Practical Neurology, 4th Ed.

7. Approach to the Patient with Syncope

Syncope is usually defined as transient loss of consciousness and postural tone followed by spontaneous recovery. It has been proposed that application of this term be limited to the subgroup of these related to transient global cerebral hypoperfusion (distinguishing transient loss of consciousness from other causes such as seizure, trauma, or psychogenic causes); however, usage of the term varies. In the United States alone, up to 5% of all emergency room visits and hospital admissions are due to syncope, thereby accounting for approximately 300,000 emergency department visits and 100,000 admissions per year. More than a million individuals a year are evaluated for syncope and related injuries (e.g., falls, fractures, etc.), thus imposing a high cost burden on the health care system.

I. ETIOLOGY

Syncope broadly defined is most commonly cardiovascular in etiology. Most often, a generalized or local cerebral impairment of blood/oxygen delivery causes the loss of consciousness. Despite frequent referral for neurologic investigation after syncope, primary neurologic causes of syncope are uncommon (excepting neurocardiogenic/vasovagal episodes).

Even in cases where seizure-like motor activity is witnessed after the loss of consciousness, these may be a consequence of a cardiovascular etiology and an assessment for such is often warranted. Other causes of transient loss of consciousness may present similarly and at times may be difficult to distinguish on initial evaluation.

Cardiovascular causes include decreased cardiac output secondary to abnormalities in heart rate and/or stroke volume, impairment of cerebral blood flow, and decreased blood pressure related to hypovolemia or decreased peripheral vascular resistance. Any medical condition causing one of these features may lead to the development of syncope. As shown in Table 7.1, the causes of syncope can be classified into broad categories: neurally mediated syncope, orthostatic hypotension, cardiac arrhythmias, structural heart disease, and cerebrovascular steal syndromes. Based on pooled data from five studies, the incidence of the major causes of syncope is shown in Table 7.2.

Often multiple mechanisms can contribute to the syncope. For example, medications or postprandial fluid shifts can exacerbate mild preexisting orthostatic hypotension, sinus node dysfunction, and impaired autoregulation of cerebral blood flow. This is especially true in the elderly in whom syncope is commonly multifactorial.

A. Neurally mediated syncope, also referred to as neurocardiogenic or vasodepressor syncope, is common, and results from the activation of a reflex that produces a significant vasodilatory (vasodepressor) and/or bradycardic (cardioinhibitory) response. Typically, it occurs after prolonged standing or sitting and may be reproduced on tilt-table testing. Long-term follow-up studies have shown that neurally mediated syncope carries a benign prognosis and a similar survival outcome to those patients with no history of syncope. Several different etiologies can lead to neurally mediated syncope as shown in Table 7.1. Almost all of these etiologies can be diagnosed by a carefully taken history. Classic vasovagal syncope may be considered in this group, and usually occurs in the setting of emotional or orthostatic stress, although it can also have an atypical presentation with no clear triggering events or premonitory signs. A careful history should also diagnose the etiology of several causes of situational syncope (e.g., postprandial, postmicturition, postdefecation, etc.). Syncope due to carotid sinus hypersensitivity occurs in the setting of inadvertent mechanical pressure on the carotid sinus and can be reproduced by carotid sinus massage. Glossopharyngeal neuralgia may present with syncope associated with painful swallowing.

TABLE 7.1 Causes of Syncope

Neurally Mediated

Vasovagal syncope

Carotid sinus syncope

Situational syncope (cough, swallow, micturition, defecation, postprandial, etc.)

Glossopharyngeal neuralgia

Orthostatic Hypotension

Volume depletion

Medications

Autonomic failure syndromes

Primary autonomic failure (Parkinson’s disease, MSA)

Secondary autonomic failure (diabetes mellitus, amyloidosis)

Alcohol or illicit drugs

Post-exercise

Cardiac Arrhythmias

Sinus node dysfunction

AV conduction system disease

Paroxysmal supraventricular and ventricular tachycardias

Channelopathies (long QT syndrome, Brugada’s syndrome)

Arrhythmogenic right ventricular dysplasia

Drug-induced (torsades de pointes, bradycardia)

Implantable device malfunction (pacemaker or defibrillator)

