Syncope: An Uncommon Presentation of Ischemic Cardiomyopathy

Syncope: An Uncommon Presentation of Ischemic Cardiomyopathy Salah S. Al-Zaiti, ANP-BC, Mohamad K. Khasawneh, MD, and Mary G. Carey, PhD

ABSTRACT A case report of an uncommon presentation of ischemic cardiomyopathy is described. The current evidence regarding risk stratification, diagnosis, and management of cardiac-related syncope is summarized and then applied to the current presentation. Conclusions and clinical implications are discussed. Keywords: ischemic cardiomyopathy, syncope © 2011 American College of Nurse Practitioners

A

53-year-old man presented to the emergency department (ED) for new episode of syncope. The episode occurred at work after prolonged standing and was accompanied with sudden palpitations and blurred vision. A few minutes later, he woke with a coworker by his side and was transported to the ED. Notably, he was exhausted at the time of the attack but reported the loss of consciousness was transient and that he recovered without any residual limitations. He had worked in constructions for 20 years and denied any medications use or cardiac disease; however, he was a heavy smoker for 30 years. A detailed health history revealed that his father died of a myocardial infarction (MI) at age 60. During the physical exam he was alert and oriented, his supine blood pressure (BP) was 120/60 mmHg and his standing BP was 115/55 mmHg, lungs were clear, and there was no abnormal heart sounds or carotid bruits. Motor and sensory functions were intact during the neurologic exam, and head-up tilt test was negative. The complete blood count and comprehensive metabolic panel were within normal limits, and the cardiac enzymes were negative. His lipid panel was abnormal; specifically his triglycerides and low-density lipoprotein (LDL) were 316 and 135 mg/dL, respectively. The chest X-ray was not clinically significant, and the standard 12-lead electrocardiogram (ECG) showed normal sinus rhythm at 75 beats per minute with pathologic Q waves and T wave inversion in leads II, III, aVF, and V5-V6 (Figure 1). www.npjournal.org

The patient was admitted to the hospital for further evaluation, and an urgent echocardiogram revealed cardiomyopathy with an ejection fraction (EF) of 35%; there was no valvular heart disease. The patient then underwent a diagnostic coronary angiogram that revealed triple vessel disease (right coronary artery, left anterior descending artery, and circumflex coronary artery blockages at 95%, 50%, and 100%, respectively). Myocardial viability studies indicated that coronary artery bypass surgery would be unfavorable. Given his poor EF, the patient eventually underwent implantable cardioverter-defibrillator (ICD) placement and was discharged home with ambulatory Holter monitoring for 24 hours, which revealed no major arrhythmias. No recurrent syncopal episodes were reported. DEFINING THE PROBLEM Syncope is a common clinical problem characterized by transient, self-terminating loss of consciousness with complete and prompt recovery; the cause is insufficient cerebral oxygen supply, usually the result of a transient fall of systemic arterial pressure beyond those tolerated by the central nervous system.1 Because of the increased risk of mortality in patients with underlying coronary artery disease (CAD) or structural heart disease (SHD), medical attention is directed toward evaluating the underlying etiology and identifying those at higher risk to achieve more desirable outcomes.2 The management of syncope patients in the ED is a challenging problem for clinicians. Despite obvious The Journal for Nurse Practitioners - JNP

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Figure 1. The initial 12-Lead ECG in the Emergency Department

Shows normal sinus rhythm at 75 beats per minute with pathologic Q waves and T wave inversion in leads II, III, aVF, and V5-V6

symptoms, fewer than half of patients who experience a syncopal episode seek medical assistance, yet syncopal episodes account for 3%-5% of all visits to hospital EDs and account for up to 6% of hospital admissions from ED. Although syncope is more common among young adults, the average age of those admitted is between 65 and 75. This may imply that cases of syncope presenting to ED are more severe with higher rates of heart disease.3-5 The purpose of this article is to provide nurse practitioners with the current evidence regarding syncope risk stratification, diagnosis, and management as it applies to current clinical presentation. REVIEWING THE EVIDENCE Definition and Prevalence Syncope refers specifically to a sudden, transient loss of consciousness caused by inadequate cerebral perfusion that is self-limited and followed by prompt and complete recovery.1,2,4,6 Symptoms include not only dizziness or blurred vision (usually referred to as presyncope) but also physical collapse with inability to remember the episode itself. In the United States, the lifetime prevalence of syncope is estimated to be 11% to 50%; that is 1 to 2 million patients are evaluated for syncope in ED annually, which accounts for 1%-5% of ED visits and 3%-6% of urgent hospital admissions.3,4,7 Among those evaluated for syncope in the ED, 54% are women, and more than half (59%) are admitted.8 Once admitted, medical attention is focused on risk stratification for identifying those at 386

