eMedicine Specialties > Cardiology > Arrhythmias
Holiday Heart Syndrome
Updated: Apr 21, 2009
Introduction
Background
Alcohol consumed in large quantities for many years has long been recognized to induce an alcoholic cardiomyopathy. Clinically identical to idiopathic dilated cardiomyopathy, alcoholic cardiomyopathy is a major form of secondary dilated cardiomyopathy in the Western world. (See eMedicine articles Cardiomyopathy, Alcoholic and Cardiomyopathy, Dilated.) With this change in cardiac structure and decline in function, there exists the substrate for atrial and ventricular arrhythmias. However, only within the past 20-25 years has the arrhythmogenic potential of short-term alcohol consumption been elucidated in patients without clinically evident heart failure.
In 1978, Ettinger et al conducted a study evaluating 32 separate dysrhythmic episodes in 24 patients. These patients consumed alcohol heavily and regularly; in addition, they took part in a weekend or holiday drinking binge immediately prior to evaluation. Based on the results of this study, the term holiday heart syndrome was coined. It was defined as an acute cardiac rhythm and/or conduction disturbance, most commonly supraventricular tachyarrhythmia, associated with heavy ethanol consumption in a person without other clinical evidence of heart disease. Typically, this resolved rapidly with spontaneous recovery during subsequent abstinence from alcohol use.1
Holiday heart syndrome now most commonly refers to the association between alcohol use and rhythm disturbances, particularly supraventricular tachyarrhythmias in apparently healthy people. Similar reports have indicated that recreational use of marijuana may have similar effects.2 The most common rhythm disorder is atrial fibrillation, which usually converts to normal sinus rhythm within 24 hours.3 Holiday heart syndrome should be particularly considered as a diagnosis in patients without structural heart disease and with new-onset atrial fibrillation.4 Although the syndrome can recur, its clinical course is benign, and specific antiarrhythmic therapy is usually not indicated. Interestingly, even modest alcohol intake can be identified as a trigger in some patients with paroxysmal atrial fibrillation.5
Pathophysiology
Several mechanisms are theorized to be responsible for the arrhythmogenicity of alcohol. These include an increased secretion of epinephrine and norepinephrine, increased sympathetic output, a rise in the level of plasma free fatty acids, and an indirect effect through acetaldehyde, the primary metabolite of alcohol, or fatty acid ethyl esters, a cardiac alcohol metabolite.6 Alcohol can also directly decrease sodium current and can affect intracellular pH, ether causing acidosis with low doses or alkalosis with higher doses. Interestingly, these effects may be species specific, with rabbits7 and humans being similarly affected while the dog atria appear unaffected8 .
Analysis of ECGs performed following resolution of arrhythmias in patients who have consumed a large quantity of alcohol show significant prolongation of the PR, QRS, and QT intervals compared with patients who experienced arrhythmias in the absence of alcohol consumption.9 The arrhythmogenicity of alcohol has also been examined in the electrophysiology laboratory.
One study evaluated 14 patients with a history of significant alcohol consumption. Initially, the atrial and ventricular extrastimulus technique induced nonsustained ventricular tachycardia in 1 patient, nonsustained atrial fibrillation in 1 patient, paired ventricular responses in 1 patient, and no response in the remaining 11 patients. Following administration of alcohol, 10 of the 14 patients developed sustained or nonsustained tachyarrhythmias in response to the extrastimulus technique, with significant prolongation of His-ventricular conduction.10
In another study, ingestion of whiskey resulted in no change in the atrial refractory period but facilitated induction of atrial flutter in individuals who were chronic drinkers and those who were nondrinkers. This evidence strongly suggests that alcohol possesses proarrhythmic properties. These seem to be more pronounced in patients with larger P wave dispersion. Although ventricular repolarization abnormalities on surface ECG were described, whether ventricular myocardium responds similarly to ethanol is uncertain. One case of ventricular fibrillation was described in a patient with heavy alcohol ingestion, but an electrophysiologic study (EPS) revealed only inducibility of atrial fibrillation with rapid ventricular response but no ventricular arrhythmias.