Structural Cardiovascular Disease

Obstructive valvular disease, particularly aortic stenosis

Hypertrophic obstructive cardiomyopathy

Atrial myxoma

Aortic dissection

Pericardial tamponade

Pulmonary embolism

Cerebrovascular

Subclavian steal syndrome

Stroke/TIA (uncommon)

Metabolic and other conditions:

Electrolyte derangements

Hypoglycemia

Hypoxemia

Anemia

TABLE 7.2 Incidence of Major Causes of Syncope

 

Cause

Percentage

 

Vasovagal

18

Situational

5

Orthostatic

8

Cardiac

18

Medication

3

Psychiatric

2

Neurologic

10

Carotid sinus

1

Unknown

34

B. Orthostatic hypotension can cause inadequate cerebral perfusion leading to syncope upon rising from a sitting or supine to an upright position. The most common mechanism of hypotension is the loss of peripheral vascular tone due to the failure of the autonomic nervous system to maintain peripheral vascular resistance. This can occur due to a primary dysfunction of the autonomic nervous system associated with several neurodegenerative conditions (multiple systems atrophy [MSA]) or due to diseases causing secondary autonomic nervous system failure (e.g., diabetes, amyloidosis, etc.). MSA encompasses a group of sporadic progressive neurologic disorders characterized clinically by autonomic dysfunction (i.e., orthostatic hypotension, impotence, urinary retention or incontinence, etc.), parkinsonism, and ataxia in any combination. Medications, alcohol, and drug toxicity should also be considered when evaluating orthostatic hypotension. Volume depletion (e.g., dehydration, hemorrhage, Addison’s disease, etc.) may cause orthostatic syncope.

C. Cardiac arrhythmias often present with syncope due to a decrease in cardiac output. This can occur in bradycardia (e.g., sinus arrest, heart block, etc.) or tachycardia (e.g., nonsustained ventricular tachycardia/fibrillation). It is relatively uncommon for supraventricular tachycardias to cause syncope in the absence of other structural heart disease or the Wolff–Parkinson–White’s syndrome (i.e., preexcited atrial fibrillation). Arrhythmic syncope may indicate a risk for sudden death and should be aggressively managed. In patients with congestive heart failure (CHF), syncope is associated with an increased risk for cardiovascular and total mortality.

D. Structural heart disease can cause syncope due to the inability to produce sufficient cardiac output to match demand. Obstructive valvular heart disease and hypertrophic cardiomyopathy are common etiologies. Primary pump failure due to myocardial dysfunction can also lead to syncope; however, associated ventricular arrhythmias are a more common cause. Other less common conditions include atrial myxoma, pericardial tamponade, and acute aortic dissection.

E. Cerebrovascular causes of syncope are rare. These include steal syndromes, such as subclavian steal, in which cerebral blood is shunted away from the brain. Obstruction of cerebral blood flow is a rare cause of true syncope. Most carotid artery distribution transient ischemic attacks (TIAs) cause unilateral visual impairment, weakness, or loss of sensation. Posterior circulation TIAs generally manifest as diplopia, vertigo, ataxia, or “drop attacks,” but not loss of consciousness. Rare patients with TIA may have transient loss of consciousness, but isolated syncopal episodes without accompanying neurologic symptoms should generally not be ascribed to a TIA.

F. Psychogenic syncope occurs without any substantial changes in hemodynamics and is often associated with a prior significant psychologic event. Physical causes must be excluded. It and other causes are included in the differential diagnosis of transient loss of consciousness, but are usually distinguished from true syncope.

G. Syncope of unknown origin is a legitimate diagnosis made after a careful history, physical examination, and selected laboratory tests have failed to elucidate a specific etiologic factor. This diagnosis is clinically useful because it is associated with a prognosis that is considerably better than that of patients who have identifiable cardiac or neurologic causes of syncope. Although long-term follow-up studies have shown that patients with syncope and a history of cardiac or neurologic disease have increased long-term mortality, those patients with syncope of unknown causation have a distinctly better prognosis.

II. EVALUATION

Initial evaluation of syncope should address three key questions:

• Is the loss of consciousness attributable to true syncope or to other nonsyncopal factors? A careful history is crucial for making the diagnosis and excluding nonsyncopal etiologies. Table 7.3 lists some conditions that are commonly distinguished from syncope, some of which are associated with a transient loss of consciousness.