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increased risk for mortality; patients with underlying myocardial ischemic or SHD are at high risk of sudden cardiac death (SCD).2,9 Importantly, the 12-month mortality rate for patients with a cardiovascular cause of syncope has been reported to be as high as 30%, compared to 12% in those with non-cardiovascular causes.10 Classification and Pathophysiology The most common mechanism of syncope is insufficient cerebral perfusion. Normal cerebral blood flow is 50-60 mL/min that is usually maintained with a mean arterial pressure of 60 mmHg. Two main causes can compromise cerebral blood flow and cause cerebral dysfunction or altered autoregulation that eventually lead to syncope (or presyncope). These include decreased cardiac output from inadequate venous return, diminished blood volume, tachyarrhythmias, bradyarrhythmias, valvular disease, or decreased peripheral vascular resistance from vasovagal attacks, thermal stress, visceral pain reflexes, vasodilators, or autonomic neuropathies.11-13 Despite guidelines to establish a medical diagnosis of syncope, it is not often possible to conclude a single cause because multiple comorbidities are common. Based on data from syncopal ED visits, a neurally mediated cause of syncope is most commonly reported, followed by orthostatic hypotension, primary cardiac arrhythmias, SHD or cardiopulmonary disease, and nonsyncopal attacks. An unknown etiology is reported in 2%-37% of cases.3,5,7,14 Most common types of syncope are illustrated in Table 1. Diagnosis The initial and most important tool for establishing a diagnosis of syncope is a thorough medical history and careful physical examination, including orthostatic blood pressure measurements and standard 12-lead ECG.1,2,14 Findings addressing the presence of SHD are of great importance (eg, abnormal heart sounds) because such findings can predict or rule out a cardiac cause of syncope with high sensitivity and specificity.1 The 12-lead ECG and echocardiogram are essential elements in the initial evaluation of syncope if a cardiac cause is suspected. Although it is rare that either can provide a definitive cardiac diagnosis, they facilitate the selection of subsequent diagnostics tests (eg, coronary angiogram). However, it is challenging to establish a cardiac diagnosis if a transient cardiac arrhythmia (eg, nonsustained ventricular tachycardia) is the primary cause of syncope, Volume 7, Issue 5, May 2011

Table 1. Classification of Selected Causes of Syncope in Descending Order of Frequency3,5,7,14 Etiology

in Emergency Departments

Prevalence

Neurally mediated syncope 1. Vasovagal faint 2. Carotid sinus syndrome 3. Situational faints

21%-66%

Arrhythmias 1. Sinus node dysfunction 2. Paroxysmal supraventricular and ventricular tachycardias 3. Implanted device malfunction

10%-11%

Orthostatic syncope 1. Secondary autonomic failure (eg, drugs and alcohol) 2. Volume depletion (eg, hemorrhage) 3. Primary autonomic failure

9%-10%

Cardiac disease 1. Acute myocardial infarction 2. Cardiac valvular disease 3. Obstructive cardiomyopathy 4. Acute aortic dissection 5. Pulmonary embolus

5%-10%

Others Cerebrovascular, non-syncope causes, unidentified, etc

8%-37%

All patients admitted to the ED with a syncopal episode should be assessed before the final diagnosis is established, more sophisticated tests are selected as needed, and medical treatment is based on the etiology.

especially if the arrhythmic events are occurring infrequently. In such cases a continuous ECG monitoring (eg, 24-hour ambulatory Holter recording) can be valuable for identifying the etiology.1,2 A helpful algorithm for the diagnosis and management of syncope in ED can be summarized as follows (Figure 2). 1. Medical History2,14 • Syncope associated with auras, prodromal symptoms, focal neurological signs, seizure-like activity, unpleasant sight or smell, prolonged standing, nausea, vomiting, meals, head rotations, or exertion, with a long history of syncope and absence of cardiac disease, are indicative of neutrally mediated syncope. • Syncope that occurs after standing up or is associated with prolonged standing, crowded hot places, autonomic neuropathy, parkinsonism, exertion, or starting antihypertensive, phenothiazide, or tricyclic medications is more likely to be caused by orthostasis. • Syncope that occurs in supine position or is associated with exertion, palpitation, chest pain, or familial history of SHD or SCD is more likely to be cardiac in origin. www.npjournal.org

