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  • syncope - HCM and other causes

    Post Graduate Medicine

    January, 2003

    SECTION: CME CREDIT ARTICLE; Vol. 113, No. 1; Pg. 31

    LENGTH: 4696 words

    HEADLINE: Discovering the cause of syncope

    BYLINE: Karen E. Hauer, MD; Karen E. Hauer, MDDr Hauer is assistant clinical
    professor of medicine and director of internal medicine clerkships, University
    of California, San Francisco, School of Medicine. Correspondence: Karen E.
    Hauer, MD, University of California, San Francisco, School of Medicine, Division
    of General Internal Medicine, 400 Parnassus Ave, Box 0320, San Francisco, CA
    94143. E-mail: [email protected].

    HIGHLIGHT:
    A guide to the focused evaluation

    BODY:

    PREVIEW Syncope has many causes. Although the most common ones are generally
    benign and do not require extensive evaluation, cardiac syncope has high rates
    of recurrence and death. In this article, Dr Hauer describes how physical
    examination and electrocardiographic findings can guide further evaluation to
    provide the largest diagnostic yield at the lowest cost.

    Syncope is a common problem, accounting for 3% of emergency department
    visits.1 (Reference) Evaluation of syncope can be challenging for many reasons.
    First, syncope is not a diagnosis; rather, it is a symptom with many possible
    causes. Common causes, such as the vasovagal faint, are not serious. However,
    other causes are deadly and require further investigation. In addition, the
    history of a syncopal event often is unclear because the patient has amnesia and
    there were no witnesses to the event. As many as 45% of cases elude diagnosis
    after a standard workup, and many tests commonly used in syncope evaluation are
    costly and have a low diagnostic yield.2,3 (Reference) Syncope is caused by
    transient loss of blood flow to the areas of the brain necessary for
    consciousness, the brainstem reticular activating system and the bilateral
    cerebral cortices. Cerebral perfusion can be diminished because of decreased
    cardiac output, loss of vascular tone, or cerebrovascular disease. Differential
    diagnostic considerations include other disorders that can cause loss of
    consciousness, such as seizure, narcolepsy, and metabolic or drug-induced
    encephalopathy. Drop attacks are characterized by a sudden loss of postural tone
    without loss of consciousness. Sudden cardiac death is similar to syncope but
    requires intervention (ie, electrical or chemical cardioversion for
    tachyarrhythmias or atropine sulfate or a pacemaker for bradyarrhythmias) to
    restore normal mental status and cardiac rhythm.

    Causes

    The chief causes of syncope and the approximate percentage of patients with each
    diagnosis are shown in table 1.

    Cardiac disease Historical clues that suggest a cardiac origin of syncope
    include associated palpitations, sudden syncope without preceding symptoms, and
    known organic heart disease. Syncope due to aortic stenosis or hypertrophic
    cardiomyopathy is often preceded by exertion, when cardiac output cannot meet
    increased demand. Palpitations may signal supraventricular or ventricular
    tachyarrhythmias, and patients with bradyarrhythmias or conduction block may
    have weakness, dizziness, or symptoms of associated tachyarrhythmias.

    Physical examination may show left or right ventricular hypertrophy or
    dilation, murmurs (ie, of aortic stenosis, hypertrophic subaortic stenosis, or
    tricuspid regurgitation), gallops, irregular cardiac rate or rhythm, or a loud
    S2 suggestive of pulmonary hypertension. Some disorders that cause cardiac
    outflow obstruction also predispose patients to arrhythmogenic syncope. For
    instance, genetic hypertrophic cardiomyopathy is associated with ventricular
    arrhythmias and sudden cardiac death, and infiltrative cardiomyopathy due to
    sarcoidosis or amyloidosis can cause conduction system disease.