• Are there any distinguishing features in the history that may suggest the diagnosis?Table 7.4 lists features of vasovagal syncope, seizures, and cardiac syncope.

• Does the patient have heart disease? Patients with syncope have a fairly benign clinical course in the absence of heart disease. On the other hand, the presence of cardiac disease carries a much more ominous prognosis.

A. History. In order to address the above questions, a detailed history is required. The history is the most crucial component of the evaluation of syncope. Particular attention should be paid to the following points:

1. Events leading to syncope. A patient’s activity and posture before the episode should be noted. An episode occurring in a supine position suggests either an arrhythmic etiology or seizure, and makes a neurally mediated etiology or orthostatic hypotension unlikely. Conversely, syncope occurring during prolonged standing is likely neurocardiogenic. Vasovagal syncope should be suspected if the event was triggered by fear, pain, emotional distress, or instrumentation.

TABLE 7.3 Conditions to be Distinguished from Syncope

Disorders Not Associated with Loss of Consciousness

Falls

Drop attacks

Disorders Associated with Loss of Consciousness

Psychogenic (may or may not have loss of consciousness)

Metabolic disorders

Hypoglycemia

Hypoxia

Hyperventilation with hypocapnia

Epilepsy

Medication/pharmacologic (anesthetic/sedating including recreational drugs, alcohol)

TABLE 7.4 Typical Features of Vasovagal Syncope, Seizure, and Cardiac Syncope

Syncope that occurs after rising from a supine or sitting position is consistent with orthostatic hypotension. Syncope occurring during or immediately after urination, defecation, coughing, or swallowing is a feature of situational syncope. Postprandial syncope is characterized by episodes that occur 15 to 90 minutes following meals. Syncope in the setting of neck manipulation such as extension, flexion, rotation, or compression (e.g., a tight shirt collar, necktie, or during shaving) may suggest carotid sinus hypersensitivity.

Syncope in the setting of exercise is particularly worrisome for a cardiac etiology. Syncope during physical exertion is a characteristic finding in aortic stenosis, atrioventricular (AV) block, or tachyarrhythmias, whereas loss of consciousness after exercise should arouse suspicion for hypertrophic cardiomyopathy or ventricular arrhythmia.

2. Prodromal signs and symptoms often provide clinically relevant information. Very brief prodromal symptoms lasting only seconds are a characteristic of cardiac causes, situational syncope, and orthostatic hypotension. Cardiac causes of syncope often do not have any prodromal symptoms or may present with dizziness and/or palpitations. On the other hand, vasovagal syncope typically has a more sustained warning period accompanied by symptoms of nausea, diaphoresis, and flushing. Focal neurologic symptoms such as vertigo, diplopia, ataxia, dysarthria, hemiparesis, and unilateral numbness may be indicative of a TIA as the cause of the loss of consciousness.

3. Events during the syncopal period. Obtaining as much detail as possible from witnesses regarding the events during the syncopal episode may be highly valuable. The patient may be amnestic for events before, during, and after the episode. A detailed history confirming the presence of true loss of consciousness and describing neuromuscular activity is extremely important. Although prolonged episodes of cerebral anoxia (more than 10–15 seconds) can induce brief involuntary motor activity, the presence of more sustained episodes of alternating tonic and clonic muscle action is strongly suggestive of a seizure. Urinary incontinence is more frequent among patients with seizure, although it can accompany syncope of any cause. Fecal incontinence is more specific for seizures.

4. Postsyncopal events. Details of events immediately following the loss of consciousness may provide important diagnostic clues. This history may also need to be obtained from witnesses. Prolonged duration of confusion, amnesia, or lethargy is more consistent with seizure activity rather than a cardiac or neurally mediated event. Similarly, the presence of focal neurologic symptoms or signs point to an inciting neurologic event such as a seizure with residual functional deficit (Todd’s paralysis) or ischemic injury. Facial pallor points to syncope, facial plethora is more suggestive of seizure, and diffuse muscle soreness suggests seizure activity (see Chapter 6).

5. Family history. A family history of syncope, arrhythmias, or early sudden cardiac death may point to a genetic condition linked to ventricular arrhythmias, even in the absence of structural heart disease. Such a history should prompt more detailed cardiac investigation.