Figure 2. Initial Approach to Evaluate and Manage Syncope

• Syncope associated with palpitations, post-episode fatigue, history of MI or left ventricular dysfunction, or starting antiarrhythmic medications is more likely to be caused by arrhythmias. • Syncope associated with arm exercise, head trauma, focal neurological symptoms, or differences in blood pressure in the 2 arms is indicative of cerebrovascular syncope. 2. Physical Examination14,15 • Vital signs plus cardiopulmonary and neurologicfocused examinations are important to identify orthostasis, autonomic dysfunction, and organic heart diseases. A reduction in systolic blood pressure of 20 mmHg upon standing from sitting position or a systolic blood pressure ⬍ 90 mmHg during standing is indicative of orthostatic hypotension. • Abnormal heart sounds may imply valvular heart disease, whereas carotid bruits may imply carotid artery disease. • Abnormalities in speech, cognition, visual fields, motor strength, sensation, tremor, or gait disturbances may imply neurologic disease.2 • Head-up tilt test can be sometimes used to provoke vasovagal syncope when the etiology cannot be explained. 3. Electrocardiogram2,14 • Prolonged QRS duration (ⱖ 120 msec), left or right bundle branch blocks (BBB), Mobitz type II atrioventricular block, third-degree heart block, sinus bradycardia, sinus pause (ⱖ 3 seconds), prolonged QT The Journal for Nurse Practitioners - JNP

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interval (⬎ 450 msec), or right BBB with ST elevation in leads V1-V3 (Brugada syndrome) are diagnostic for cardiac arrhythmia as a cause of syncope. • The presence of ST elevation, T-wave inversion, or Q-waves is diagnostic for CAD. • The standard ECG is less useful when arrhythmias occur less frequently, which becomes a challenging diagnosis. 4. Echocardiogram2,16 • Evidence shows that echocardiogram adds no additional diagnostic benefit when initial evaluation does not support possible cardiac disease. • For patients with suspected cardiac disease, echocardiogram is very useful in screening for valvular diseases, pulmonary hypertension, right or left ventricular hypertrophy, or cardiomyopathy. • Echocardiogram can guide the selection of further diagnostic tests like CT or MRI scans. 5. Electrophysiological Study14 • Electrophysiological testing is useful in identifying the presence of ventricular tachyarrhythmias and evaluating the risk of sudden death in patients with CAD. • An electrophysiological procedure is indicated when the initial evaluation suggests an arrhythmic cause of syncope or the presence of CAD. • Normal electrophysiological findings cannot completely exclude an arrhythmic cause of syncope, and further evaluations (eg, ECG, continuous monitoring) are then warranted. 6. Noninvasive ECG Monitoring2,17 • The type and duration of monitoring are determined by the frequency of events. Holter monitoring is carried out for 24-72 hours and can record major abnormalities in 27% of patients. • Implantable loop recorders can monitor ECG for 14 months and can yield diagnostic information in 90% of patients. • Holter monitoring is indicated in patients who have clinical or ECG features suggesting an arrhythmic syncope after inconclusive initial evaluation, but when the mechanism of syncope remains unclear after full evaluation, an implantable loop recorder is indicated.

presenting with transient loss of consciousness at ED is important.1,2 Clinicians need to differentiate between real syncope and non-syncopal episodes (eg, falls, traumas, pseudosyncope, seizures, etc) before admitting patients for further evaluation and management. The European Society of Cardiology14 recommends admitting patients with real syncope for further evaluation or management as follows: • Patients with significant heart disease, ECG abnormalities that suggest arrhythmia, or family history of SCD need to be admitted for further evaluation. • Patients with cardiac arrhythmia, ischemia, SHD, or cardiopulmonary disease need to be admitted for initial management. • Patients with minimal or no heart disease or who suffered recurrent episodes with syncope in supine position occasionally need to be admitted. Many attempts have been made to stratify those at increased risk for mortality. San Francisco Rule Study (SFRS)8 predicts those at increased risk for serious outcomes with 98% sensitivity and 56% specificity using a simple mnemonic: CHESS. At least one of the following exist: congestive heart failure (CHF), hematocrit ⬍ 30%, ECG that is abnormal, shortness of breath, or systolic hypotension ⬍ 90 mmHg. The OESIL Risk Score18 was developed as a prognostic tool to be used in the ED for patients with syncope. It can predict 12-month, all-cause mortality using 4 predictors in a simple mnemonic: SAHA (syncope without prodromes, age ⬎ 65 years, history of heart disease, and abnormal ECG). A more comprehensive risk-stratification approach was done in the Syncope Evaluation in the Emergency Department (SEED) study4 that was successful in reducing hospital admissions and total length of stay without affecting mortality. The SEED study classified patients into 3 groups: • High-risk group: chest pain, CHF, valvular disease, arrhythmia, ischemia, sinus pauses, third-degree heart block, QTc ⬎ 500 msec, sinus bradycardia, atrial fibrillation, or malfunctioning pacemaker/ICD • Intermediate-risk group: age ⱖ 50 years, history of CAD, presence of BBB, family history of SCD, or pacemaker/ICD in place • Low-risk group: age ⬍ 50 years, normal cardiovascular examination, and normal ECG findings

