspeptic symptoms with both dabigatran doses and the increased risk of gastrointestinal bleeding with the 150-mg dose.
The benefit of dabigatran may be explained in part by the twice-daily dosing regimen. Since dabigatran has an elimination half-life of 12 to
17 hours, twice-daily dosing reduces variability in the anticoagulation effect, especially as compared with the anticoagulation effect of
warfarin, which is difficult to control. Warfarin broadly inhibits coagulation (inhibiting factors II, VII, IX, and X and proteins C and S). By
selectively inhibiting only thrombin, dabigatran may have antithrombotic efficacy while preserving some other hemostatic mechanisms in the
coagulation system and thus potentially mitigating the risk of bleeding.
The use of open-label warfarin could have introduced a bias in the reporting or adjudication of events. This risk was reduced by the
implementation of several validated procedures, including blinded evaluation of outcome events. The unexpectedly different rates of
myocardial infarction and gastrointestinal bleeding among the three treatment groups support an absence of bias. Control of anticoagulation
with warfarin in our study was similar to that in previous international clinical trials, even though half our patients had not previously had
extensive treatment with warfarin.10,17
The net clinical benefit outcome, which is a measure of the overall benefit and risk, was similar between the two doses of dabigatran, owing
to the lower risk of ischemia with the 150-mg dose and the lower risk of hemorrhage with the 110-mg dose. These findings suggest that the
dose of dabigatran could potentially be tailored to take into consideration the risk characteristics of a specific patient, although this
concept was not specifically tested in our trial.
In conclusion, we compared two doses of dabigatran with warfarin in patients who had atrial fibrillation and who were at risk for stroke. As
compared with warfarin, the 110-mg dose of dabigatran was associated with similar rates of stroke and systemic embolism and lower rates of
major hemorrhage; the 150-mg dose of dabigatran was associated with lower rates of stroke and systemic embolism but with a similar rate of
major hemorrhage.
Slide 84
SUMMARY (1 of 2)
• Precise classification of dizziness into vertigo,
presyncope, disequilibrium, and lightheadedness
is often difficult, and multiple causes of the same
symptoms are common
• Most dizziness resolves within days to several
months
• Key physical exam steps include checking for
orthostatic hypotension, performing the headhanging (Dix-Hallpike) test, and observing gait
Slide 85
SUMMARY (2 of 2)
• In older adults the cause of syncope is often
multifactorial
• Most diagnostic procedures for syncope are
expensive and have a low yield unless findings
from the H & P suggest a particular cause
• The absence of cardiac disease strongly suggests
that the cause of syncope is not cardiac
• Treatment of dizziness and syncope focuses on
treating the underlying disorder
Slide 86
CASE 1 (1 of 3)
• For the past several weeks, a 69-year-old man has had
recurrent spells of room-spinning vertigo that last for
about 4 minutes.
• The spells occur spontaneously and are unassociated
with positional changes. They are accompanied
occasionally by double vision and sometimes by
weakness on the right side.
• Several times, the patient has had sudden drop attacks,
followed by mild weakness of both legs lasting several
minutes.
• The patient has a history of diabetes mellitus and CAD.
Slide 87
CASE 1 (2 of 3)
Which of the following is the most likely cause of
the vertigo?
(A)
Vestibular neuronitis
(B)
Vertebrobasilar insufficiency
(C)
Labyrinthitis
(D)
Migraine-associated vertigo
(E)
Ménière’s disease
Slide 88
CASE 1 (3 of 3)
Which of the following is the most likely cause of
the vertigo?
(A)
Vestibular neuronitis
(B)
Vertebrobasilar insufficiency
(C)
Labyrinthitis
(D)
Migraine-associated vertigo
(E)
Ménière’s disease
Slide 89
CASE 2 (1 of 3)
• A 75-year-old woman reports repeated episodes of
profound dizziness and near loss of consciousness, along
with at least two episodes in which she found herself on
the floor but was unaware of how she fell. She denies any
confusion after the episode or any significant trauma.
• The patient takes amlodipine 5 mg/day for hypertension.
• BP is 152/84 and pulse is 76 when the patient is supine.
In the upright posture, BP is 146/86 and pulse is 86.
There is no jugular venous distension or carotid bruit.
Lungs are clear. There is a slightly delayed carotid
upstroke and a II/VI systolic murmur at the base with an
intact S2 but no gallop.
Slide 90
CASE 2 (2 of 3)
Which of the following is the most appropriate
next step in the evaluation of this patient to
stratify her risk of adverse outcomes?
(A)
Blood tests
(B)
Electrocardiography
(C)
Holter monitoring
(D)
Event monitor
(E)
Tilt-table test
Slide 91
CASE 2 (3 of 3)
Which of the following is the most appropriate
next step in the evaluation of this patient to
stratify her risk of adverse outcomes?