Frequency
United States
The frequency with which cardiac arrhythmias can be attributed to alcohol use is unclear owing to differing data. One study showed alcohol as the causative agent in 35% of cases of new-onset atrial fibrillation and in 63% of cases in patients younger than 65 years.11 Conversely, another study showed only about 5-10% of all new episodes of atrial fibrillation to be explainable by alcohol use.
Atrial fibrillation is the most common rhythm disturbance associated with alcohol consumption. Atrial flutter, isolated ventricular premature beats, isolated atrial premature beats, junctional tachycardia, and various other rhythm disturbances may occur with less frequency.
International
Worldwide prevalence is not well documented. Prevalence is presumably increased in countries with higher rates of alcohol ingestion and alcoholism.
Mortality/Morbidity
Regular consumption of alcohol in modest amounts does not seem to have the same potential to cause arrhythmias as alcohol consumed in heavy amounts. In fact, it has been shown in a sample of patients whose usual daily alcohol intake exceeds 6 drinks that the risk of developing atrial fibrillation, atrial flutter, and atrial premature beats is at least twice that of patients who drink alcohol at least monthly but who on average consume less than a single drink daily.
Race
Evidence regarding race is unavailable.
Sex
An increased incidence of the holiday heart syndrome has not been clearly documented in males; however, this can be inferred as males have a higher incidence of atrial fibrillation and alcoholism.
Age
Although atrial fibrillation increases with age, it is unclear if holiday heart syndrome is more common in elderly patients, since this age group is more likely to have structural heart disease.
Clinical
History
Patients with acute exposure to alcohol can present with a variety of symptoms.
- Palpitations are the most common symptom. These can be intermittent or persistent, depending on the presence or absence of sustained arrhythmia and the ventricular response to atrial fibrillation. Patients with rapid ventricular responses can present with near syncopal symptoms, dyspnea on exertion, and angina.
- Patients often have a history of previous alcohol exposure. This often occurs in binges on weekends, during vacations, and, of course, on holidays. A history of alcoholism should alert physicians to concomitant illnesses such as alcohol-related cardiomyopathy and chronic liver disease. These coexisting illnesses have important prognostic implications and affect patient management.
Physical
On physical examination, the patient may show signs of alcohol intoxication and have alcohol on the breath. Depending on the cardiac rhythm, the patient may have an irregular or thready pulse. Cardiac auscultation is usually normal except for possibly irregular and/or rapid heart tones. Mental status may be impaired consistent with alcohol intoxication.
Differential Diagnoses
Alcoholism
Atrial Fibrillation
Atrial Flutter
Hyperthyroidism
Paroxysmal Supraventricular Tachycardia
Pulmonary Embolism
Other Problems to Be Considered
Excessive use of caffeine or over-the-counter decongestants (eg, ephedrine, phenylpropanolamine [recalled from US market])
Workup
Laboratory Studies
- Assess serum electrolyte levels, particularly potassium, in all patients with acute arrhythmias.
Imaging Studies
- Echocardiography has become the standard diagnostic modality to assess chamber enlargement, left ventricular (LV) wall motion abnormalities, hypertrophy, valvular disease, and systolic dysfunction.
- In patients at risk for coronary artery disease, additional cardiac imaging (eg, perfusion imaging, echocardiography) may be required.
Other Tests
- Twelve-lead ECG is essential to exclude other cardiac pathology such as ischemia, infarction, pulmonary embolism, or hypertrophy.
- Upon resolution of holiday heart syndrome and return to sinus rhythm, treadmill stress testing is reasonable in some patients to look for exercise-related arrhythmia after the acute effects of alcohol have resolved.