    Neurologic disease Although seizure is not a true cause of syncope, it is often
    a differential diagnostic consideration. Historical features suggestive of
    seizure include tonic-clonic movements, incontinence, postictal mental status
    changes, loss of consciousness for longer than 5 minutes, and lateral tongue
    biting.4 (Reference) A postictal state is the most helpful historical feature
    for diagnosis of seizure. Because tonic-clonic activity and incontinence also
    can be caused by cardiac syncope, these features alone do not confirm a
    diagnosis of seizure. Cerebrovascular disease is an uncommon cause of syncope.
    Vertebrobasilar insufficiency causing syncope generally has other associated
    symptoms of posterior circulation insufficiency, such as vertigo, diplopia,
    ataxia, and dysarthria. Carotid artery disease does not cause loss of
    consciousness unless both carotid arteries are involved.

    Reflex-mediated syncope Neurocardiogenic syncope results from an exaggerated
    reflex response, usually to upright posture. Normally, decreased venous return
    stimulates increased cardiac contractility and peripheral vasoconstriction to
    maintain blood pressure. In some patients, this physiologic response stimulates
    cardiac mechanoreceptors in the left ventricular wall, leading to a complex
    cascade of sympathetic inhibition and parasympathetic stimulation (figure 1).

    Vasovagal syncope, the most common type of syncope, results from this
    mechanoreceptor reflex and is usually triggered by pain, strong emotion,
    prolonged standing, or stress. ''Situational'' syncope is similar to vasovagal
    syncope but is stimulated by micturition, defecation, cough, or deglutition.
    Carotid sinus hypersensitivity can cause bradycardia, hypotension, or both.
    Abnormal carotid hypersensitivity is common in older men with other
    cardiovascular disease, although not all of them experience syncope.

    Orthostatic hypotension is defined as a fall in systolic blood pressure of
    greater than 20 mm Hg upon assuming upright posture. This condition results from
    volume depletion, use of certain medications (particularly
    antihypertensives, vasodilators, and negative chronotropes), primary autonomic
    insufficiency, or secondary autonomic insufficiency due to diabetes mellitus,
    amyloidosis, or alcohol abuse. Orthostatic intolerance is more common in the
    elderly than in the young.

    Psychiatric disease Psychiatric disease as a cause of syncope is always a
    diagnosis of exclusion. Dizziness and syncope may be symptoms of a variety of
    psychiatric diseases, such as anxiety, depression, somatization, panic disorder,
    and substance abuse. Patients with unexplained syncope and psychiatric diagnoses
    are more likely to have multiple somatic complaints, to report frequent syncope,
    and to be younger than those without psychiatric diagnoses.5 (Reference)

    Diagnostic evaluation

    A diagnostic algorithm for syncope is shown in figure 2. A carefully taken
    history and thorough physical examination yield a diagnosis in 45% of patients
    with syncope.6 (Reference) Helpful information regarding the setting includes
    any precipitant of reflex-mediated syncope, such as posture change, coughing,
    swallowing, head turning, defecation, pain, strong emotion, fear, or prolonged
    standing. Associated symptoms of reflex-mediated syncope include nausea, pallor,
    warmth, diaphoresis, confusion, and palpitations. Patients rapidly recover clear
    mental status after the event, although bradycardia may persist for minutes to
    hours. The speed of recovery is helpful in distinguishing syncope from seizure,
    which typically has a postictal state.

    Palpitations or sudden syncope suggests underlying arrhythmia (although
    nonsudden syncope does not exclude arrhythmia). A personal or family history of
    cardiac disease (eg, hypertrophic cardiomyopathy), sudden cardiac death (due,
    for example, to hypertrophic cardiomyopathy, long QT syndrome), or neurologic
    disease (eg, seizure, cerebrovascular disease) is another clue.

    Antiarrhythmic agents and tricyclic antidepressants are potentially
    proarrhythmic, meaning that normally nontoxic drug levels can provoke
    arrhythmias, especially in the presence of underlying congestive heart failure
    (CHF). Oral hypoglycemic agents can cause hypoglycemia-induced loss of
    consciousness. Beta blockers and calcium channel blockers can cause bradycardia
    and hypotension, both of which can precipitate syncope.