Risk Stratification Because of the increased risk of mortality among patients with cardiac cause of syncope, risk stratification of patients

Management The first and most important decision in the management of patients presenting with syncope to the ED is

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Table 2. Management Guidelines for Syncope1,3,6,14 Classification

Recommendations

Neurally mediated syncope and orthostatic hypotension

• Reassurance and education about pathophysiology and prevention measures • Controlling contributing psychological/psychiatric factors • Techniques to abort imminent attacks (eg, physical maneuvers, hydration, salt intake, etc) • Avoiding syncope triggers • Desensitization techniques for situational syncope • Cardiac pacing for carotid sinus syndrome • Physical maneuvers (eg, leg crossing with lower body tensing, squatting, arm tensing, tilt training) • Modification of hypertension drugs and pharmacological interventions to improve vascular tone and counteract intravascular volume depletion • Bolus water intake in the morning with gradual, slow rising from bed

Arrhythmia

• Cardiac pacemakers for bradyarrhythmias • Ablation therapy, antiarrhythmias, or ICD for tachyarrhythmia • ICD for channelopathies (Brugada syndrome, long QT syndrome)

Structural heart disease

• Surgery for valvular disease • Pharmacological intervention and pacing for cardiomyopathies • Specific intervention to correct underlying pathology

Cerebrovascular disease

• Management of migraines (if present) with beta blockers and cranial artery vasoconstrictors • Specific intervention to correct underlying pathology

ICD = implantable cardioverter defibrillator.

whether to hospitalize the patient or not.6 Syncope with a suspected heart disease or arrhythmic origin, occurring during exercise, causing severe injury, or associated with family history of SCD needs to be admitted to the hospital for further management.14 Once the diagnosis is established, further evaluation and management of each type of syncope can be started. Table 2 summarizes management guidelines for patients with syncope.1,3,6,14 IMPLEMENTING THE EVIDENCE The first step in evaluating a patient with transient loss of consciousness is to determine whether the episode was a true syncope or not. In the current case scenario, based on the eyewitness reports of complete physical collapse provided by the patient’s coworkers, true syncope initially was diagnosed. Thus, the patient was evaluated with a thorough medical history, physical exam, and standard 12-lead ECG. Whereas the neurologic and cardiopulmonary exams were normal, the medical history was suspicious for a cardiac cause of syncope, suggesting further intensive evaluation. Age, sex, smoking history, the absence of prodromal symptoms before the single attack, the accompanying palpitations during the attack, and the family history of heart disease and sudden death are features suggestive of cardiac www.npjournal.org

cause of syncope. Additionally, the hyperlipidemia and the abnormal ECG were indicative of possible CAD. On the other hand, arrhythmia as a cause of syncope might also be suspected in the current scenario because the attack was accompanied by palpitations. However, no evidence of arrhythmia was seen on the ECG, but since standard resting 12-lead ECG does not document infrequent events like ventricular or supraventricular tachycardias, this etiology cannot be excluded. Further evaluation (eg, ambulatory continuous ECG monitoring) is warranted to rule out arrhythmia-related syncope. Moreover, other etiologies, including orthostatic hypotension, are less likely. The vital signs revealed neither a drop of blood pressure ⬎ 20 mmHg nor a systolic blood pressure ⬍ 90 mmHg between standing and supine readings, which can help to rule out orthostatichypotension-related syncope. At this point in the case scenario, the right decision was made to admit the patient to the hospital for further evaluation and management. Initial interventions include continuous cardiac monitoring, fall precautions, frequent neurological checks (eg, every 4 hours), oxygen administration if needed, and pharmacological support (prophylactic aspirin, antihyperlipidemic drugs). The Journal for Nurse Practitioners - JNP