(A)
Blood tests
(B)
Electrocardiography
(C)
Holter monitoring
(D)
Event monitor
(E)
Tilt-table test
Slide 92
CASE 3 (1 of 2)
Of the following features that may be available
from a patient history, which best distinguishes
syncope from an unexplained fall?
(A)
Tonic-clonic movements
(B)
Urinary incontinence
(C)
Postictal state
(D)
Loss of consciousness
(E)
Loss of postural tone
Slide 93
CASE 3 (2 of 2)
Of the following features that may be available
from a patient history, which best distinguishes
syncope from an unexplained fall?
(A)
Tonic-clonic movements
(B)
Urinary incontinence
(C)
Postictal state
(D)
Loss of consciousness
(E)
Loss of postural tone
Slide 94
Vertigo
•
•
•
•
(A) Illusion of movement where none exists
(B) Often occurs after upper respiratory infection;
patients present with nystagmus
(C) Characterized as dizziness without hearing
loss;
• treated with topiramate
• (D) Seen in ototoxicity and in patients on
chemotherapy;
• patients complain of blurred vision
Slide 95
Answer
• (A) Illusion of movement where none exists
Slide 96
Oscillopsia
•
•
•
•
(A) Illusion of movement where none exists
(B) Often occurs after upper respiratory infection;
patients present with nystagmus
(C) Characterized as dizziness without hearing
loss;
• treated with topiramate
• (D) Seen in ototoxicity and in patients on
chemotherapy;
• patients complain of blurred vision
Slide 97
Answer
• (D) Seen in ototoxicity and in patients on
chemotherapy; patients complain of blurred
vision
Slide 98
Vestibular neuritis
•
•
•
•
(A) Illusion of movement where none exists
(B) Often occurs after upper respiratory infection;
patients present with nystagmus
(C) Characterized as dizziness without hearing
loss;
• treated with topiramate
• (D) Seen in ototoxicity and in patients on
chemotherapy;
• patients complain of blurred vision
Slide 99
Answer
• (B) Often occurs after upper respiratory
infection; patients present with nystagmus
Slide 100
Choose the correct statement about
benign paroxysmal positional vertigo
(BPPV).
(A) Rotary nystagmus occurs
immediately after movement (eg, to
lying down position)
(B) Uncomplicated BPPV improves
within days to weeks
(C) Epley maneuver recommended for
elderly patients
(D) Most commonly caused by alcohol
and drug use
Slide 101
Answer
• (B) Uncomplicated BPPV improves within
days to weeks
Slide 102
Which of the following medications
is recommended for severe
endolymphatic hydrops?
(A) Dimenhydrinate
(B) Prednisone
(C) Sublingual lorazepam
(D) Nortriptyline
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Answer
• (C) Sublingual lorazepam
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If a patient is found to have shortterm memory loss, headaches, and
loss of sense of smell after head
trauma, the
most likely cause is:
(A) A central concussion
(B) A cervical injury
(C) A perilymph fistula
(D) Whiplash
Slide 105
Answer
• (A) A central concussion
Slide 106
In the Atrial Fibrillation Follow-up
Investigation of Rhythm
Management (AFFIRM) trial,
patients randomized to
rate control therapy had a
significantly higher incidence of
stroke than those who received
rhythm control therapy.
(A) True (B)False
Slide 107
Answer
• (B)False
Slide 108
When considering therapy for
patients with atrial fibrillation (AF),
which of the following factors might
favor rate
control over rhythm control therapy?
(A) Persistent AF
(B) Older age
(C) Hypertension
(D) All the above
Slide 109
Answer
• (D) All the above
Slide 110
Which of the following therapies is
recommended for a patient with AF
and CHADS2 score of 0?
(A) Warfarin with maintenance of
international normalized ratio at 2 to
3
(B) Aspirin or warfarin
(C) Aspirin or no medication
(D) Aspirin and clopidogrel
Slide 111
Answer
• (C) Aspirin or no medication
Slide 112
In elderly patients, warfarin appears
to be more effective than aspirin at
preventing thromboembolism, but is
associated with increased risk of
bleeding.
(A) True (B) False
Slide 113
Answer
• (A) True
Slide 114
ACKNOWLEDGMENTS
Co-Editors:
Karen Blackstone, MD
Elizabeth L. Cobbs, MD
GRS6 Chapter Authors:
David Bush, MD
Kurt Kroenke, MD
GRS6 Question Writers:
Gail Ishiyama, MD
Mathew Maurer, MD
Medical Writer:
Barbara B. Reitt, PhD, ELS(D)
Reviewer:
Colleen Christmas, MD
Managing Editor:
Andrea N. Sherman, MS
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© American Geriatrics Society