6. Comorbid conditions. The most important prognostic factor in patients presenting with syncope is the presence of cardiac disease. Thus, special emphasis should be placed on obtaining a detailed history of any cardiovascular pathology such as coronary artery disease, hypertension, CHF, hypertrophic obstructive cardiomyopathy, and valvular disorders. Symptoms associated with cardiac conditions such as palpitations, dyspnea, fluid retention, decreased exercise tolerance, lightheadedness, or chest pain require further workup.

The medical history should address the possibility of neurologic disorders predisposing to seizures mimicking syncope. This includes primary or metastatic neoplasia, as well as a history of previous trauma, infection, ischemic, or hemorrhagic injury to the brain. Medical conditions such as diabetes mellitus, alcohol abuse, vitamin B12 deficiency, or other metabolic disorders are associated with peripheral or autonomic neuropathy and can cause orthostatic hypotension.

A brief gynecologic history should be elicited to identify risk factors for pregnancy, particularly in ectopic locations. Pregnant patients are at increased risk for syncope due to orthostatic hypotension and vasovagal reactions. Moreover, a ruptured ectopic pregnancy occasionally manifests with syncope.

TABLE 7.5 Agents Causing or Exacerbating Orthostatic Hypotension

ACE-Is

ARBs

Alpha-blockers

Beta-blockers

Calcium channel blockers

Nitrates

Sildenafil citrate

Phenothiazines

Opiates

Tricyclic antidepressants

Ethanol

Bromocriptine

Abbreviations: ACE-Is, angiotensin converting enzyme inhibitors; ARBs, angiotensin receptor blockers.

A history of anxiety disorders and depression is important to elucidate. Psychiatric illness should be suspected as a potential etiology, especially in patients with severe, atypical, repetitive, and drug-refractory episodes. Patients with psychogenic syncope may have reproducible symptoms on tilt-table testing despite a normal heart rate, blood pressure, and EEG.

Finally, careful review of the patient’s medication list is essential. Antihypertensive and other drugs can cause syncope by reducing cardiac output and lowering peripheral vascular resistance. As shown in Table 7.5, many psychotropic and antihypertensive medications can induce orthostatic hypotension. Drugs that prolong the QT interval may also present with syncope.

B. Physical examination.

1. Vital signs should include an assessment of orthostatic hypotension, which is defined as a decrease of 20-mm Hg in systolic pressure or 10-mm Hg in diastolic pressure following standing from a supine position. It is important that the supine blood pressure be obtained after at least 5 minutes of recumbency and the standing blood pressure measured initially and again after the patient has been erect for at least 2 minutes.

2. Given the prognostic importance of cardiac disease, a detailed cardiovascular examination should be performed. Palpation of the carotid arteries may demonstrate pulsus parvus et tardus (weak and delayed carotid pulsation), which occurs with hemodynamically significant aortic stenosis, or pulsus bisferiens (biphasic carotid pulsation), which may be found in hypertrophic obstructive cardiomyopathy. Similarly, particular attention should be paid to the presence of systolic-crescendo-decrescendo murmurs, implying the presence of aortic stenosis or hypertrophic obstructive cardiomyopathy. Peripheral edema, elevated jugular venous pressure, pulmonary crackles, hepatomegaly, and a third heart sound (S3) signify heart failure. The presence of a carotid bruit signifies a high likelihood of diffuse atherosclerotic vascular disease involving the cerebral, coronary, and peripheral vasculature. A supraclavicular bruit and a diminished upper extremity arterial pulsation are evidence of subclavian steal syndrome.

If carotid sinus supersensitivity is suspected, carotid massage can be performed in the absence of a bruit or known atheromatous disease. Carotid sinus hypersensitivity can be detected by means of monitoring changes in blood pressure and heart rate after 5 to 30 seconds of unilateral carotid artery massage. Responses are characterized as cardioinhibitory, vasodepressor, or mixed. Carotid sinus hypersensitivity is more common in older patients. Electrocardiographic and resuscitation equipment should be available.

3. A screening neurologic examination should be pursued to detect postictal cognitive impairment, the presence of focal neurologic defects indicative of either acute neurologic injury or a preexisting substrate for a seizure disorder, peripheral neuropathy that would predispose to orthostatic hypotension, or a movement disorder that would cause nonsyncopal falls.