Treatment
Medical Care
- Patients presenting to the emergency department with sustained tachyarrhythmia secondary to acute alcohol toxicity usually can be observed with ECG monitoring. Treatment with an AV nodal blocking agent (eg, beta-blocker, verapamil, diltiazem) may be needed if the ventricular rate is excessive. If the duration of atrial fibrillation approaches 24-48 hours, cardioversion should be considered to obviate the need for anticoagulation. In general, pericardioversion anticoagulation is required for atrial fibrillation lasting more than 48 hours.
- Most patients with structural heart disease should be admitted for observation and treatment if the arrhythmia persists.
- Young patients with no evidence of structural heart disease sometimes can be discharged without further treatment once their arrhythmia has stabilized.
- Advise all patients against the excessive use of alcohol in the future.
Consultations
Patients presenting with new-onset tachyarrhythmias and structural heart disease, such as myocardial ischemia and/or LV dysfunction, often require a more extensive evaluation, and consultation with a cardiologist may be necessary.
Diet
The use of alcohol is contraindicated. Stimulants such as caffeine should be avoided initially; the interaction of alcohol and caffeine on atrial fibrillation has not been determined.
Activity
Following alcohol-related arrhythmia, it usually is advisable for patients to refrain from significant exertion because excessive catecholamines can precipitate recurrent episodes in some cases. Most patients without underlying heart disease should be able to gradually resume full physical activity over the next few days.
Medication
Symptoms of acute alcohol toxicity often resolve spontaneously. Arrhythmia monitoring and observation are adequate in many patients. In patients with atrial tachyarrhythmias and a rapid ventricular response (eg, atrial fibrillation or flutter), ventricular rate control is important for those who are symptomatic. The use of intravenous beta-antagonists, diltiazem, or verapamil is appropriate. Digoxin has a slow onset of action, and chronic therapy with this drug is rarely indicated. As always, patients who are hemodynamically unstable patients should be treated with direct current cardioversion.
Beta-antagonists
In patients with atrial tachyarrhythmias and a rapid ventricular response (eg, atrial fibrillation or flutter), ventricular rate control is important for those who are symptomatic.
Metoprolol (Lopressor, Toprol XL)
Beta-antagonists are useful agents because of their rapid onset of action and sympatholytic effects. They are the treatment of choice if acute myocardial ischemia or myocardial infarction is present.
Dosing
Adult
5 mg IV push q5min, not to exceed 3 doses; can be followed by 25 mg PO q6h
Pediatric
Not established
Interactions
Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels of metoprolol, possibly resulting in decreased pharmacologic effects; toxicity of metoprolol may increase with coadministration of sparfloxacin, phenothiazines, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; metoprolol may increase toxicity of digoxin, flecainide, clonidine, epinephrine, nifedipine, prazosin, verapamil, and lidocaine
Contraindications
Bradycardia; second- or third-degree heart block; significant pulmonary congestion; asthma; bronchospastic lung disease
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Beta-adrenergic blockade may reduce signs and symptoms of acute hypoglycemia and may decrease clinical signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; monitor patient closely and withdraw the drug slowly; during IV administration, carefully monitor blood pressure, heart rate, and ECG
Calcium channel blockers (nondihydropyridine)
In specialized conducting and automatic cells in the heart, calcium is involved in the generation of the action potential. The calcium channel blockers inhibit movement of calcium ions across the cell membrane, thus depressing both impulse formation (automaticity) and conduction velocity.
Verapamil (Calan, Covera-HS, Verelan)
Can diminish PVCs associated with perfusion therapy and decrease the risk of ventricular fibrillation and ventricular tachycardia.