    Physical examination may demonstrate abnormalities in heart rate or blood
    pressure, including orthostatic changes. Cardiovascular examination may reveal
    evidence of chamber hypertrophy, pulmonary hypertension, murmurs, gallops, or
    CHF. In the absence of carotid bruits, cerebrovascular disease, transient
    ischemic attack, or stroke, carotid sinus massage for up to 5 seconds is useful
    to elicit carotid sinus hypersensitivity. Such hypersensitivity is defined as a
    3-second pause in rhythm, a 30-mm Hg symptomatic drop in systolic blood
    pressure, or a 50-mm Hg asymptomatic drop.7 (Reference)
    Electrocardiographic monitoring during the maneuver is essential to observe and
    characterize changes in heart rate or rhythm. A thorough neurologic examination
    is crucial to document any focal findings that would prompt further neurologic
    testing.

    The 12-lead electrocardiogram (ECG) adds only a 5% diagnostic yield to the
    history and physical examination.6 (Reference) An ECG is nonetheless routinely
    recommended because it can reveal clues to underlying cardiac disease, including
    substrate for life-threatening ventricular arrhythmias (ie, Q waves, ventricular
    hypertrophy, or long QT interval) or bradycardia (ie, baseline bradycardia or
    type II second- or third-degree heart block). Premature atrial and ventricular
    contractions are nonspecific and common. Abnormalities identified on history
    taking, physical examination, and electrocardiography should selectively guide
    further testing.

    Cardiac evaluation Cardiac testing is indicated for patients in whom cardiac
    disease is suspected on the basis of symptoms, medical history, physical
    examination, or electrocardiographic findings.

    Tests to rule out myocardial infarction generally should be limited to
    patients with anginal symptoms or electrocardiographic evidence of cardiac
    ischemia or infarction.8 (Reference)

    Telemetry may be indicated for suspected arrhythmogenic syncope. In a
    prospective study of 2,240 medical and cardiac patients admitted to a telemetry
    unit,9 (Reference) the yield of telemetry was quite low, with less than 1% of
    patients requiring transfer to the intensive care unit for management of an
    arrhythmia. Telemetry can be helpful to rule out arrhythmogenic syncope when
    symptoms occur with concurrent normal telemetry.

    The diagnostic yield of echocardiography is about 5% to 10% in unselected
    syncope patients.6 (Reference) Echocardiography is indicated when structural
    heart disease is suspected. Evidence of myocardial infarction or CHF indicates a
    possible arrhythmia focus. Echocardiography should always be performed before a
    stress test if left ventricular outflow obstruction due to aortic stenosis or
    hypertrophic cardiomyopathy is suspected; these conditions are
    contraindications to stress testing.

    Exercise stress testing is indicated in the evaluation of exertional syncope
    after left ventricular outflow obstruction has been excluded by examination or
    echocardiography. Stress testing can rule out cardiac ischemia or
    catecholamine-mediated ventricular tachycardia. In the absence of a history of
    exertional syncope, the diagnostic yield of stress testing in unselected syncope
    patients is only 1%.6 (Reference)

    Additional evaluation for arrhythmia can be performed with more prolonged or
    invasive testing. The ambulatory Holter monitor is worn for 24 to 48 hours while
    the patient performs usual daily activities. The brief duration of monitoring is
    the main limitation except in patients with daily symptoms. Patients must be
    able to keep an accurate diary of symptoms so changes in rhythm can be
    correlated with symptoms.

    The continuous-loop event recorder is a convenient and cost-effective device
    that monitors cardiac arrhythmias over several weeks, overcoming the main
    limitation of the Holter monitor. Diagnostic yield ranges from 6% to 31%.10
    (Reference) Electrodes placed on the chest wall transmit data to a small
    monitoring device worn on the belt or wrist. Data are stored and discarded
    continuously. The patient must be able to activate the device before or after
    symptoms occur, prompting it to save data for about 1 minute prior to and
    several minutes after activation. Pacemaker-sized surgically implanted event
    monitors can be helpful in evaluating syncope that occurs less than once a
    month.11 (Reference)

    The signal-averaged ECG filters multiple QRS complexes to uncover late
    potentials arising from abnormal myocardium, in which reentry and ventricular
    tachycardia may arise. A normal signal-averaged ECG predicts a low risk of
    subsequent ventricular tachycardia, particularly when the ejection fraction is
    normal. However, the test is less accurate than electrophysiologic studies in
    predicting ventricular arrhythmias and cannot obviate the need for further
    cardiac evaluation regardless of the result among patients with known coronary
    artery disease or left ventricular dysfunction.