4. A digital rectal examination should be considered if there is concern about gastrointestinal bleeding.

C. Laboratory studies.

1. ECG.

a. Although it carries a low diagnostic yield, the resting 12-lead ECG is an important test for both prognosis and triage. Although it is relatively uncommon for the snapshot in time that the ECG is taken to demonstrate a culprit arrhythmia, the presence of pathologic Q waves, left axis deviation, left bundle branch block, or left ventricular hypertrophy may point to underlying cardiac pathology. Severe sinus bradycardia or AV block may be diagnostic.

Repolarization abnormalities also may provide clues to the etiology of the syncope. These include a long QT interval (long QT syndrome), epsilon wave and precordial T-wave inversions (arrhythmogenic right ventricular dysplasia/cardiomyopathy), and right bundle branch block with saddle back ST elevation in leads V1–V3 (Brugada’s syndrome). Other ECG signs of right heart strain (S1Q3T3 or right bundle branch block pattern) suggest pulmonary embolism.

b. Ambulatory ECG. Patients with recurrent episodes may benefit from ambulatory ECG. This should generally be performed in patients with no significant structural heart disease in whom an arrhythmia is either suspected or needs to be ruled out. Several types of monitors could be used, depending on the frequency of the symptoms: 24-hour continuous recordings, patient-activated looping and nonlooping event monitors that can be worn up to a period of 4 weeks, continuous 24-hour monitors that can also be worn for 4 weeks, and subcutaneous implantable loop recorders for long-term monitoring. Sensitivity and optimal recording duration are dependent on the frequency of events.

Ambulatory monitoring has limited specificity because certain rhythm disturbances, such as brief pauses, premature atrial and ventricular contractions, and nonsustained ventricular tachycardia, can be detected even when they are not responsible for the syncope. Thus, it is important to correlate the findings of ambulatory monitoring with symptoms. If symptoms occur during monitoring and no ECG abnormalities are detected, a rhythm disturbance is effectively excluded as an etiologic factor.

2. Echocardiography is a powerful tool that should be commonly used when disease cardiac cause is suspected clinically. It can provide clues regarding the etiology of syncope such as valvular heart disease or atrial myxoma. More importantly, it can confirm or exclude the presence of left ventricular dysfunction, which is associated with a risk of sudden cardiac death and which carries important prognostic implications.

3. Blood laboratory testing. Serum electrolyte abnormalities should be excluded. Elevated prolactin levels have been reported in some patients hours after generalized tonic–clonic seizures. The same is true for creatine kinase levels, although increased serum concentrations can also be caused by injury during a syncopal episode. Serum glucose levels are most valuable at the time of the event, particularly in the evaluation of diabetic patients who have recently increased their insulin or oral hypoglycemic therapy or decreased their caloric intake. A complete blood count is occasionally helpful if blood loss or severe anemia is suspected.

Arterial blood gas analysis can be useful in the evaluation of the occasional patient in whom pulmonary embolism is suspected because of the history, physical examination findings, or ECG results.

4. Stress testing or coronary angiography to assess for coronary ischemia is appropriate in some patients, particularly the elderly, those with exertional symptoms (syncope, chest pain, or dyspnea), cardiomyopathy, or ventricular arrhythmias.

5. Electrophysiologic testing is used to assess the integrity of the sinus node, cardiac conduction system, as well as the predisposition to ventricular and supraventricular arrhythmias. However, sensitivity is limited. The results are most often abnormal in patients with known heart disease or those with significant abnormalities on a routine ECG. Findings of greatest diagnostic value include inducible monomorphic ventricular tachycardia, markedly abnormal sinus node recovery times, inducible supraventricular tachycardia with hypotension, significant infra-Hisian disease, and pacing-induced infra-Hisian block. Recent studies have shown that patients with underlying left ventricular dysfunction are at high risk for arrhythmic death and benefit from prophylactic defibrillator insertion even in the absence of syncope. Thus, patients with syncope and left ventricular dysfunction may not necessarily benefit from electrophysiological testing to assess inducibility of ventricular arrhythmias.