Dosing
Adult
5-10 mg IV over 2 min, followed by second dose 15-30 min later if patient does not satisfactorily respond to initial dose
Pediatric
Not recommended
Interactions
Verapamil may increase carbamazepine, digoxin, and cyclosporine levels; coadministration with amiodarone, can cause bradycardia and a decrease in cardiac output; when administered concurrently with beta-blockers may increase cardiac depression; cimetidine may increase verapamil levels; verapamil may increase theophylline levels
Contraindications
Documented hypersensitivity; severe CHF, sick sinus syndrome or second- or third-degree AV block, and hypotension (<90 mm Hg systolic)
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Hepatocellular injury may occur; transient elevations of transaminases with and without concomitant elevations in alkaline phosphatase and bilirubin have occurred (elevations have been transient and may disappear with continued verapamil treatment); periodically monitor liver function
Diltiazem (Cardizem CD, Dilacor, Tiazac)
For symptomatic supraventricular tachycardias. In many situations, this may be the drug of choice if used IV, since it is relatively short acting and can be stopped if there is resolution of arrhythmia following recovery from acute alcohol toxicity. This is an excellent approach in patients without evidence of underlying cardiac disease.
Dosing
Adult
0.25 mg/kg IV over 2 min; repeat 0.35 mg/kg over 2 min if no response; start infusion at 5-15 mg/h
Pediatric
Not recommended
Interactions
May increase carbamazepine, digoxin, and cyclosporine, theophylline levels; when administered with amiodarone, may cause bradycardia and a decrease in cardiac output; when administered with beta-blockers may increase cardiac depression; cimetidine may increase diltiazem levels
Contraindications
Documented hypersensitivity; severe CHF, sick sinus syndrome, second- or third-degree AV block, and hypotension (<90 mm Hg systolic)
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in impaired renal or hepatic function; may increase LFT levels, and hepatic injury may occur
Digoxin (Lanoxin, Lanoxicaps)
Cardiac glycoside with direct inotropic effects in addition to indirect effects on the cardiovascular system. Acts directly on cardiac muscle, increasing myocardial systolic contractions. Its indirect actions result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure.
Dosing
Adult
0.75-1.25 mg/d PO in divided doses (0.25 mg q4h x 4)
Pediatric
Not established
Interactions
Medications that may increase digoxin levels include alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, quinidine, diltiazem, aminoglycosides, oral amiodarone, anticholinergics, diphenoxylate, erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, tolbutamide, and verapamil
Medications that may decrease serum digoxin levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, oral colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (including carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid
Contraindications
Documented hypersensitivity; beriberi heart disease, idiopathic hypertrophic subaortic stenosis, constrictive pericarditis, and carotid sinus syndrome
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Hypokalemia may reduce positive inotropic effect of digitalis; IV calcium may produce arrhythmias in digitalized patients; hypercalcemia predisposes patient to digitalis toxicity, and hypocalcemia can make digoxin ineffective until serum calcium levels are normal; magnesium replacement therapy must be instituted in patients with hypomagnesemia to prevent digitalis toxicity; patients diagnosed with incomplete AV block may progress to complete block when treated with digoxin; exercise caution in hypothyroidism, hypoxia, and acute myocarditis
Follow-up
Further Inpatient Care
Upon resolution of holiday heart symptoms and return to sinus rhythm, treadmill stress testing is reasonable in some patients to look for exercise-related arrhythmia when the acute effects of alcohol have resolved. This is also important in patients at risk for coronary artery disease; occasionally, additional cardiac imaging (eg, perfusion imaging, echocardiography) is required.
Further Outpatient Care
Alcohol-induced atrial fibrillation without other unrelated episodes would not typically be considered a current indication for atrial fibrillation surgical or catheter ablation.
Inpatient & Outpatient Medications
Upon resolution of the alcohol-related arrhythmia, most patients do not require further therapy if they refrain from alcohol use. Patients with underlying heart disease or those with severe symptoms on presentation (eg, syncope, hypotension) may be candidates on discharge for oral agents such as beta-antagonists.
Transfer
Persons with alcoholism should be considered for transfer to facilities for detoxification/rehabilitation.
Deterrence/Prevention
Advise patients to refrain from alcohol and stimulants and to avoid excessive fatigue.
Prognosis
Prognosis depends on the presence of underlying heart disease. Long-term alcohol use increases the risk of cardiomyopathy and chronic liver disease.