    Electrophysiologic testing is the ''gold standard'' for diagnosis of
    arrhythmias. It is recommended for patients with syncope and a history
    suggestive of arrhythmia or with idiopathic syncope and known underlying heart
    disease. The diagnostic yield is low in patients without underlying cardiac
    disease.

    Reflex-mediated syncope Tilt table testing demonstrates neurocardiogenic syncope
    that is suspected but not confirmed by history taking and physical examination.
    In the passive tilt table test, the patient lies on a board in the supine
    position and then the table is tilted, usually to an angle of 60 degrees for 40
    minutes.12 (Reference) A positive response, defined as a symptomatic drop in
    heart rate or blood pressure, occurs after an average of 24 minutes. If the
    response is negative, injection of isoproterenol hydrochloride (Isuprel) may
    increase the diagnostic yield by augmenting cardiac contractility and
    stimulating the neurocardiogenic cascade. Typically, isoproterenol is given at a
    rate of 1 g/min while the patient is tilted to 60 degrees, and the dose is
    adjusted upward until a positive response is achieved. Among patients with
    idiopathic syncope, 49% have a positive response to the passive tilt test and
    66% have a positive response after injection of isoproterenol. The specificity
    of the passive tilt test for neurocardiogenic syncope is about 90%. Specificity
    is lower with isoproterenol.12,13 (Reference)

    The accuracy of tilt table testing is difficult to determine. The test is
    not performed unless findings from history taking and physical examination are
    ambiguous, thus leaving no ''gold standard'' with which to compare the results.
    The protocol for the tilt table test (ie, angle, duration, and use of
    isoproterenol) is not standardized, and the reproducibility is only 71% to 87%
    owing to the many factors that influence autonomic function.

    Treatment options for recurrent neurocardiogenic syncope include lifestyle
    modifications, such as avoiding triggers and liberalizing salt intake to enhance
    intravascular volume. Beta blockers, anticholinergics, the antiarrhythmic
    disopyramide (Norpace), and the alpha agonist midodrine hydrochloride
    (ProAmatine) blunt the neurocardiogenic reflex, and the corticosteroid
    fludrocortisone (Florinef) acetate increases volume. Fluoxetine hydrochloride
    (Prozac) also may be effective. Tilt table testing can be repeated to document
    therapeutic efficacy, although as many as 30% of patients with a positive
    response have a negative response to the second test regardless of therapy.
    Cardiac pacing is helpful for cardioinhibitory (bradycardic) syncope. Dual
    chamber pacing helps avoid vasodilation resulting from
    atrioventricular dissociation.

    Neurologic disease All syncope patients with focal neurologic signs or symptoms
    should undergo neuroimaging. Patients without focal neurologic findings should
    not routinely undergo neuroimaging. Similarly, electroencephalography has a low
    diagnostic yield and is not indicated in the absence of findings suggestive of
    seizure. It may be helpful in evaluating suspected seizure, although the limited
    sensitivity and specificity must be recognized; normal findings in a patient
    with a convincing seizure history do not rule out seizure, and abnormal findings
    alone do not necessarily confirm the presence of a seizure disorder.

    Psychiatric disease Because half of all psychiatric diagnoses may go
    unrecognized during routine syncope evaluation,5 (Reference) physicians need a
    high index of suspicion for psychiatric disease among syncope patients in whom
    medical evaluation was nondiagnostic. Anxiety or panic disorder with
    hyperventilation can be diagnosed by instructing the patient to hyperventilate
    in the office to elicit syncope or presyncopal symptoms. Formal psychiatric and
    substance abuse evaluation may be indicated when the cause of syncope has not
    been determined.