6. Tilt-table testing. The utility of tilt-table testing for the diagnosis of neurocardiogenic syncope remains poorly defined. It is only a moderately sensitive and specific test. A positive result is reproducible only 70% of the time. The limited reproducibility of the test and the variable natural history of unexplained syncope reduce its utility. Abnormal response patterns to tilt-table testing include the vasovagal response, which consists of a decrease in blood pressure (vasodepressor) and bradycardia (cardioinhibitory), and the dysautonomic response, which represents a failure of the autonomic system to compensate for an acute decrease in venous return that occurs with upright posture. Thus, the heart rate does not significantly change while the blood pressure declines. A third response to tilt-table testing is the postural orthostatic tachycardia response in which there is a significant increase in heart rate in response to upright positioning.

7. Radiographic studies. Routine CT and MRI of the brain have low yields but may be useful in the evaluation of patients who have sustained major head trauma, have a newly diagnosed seizure disorder, or have focal deficits on the neurologic examination.

8. Electroencephalography is not required routinely, but should be performed when clinical evaluation points to seizure or in syncope of undetermined etiology when there is adequate suspicion.

9. Device interrogation. Patients with implanted pacemakers or ICDs should have the devices checked by appropriate personnel. Not only should device malfunction be excluded as a cause of syncope, but modern devices store a plethora of diagnostic information that may be useful in diagnosis.

III. DIAGNOSTIC APPROACH

The majority of syncope is of cardiovascular cause, and the diagnosis often is suggested after a complete history and physical examination. In a new patient without prior evaluation, in addition to establishing the etiology when possible, a primary goal is defining whether the patient is at increased risk for mortality, particularly sudden cardiac death. Some patients with life threatening cardiac disorders may be otherwise asymptomatic. For example highly functional athletes, including at the professional level, may have malignant conditions (hypertrophic cardiomyopathy, genetic causes of ventricular arrhythmias, etc.) that lead to sudden cardiac death.

If the cause is unclear, evaluation of a resting 12-lead ECG should be performed in nearly all patients. Patients with symptoms or signs of cardiac disease, or those with abrupt syncope without warning should receive more detailed cardiac evaluation, which often includes echocardiography, evaluation for coronary artery disease, and referral to a cardiologist or electrophysiologist. Further cardiac testing, including electrophysiological studies and/or long-term cardiac monitoring, may be appropriate. Patients with unexplained syncope at high risk may be appropriate for preventive therapies, including the implantation of cardiac rhythm devices. Those with likely neurocardiogenic syncope should be treated for that disease. If needed, tilt-table testing could be performed to confirm the diagnosis. When the symptoms are deemed not to be of cardiovascular etiology or are nonsyncopal (e.g., seizure, psychogenic, traumatic, etc.), the patient should be managed accordingly or referred to the appropriate specialist.

Recommended Readings

Brignole M. Diagnosis and treatment of syncope. Heart. 2007;93:130–136.

Brignole M, Albani P, Benditt D, et al. Guideline on management (diagnosis and treatment) of syncope. Eur Heart J. 2004;25:2054–2072.

Fenton AM, Hammill SC, Rea RF, et al. Vasovagal syncope. Ann Intern Med. 2000;9:714–725.

Grubb BP, Kosinski D. Dysautonomic and reflex syncope syndromes. Cardiol Clin. 1997;15:257–268.

Kapoor WN. Syncope. N Engl J Med. 2000;25:1856–1862.

Middlekauff HR, Stevenson WG, Stevenson LW, et al. Syncope in advanced heart failure: high risk of sudden death regardless of origin of syncope. J Am Coll Cardiol. 1993;21:110–116.

Moss AJ, Zareba W, Hall J, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med. 2002; 346:877–883.

Moya A, Sutton R, Ammirati F, et al. Guidelines for the diagnosis and management of syncope (version 2009) (Task Force for the Diagnosis and Management of Syncope of the European Society of Cardiology [ESC]; European Heart Rhythm Association [EHRA]; Heart Failure Association [HFA]; Heart Rhythm Society [HRS]). Eur Heart J. 2009;30(21):2631–2671.

Olshansky B, Poole JE, Johnson G, et al. Syncope predicts the outcome of cardiomyopathy patients: analysis of the SCD-HeFT study. J Am Coll Cardiol. 2008;51(13):1277–1282.

Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med. 2002;347:878–885.

Zaidi A, Clough P, Cooper P, et al. Misdiagnosis of epilepsy: many seizure-like attacks have a cardiovascular cause. J Am Coll Cardiol. 2000;36:181–184.



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