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The standard 12-lead ECG taken at the ED revealed normal sinus rhythm at 75 beats per minute. Although there were no ST segment deviations indicating myocardial ischemia, there were pathologic Q waves (ⱖ 0.04 msec and ⱖ 1/4 of R wave) with T wave inversion in leads II, III, aVF, and V5-V6. Markers of myocardial scaring in the inferior and lateral walls strongly suggest CAD. In addition, the ECG revealed QRS fragmentation (RSR morphology, notching of the nadir of S wave, or more than 1 R wave) along the same leads with pathologic Q waves, which suggests the presence of a myocardial scar with poor prognosis rate.19 In a previous investigation,20 we found that in patients with ischemic cardiomyopathy, number of leads with Q waves are sensitive and can predict 10% of the myocardial scar of the left ventricle, which is estimated to be large in the current case study. Upon admission an urgent echocardiogram revealed cardiomyopathy with EF of 35%. Left ventricular systolic dysfunction (LVSD), defined as EF ⬍ 35%-45%, is a significant clinical finding; approximately 50% of deaths among patients with LVSD are attributed to SCD.21 It is uncommon for patients with LVSD to be asymptomatic, which was an unexpected finding in the current presentation. Evidence highly recommends prophylactic ICD implantation as secondary prevention of SCD in patients with EF ⱕ 35%. This approach has shown to reduce absolute mortality by 7.9% in patients at high risk.21 However, to further investigate the possible CAD in the current presentation, the patient underwent a diagnostic coronary angiogram. The current guidelines recommend exercise treadmill testing for patients with syncope to rule out CAD,2 but because of the documented inferior-lateral myocardial scar on the ECG and the increased risk of death for patients with LVSD, this patient was routed for direct angiogram. The cardiac catheterization revealed ischemic cardiomyopathy and triple vessel disease, including left anterior descending artery involvement, which meets the clinical criteria for coronary artery bypass surgery (CABG). However, subsequent nuclear imaging scan revealed the myocardium around the scar was nonviable (sometimes referred to as “hibernating” myocardium), and thus, CABG would not be therapeutic. Ischemic cardiomyopathy is characterized by impaired cardiac contractility that mainly results from CAD. A history of MI is commonly seen in these cases; however, 390

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longstanding myocardial ischemia can be severe enough to result in impaired myocardial contractility without precipitating MIs. The pathophysiological consequences of the resulting myocardial scaring is frequently associated with increased risk for morbidity and SCD.22 Current medical advances in cardiac surgery and ICDs have had an impact on the reduction of SCD rates, with improved survival.9 Ischemic cardiomyopathy is also associated with high prevalence of fatal cardiac arrhythmias; literature describes a patient who had recurrent syncopal episodes that were precipitated by asymptomatic, advanced, second-degree AV block and episodes of ventricular tachycardia detected by implantable loop recorder.23 In the current case study, the medical management was congruent with the current evidence where the patient underwent an ICD placement to minimize the risk of SCD and completed 24-hour Holter recording to rule out fatal arrhythmias. Even though the Holter did not reveal any arrhythmias, the short duration of recording has limited the diagnostic scope and does not completely rule out the absence of cardiac arrhythmias.2 This patient needs to be medically managed by optimal pharmacological support (eg, aspirin, statins, beta blockers, etc) and modification of risk factors, along with lifestyle changes, including smoking cessation. IMPLICATIONS TO CLINICAL PRACTICE Careful medical history, physical examination, and standard 12-lead ECG are the basis of initial evaluation of syncope and subsequent evaluation and management. Cardiac causes of syncope are associated with increased risk of morbidity and mortality. Even though cardiac syncope is not common, an approach based on initial risk stratification is more likely to yield a correct diagnosis and initiate an effective treatment in a cost-effective approach. References 1. Benditt G, Nguyen J. Syncope: therapeutic approach. J Am Coll Cardiol. 2009;53(19):1741-1751. 2. Strickberger S, Benson D, Biaggioni I, et al. AHA/ACCF Scientific Statement on the Evaluation of Syncope. Circulation. 2006;113:316-327. 3. Brignole M, Menozzi C, Bartoletti A, et al. A new management of syncope: prospective systematic guideline-based evaluation of patients referred urgently to general hospitals. Eur Heart J. 2006;27(1):76-82. 4. Shen WK, Decker WW, Smars PA, et al. Syncope Evaluation in the Emergency Department Study (SEEDS): A multidisciplinary approach to syncope management. Circulation. 2004;110:3636-3645. 5. Mitjans A, Martín C. Management of patients with syncope: from guidelines to clinical practice. Rev Esp Cardiol. 2008;61(1):10-13. 6. Benditt D. Syncope management guidelines at work: first steps towards assessing clinical utility. Eur Heart J. 2006;27(1):7-9.