    Idiopathic syncope Depending on the aggressiveness of the workup, as many as 45%
    of patients may be given the diagnosis of idiopathic syncope after routine
    evaluation.6,14,15 (Reference) Although patients with idiopathic syncope have a
    good prognosis, equivalent to that of age-matched controls, recurrent syncope
    can have important lifestyle implications for driving or work. A diagnostic
    approach to unexplained syncope is included in figure 2.

    Hospitalization and prognosis

    The decision to hospitalize a patient with syncope depends on the prognosis and
    -- most important -- the physician's ability to identify patients at high risk
    for lethal arrhythmias that could be treated during hospitalization. Prognosis
    depends on whether the origin of syncope is cardiac or noncardiac. For example,
    in a prospective study of 433 syncope patients,15 (Reference) the 1-year
    mortality rate after cardiac syncope was about 25% and the 1-year risk of sudden
    cardiac death 14%. In contrast, the 1-year mortality rate after noncardiac or
    idiopathic syncope was 6% to 8% and the 1-year risk of sudden cardiac death only
    3%. Of note, cardiac syncope carries a lower mortality rate today than in the
    past because electrophysiologic testing is now more commonly used.

    Physicians in the emergency department may not know whether syncope is
    cardiac or noncardiac in origin. Four predictors of poor outcome among syncope
    patients on initial presentation are an abnormal ECG (not nonspecific ST or T
    wave changes or sinus tachycardia), prior ventricular arrhythmia (defined as at
    least 10 premature ventricular contractions an hour or repetitive [>2] or
    multifocal premature ventricular contractions), a history of CHF, and age
    greater than 45 years.16 (Reference) The risk of arrhythmia or death at 1 year
    ranges from 5% for patients with no risk factors, to 16% with one risk factor,
    to more than 60% with three or four risk factors. My colleagues and I recommend
    that patients with even one risk factor and a history suggestive of cardiac
    syncope undergo cardiac evaluation.

    The guideline for hospitalization after syncope from the American College of
    Physicians (table 2) targets patients who would benefit from inpatient
    diagnostic evaluation or from therapies that could improve outcome over several
    days of hospitalization.

    Elderly patients

    Syncope from any cause in an elderly patient portends a poor prognosis. In a
    study of syncope in elderly (age, >60) and young patients,14 (Reference) all
    patients with cardiac syncope had 2-year mortality rates of 32% to 38%; in
    patients with noncardiac syncope, elderly patients had a much higher mortality
    rate (22%) than younger patients (5%). The high mortality rate among the elderly
    may have been due to comorbidities and suggests that patients in this age-group
    should receive close follow-up care regardless of syncope origin.

    As with other geriatric syndromes, syncope in the elderly is often
    multifaceted, frustrating physicians who seek a unifying diagnosis (table 3). A
    reasonable management strategy for elderly syncope patients with multiple risk
    factors is to correct these factors before more invasive testing is done.
    Cardiac disease should be ruled out on the basis of clues provided during
    history taking, physical examination, and electrocardiography or by selective
    further testing. If not contraindicated by carotid bruit, cerebrovascular
    disease, or a history of transient ischemic attack or stroke, carotid sinus
    massage is helpful in diagnosis of carotid sinus hypersensitivity.

    Indications for referral or consultation

    Cardiologic referral is advised for syncope patients with a documented or
    suspected cardiac origin on the basis of arrhythmia, underlying cardiac disease
    or, possibly, advanced age alone. A cardiologist typically considers invasive
    testing, including an electrophysiologic study. A neurologist should evaluate
    syncope patients with abnormal findings on neurologic examination or documented
    seizures. For patients with recurrent syncope and suspected psychiatric disease,
    psychiatric consultation is helpful for both diagnostic evaluation and
    psychiatric management.

    Recommendations for driving

    Physicians often are asked to make recommendations to their patients about
    driving after a syncopal event. Laws regarding the use of private motor vehicles
    are made at the state level. Although physicians are obligated to know the laws
    of their own state regarding the reporting of syncopal events to the motor
    vehicles department and driving by patients after syncope, physicians'
    recommendations and awareness of the law are highly variable.17,18 (Reference)
    The American Heart Association and the North American Society of Pacing and
    Electrophysiology19 (Reference) issued a statement in 1996 pertaining to driving
    after syncope, with specific recommendations based on arrhythmia type and
    severity (table 4).

    Conclusion

    Syncope is a symptom with many possible causes, including cardiac, neurologic,
    reflex-mediated, and psychiatric disorders. All patients with syncope should
    provide a thorough history and undergo physical examination and
    electrocardiographic testing. Information obtained during this initial
    evaluation guides further testing. One-year mortality and sudden cardiac death
    rates are highest after syncope caused by underlying cardiac disease. Patients
    with other origins of syncope or with idiopathic syncope generally have a good
    prognosis. PGM

    The author thanks Nora Goldschlager, MD, for her critique of the manuscript.

    The author discloses no financial interests in this article.

    1. Day SC, Cook EF, Funkenstein H, et al. Evaluation and outcome of emergency
    room patients with transient loss of consciousness. Am J Med 1982;73(1):15-23
    2. Calkins H, Byrne M, el-Atassi R, et al. The economic burden of unrecognized
    vasodepressor syncope. Am J Med 1993;95(5):473-9
    3. Junaid A, Dubinsky IL. Establishing an approach to syncope in the emergency
    department. J Emerg Med 1997;15(5):593-9
    4. Benbadis SR, Wolgamuth BR, Goren H, et al. Value of tongue biting in the
    diagnosis of seizures. Arch Intern Med 1995;155(21):2346-9
    5. Kapoor WN, Fortunato M, Hanusa BH, et al. Psychiatric illnesses in patients
    with syncope. Am J Med 1995;99(5):505-12
    6. Linzer M, Yang EH, Estes NA III, et al. Diagnosing syncope. Part 1: Value of
    history, physical examination, and electrocardiography. Clinical Efficacy
    Assessment Project of the American College of Physicians. Ann Intern Med
    1997;126(12):989-96
    7. Manolis AS, Linzer M, Salem D, et al. Syncope: current diagnostic evaluation
    and management. Ann Intern Med 1990;112(11):850-63
    8. Georgeson S, Linzer M, Griffith JL, et al. Acute cardiac ischemia in patients
    with syncope: importance of the initial electrocardiogram. J Gen Intern Med
    1992;7(4):379-86
    9. Estrada CA, Rosman HS, Prasad NK, et al. Role of telemetry monitoring in the
    nonintensive care unit. Am J Cardiol 1995;76(12):960-5
    10. Zimetbaum PJ, Josephson ME. The evolving role of ambulatory arrhythmia
    monitoring in general clinical practice. Ann Intern Med 1999;130(10):848-56
    11. Krahn AD, Klein GJ, Yee R, et al. Use of an extended monitoring strategy in
    patients with problematic syncope. Reveal Investigators. Circulation
    1999;99(3):406-10
    12. Kapoor WN, Smith MA, Miller NL. Upright tilt testing in evaluating syncope:
    a comprehensive literature review. Am J Med 1994;97(1):78-88
    13. Benditt DG, Ferguson DW, Grubb BP, et al. Tilt table testing for assessing
    syncope. American College of Cardiology. J Am Coll Cardiol 1996;28(1):263-75
    14. Kapoor W, Snustad D, Peterson J, et al. Syncope in the elderly. Am J Med
    1986;80(3):419-28
    15. Kapoor WN. Evaluation and outcome of patients with syncope. Medicine
    1990;69(3):160-75
    16. Martin TP, Hanusa BH, Kapoor WN. Risk stratification of patients with
    syncope. Ann Emerg Med 1997;29(4):459-66
    17. Linzer M, Yang EH, Estes NA III, et al. Diagnosing syncope. Part 2:
    Unexplained syncope. Clinical Efficacy Assessment Project of the American
    College of Physicians. Ann Intern Med 1997;127(1):76-86
    18. Lurie KG, Iskos D, Sakaguchi S, et al. Resumption of motor vehicle operation
    in vasovagal fainters. Am J Cardiol 1999;83(4):604-6
    19. Strickberger SA, Cantillon CO, Friedman PL. When should patients with lethal
    ventricular arrhythmia resume driving? An analysis of state regulations and
    physician practices. Ann Intern Med 1991;115(7):560-3
    20. Epstein AE, Miles WM, Benditt DG, et al. Personal and public safety issues
    related to arrhythmias that may affect consciousness: implications for
    regulation and physician recommendations. A medical/scientific statement from
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    Electrophysiology. Circulation 1996;94(5):1147-66