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7. Soteriades E, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med. 2002;347:878-885. 8. Quinn J, McDermott D, Stiell I, Kohn M, Wells G. Prospective validation of the San Francisco Syncope Rule to predict patients with serious outcomes. Ann Emerg Med. 2006;47(5):448-454. 9. Spirito P, Autore C, Rapezzi C, et al. Syncope and risk of sudden death in hypertrophic cardiomyopathy. Circulation. 2009;119:1703-1710. 10. Kapoor W, Karpf M, Wieand S, Peterson J, Levey G. A prospective evaluation and follow-up of patients with syncope. N Engl J Med. 1983;309:197-204. 11. Lazarus J, Mauro V. Syncope: pathophysiology, diagnosis, and pharmacotherapy. Ann Pharmacother. 1996;30(9):994-1005. 12. Hainsworth R. Pathophysiology of syncope. Clin Auton Res. 2004;14(Suppl 1):18-24. 13. Thijs RD, Wieling W, Kaufmann H, Dijk JGv. Defining and classifying syncope. Clin Auton Res. 2004;14(Suppl 1):4-8. 14. Brignole M, Alboni P, Benditt DG, et al. Guidelines on management (diagnosis and treatment) of syncope – Update 2004. Eur Heart J. 2004;25(22):2054-2072. 15. Parry SW, Reeve P, Lawson J, et al. The Newcastle protocols 2008: an update on head-up tilt table testing and the management of vasovagal syncope and related disorders. Heart. 2009;95(5):416-420. 16. Recchia D, Barzilai B. Echocardiography in the evaluation of patients with syncope. J Gen Intern Med. 1995;10(12):649-655. 17. Bass E, Curtiss EI, Arena VC, et al. The duration of Holter monitoring in patients with syncope: is 24 hours enough? Arch Intern Med. 1990;150(5):1073-1078. 18. Colivicchi F, Ammirati F, Melina D, Guido V, Imperoli G, Santini M. Development and prospective validation of a risk stratification system for patients with syncope in the emergency department: the OESIL risk score. Eur Heart J. 2003;24(9):811-819. 19. Das MK, Suradi H, Maskoun W, et al. Fragmented Wide QRS on a 12-Lead ECG: a sign of myocardial scar and poor prognosis. Circ Arrhythm Electrophysiol. 2008;1(4):258-268. 20. Carey MG, Luisi Jr AJ, Baldwa S, et al. The Selvester QRS Score is more accurate than Q waves and fragmented QRS complexes using the MasonLikar configuration in estimating infarct volume in patients with ischemic cardiomyopathy. J Electrocardiol. 2010;43(4):318-325.

21. Nanthakumar K, Epstein AE, Kay GN, Plumb VJ, Lee DS. Prophylactic implantable cardioverter-defibrillator therapy in patients with left ventricular systolic dysfunction: A pooled analysis of 10 primary prevention trials. J Am Coll Cardiol. 2004;44(11):2166-2172. 22. Gheorghiade M, Bonow RO. Chronic heart failure in the United States: a manifestation of coronary artery disease. Circulation. 1998;97(3):282-289. 23. Arkolaki EG, Simantirakis EN, Chrysostomakis SI, Vardas PE. Appropriate management of syncope in a patient with hypertrophic cardiomyopathy: rationale behind long-term cardiac rhythm monitoring. Hellenic J Cardiol. 2009;50(2):144-146.

Salah S. Al-Zaiti, MS, ANP-BC, RN, PhD(c), is a graduate research assistant at the State University of New York in Buffalo, NY. He can be reached at [email protected]. Mohamad K. Khasawneh, MD, is a fellow at the Jonah Center for Blood and Immunological Disease in the Erie County Medical Center in Buffalo, NY, and an MD fellow in the medical oncology department at Roswell Park Cancer Institute in Buffalo. Mary G. Carey, PhD, RN, is an associate professor at the State University of New York. In compliance with national ethical guidelines, the authors report no relationships with business or industry that would pose a conflict of interest. 1555-4155/11/$ see front matter © 2011 American College of Nurse Practitioners doi:10.1016/j.nurpra.2011.01.006

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