    Table 1. Causes of syncope
    Cause Prevalence
    Cardiac
    Arrhythmia 14%
    Mechanical* 4%
    Neurologic 10%
    Neurally mediated
    Vasovagal 18%
    ''Situational'' 5%
    Orthostatic 8%
    Psychiatric 2%
    Idiopathic 34%
    *Obstruction to cardiac outflow, decreased ejection fraction, and decreased

    ventricular filling (ie, pulmonary embolus, pulmonary hypertension, and cardiac

    tamponade).
    Adapted from Linzer et al.6 (Reference)



    Table 2. American College of Physicians criteria for hospitalization after

    syncope
    Definitely hospitalize patients who meet any of the following criteria:
    -- A history of chest pain
    -- A past history of coronary artery disease, congestive heart failure, or

    ventricular arrhythmia
    -- Physical examination findings of congestive heart failure, valvular disease,

    or focal neurologic deficit
    -- An electrocardiogram showing ischemia or infarction, arrhythmia, or bundle

    branch block
    Strongly consider hospitalizing patients who meet any of the following criteria:
    -- A history of exertional syncope (in the absence of physical examination

    evidence of aortic stenosis or other left ventricular outflow obstruction),

    frequent syncope, or age >70 yr
    -- Physical examination findings of tachycardia, orthostatic changes, or injury
    -- Suspected cardiac disease
    Adapted from Linzer et al.17 (Reference)



    Table 3. Common risk factors for syncope in the elderly
    Susceptibility to situational syncope
    Polypharmacy and adverse drug effects on heart rate, intravascular volume, and

    vascular tone (with use of beta blockers, calcium channel blockers,

    antiarrhythmics, diuretics, antidepressants)
    Serious cardiac and neurologic disease, other comorbidities, or atypical

    presentation of disease
    Decreased physiologic reserve



    Table 4. Guidelines for driving after syncope or arrhythmia
    Patient with ventricular tachycardia or fibrillation treated with medical

    therapy or implantable cardiac defibrillator
    -- Risk of recurrent arrhythmia is greatest in first 6 mo, up to 10% at 1 yr
    -- Recommendation: Patient may resume driving after arrhythmia-free for 6 mo
    Patient with bradycardia and syncope
    -- Recommendation: Patient may resume driving 1 wk after successful pacemaker

    insertion
    Patient with neurocardiogenic syncope
    Mild (presyncope, clear warning, and precipitant)
    -- Recommendation: Patient may resume driving immediately
    Severe (frequent with no warning or precipitant)
    -- Recommendation: Patient should not resume driving until after institution of

    therapy and a waiting period of unspecified duration
    Adapted from Epstein et al.20 (Reference)
    Knowledge is power ... Stay informed!
    YOU can make a difference - all you have to do is try!

    Dx age 12 current age 46 and counting!
    lost: 5 family members to HCM (SCD, Stroke, CHF)
    Others diagnosed living with HCM (or gene +) include - daughter, niece, nephew, cousin, sister and many many friends!
    Therapy - ICD (implanted 97, 01, 04 and 11, medication
    Currently not obstructed
    Complications - unnecessary pacemaker and stroke (unrelated to each other)

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