Miscellaneous
Medicolegal Pitfalls
- Although long-term anticoagulation is indicated for patients with paroxysmal, persistent, or permanent atrial fibrillation and risk factors for thromboembolism, physicians should be cautious about anticoagulating patients with expected acute alcohol toxicity, especially if there is a history of possible trauma. A reasonable approach may be to provide short-term anticoagulation with heparin in the presence of risk factors for thromboembolism (eg, previous stroke, hypertension, congestive heart failure, diabetes, age >65-75 y), as long as there are no contraindications, while ascertaining risk factors for embolic events in the setting of atrial fibrillation (CHADS score). Some patients are candidates for long-term anticoagulation with warfarin.
- Many elderly patients, or those with structural heart disease, develop atrial fibrillation. A history of recent alcohol use at times can be coincidental in these patients. Physicians should not mistakenly avoid anticoagulation under the assumption that atrial fibrillation will not recur.
- Medicolegal issues related to the management of patients with acute and/or chronic problems related to alcohol should be considered.
- Many elderly patients, or those with structural heart disease, develop atrial fibrillation. A history of recent alcohol use at times can be coincidental in these patients. Physicians should not mistakenly avoid anticoagulation under the assumption that atrial fibrillation will not reoccur.
- Medicolegal issues related to the management of patients with acute and/or chronic problems related to alcohol should be considered.
References
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Kosior DA, Filipiak KJ, Stolarz P, Opolski G. Paroxysmal atrial fibrillation following marijuana intoxication: a two-case report of possible association. Int J Cardiol. Apr 2001;78(2):183-4. [Medline].
Thornton JR. Atrial fibrillation in healthy non-alcoholic people after an alcoholic binge. Lancet. Nov 3 1984;2(8410):1013-5. [Medline].
Koskinen P, Kupari M, Leinonen H, Luomanmaki K. Alcohol and new onset atrial fibrillation: a case-control study of a current series. Br Heart J. May 1987;57(5):468-73. [Medline].
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Keywords
holiday heart syndrome, short-term alcohol consumption, alcohol-related paroxysmal atrial fibrillation, acute cardiac alcohol toxicity, arrhythmia, holiday heart symptoms, holiday heart treatment, holiday heart causes, alcohol-related cardiomyopathy, idiopathic dilated cardiomyopathy, dysrhythmic episodes, acute cardiac rhythm disturbance, acute conduction disturbance, supraventricular tachyarrhythmia, binge, binge drinking
Contributor Information and Disclosures
Author
Adam S Budzikowski, MD, PhD, Assistant Professor of Medicine, Division of Cardiovascular Medicine, Electrophysiology Section, State University of New York-Downstate, University Hospital of Brooklyn
Adam S Budzikowski, MD, PhD is a member of the following medical societies: American College of Cardiology, European Society of Cardiology, Heart Rhythm Society, and Polish Society of Cardiology
Disclosure: Nothing to disclose.
Coauthor(s)
James P Daubert, MD, Associate Professor of Medicine, Director of Electrophysiology Service, University of Rochester Medical Center; Consulting Staff, Atrial Fibrillation Clinic and Adult Congenital Heart Clinic, University of Rochester Medical Center, Strong Memorial Hospital
James P Daubert, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, and Heart Rhythm Society
Disclosure: Medtronic Equity interest None; Boston Scientific Honoraria Speaking and teaching; CV Therapeutics Consulting fee Consulting; Cryocor Consulting fee Consulting
Richard H Smith, MD, Director of Echocardiography, Long Island Heart Associates, State University of New York at Stony Brook; Clinical Assistant Professor, Department of Cardiology, Winthrop-University Hospital and North Shore University Hospital
Richard H Smith, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians-American Society of Internal Medicine, and American Medical Association
Disclosure: Nothing to disclose.
Howard S Weiss, DO, Staff Physician, Department of Medicine, Winthrop University Hospital
Howard S Weiss, DO is a member of the following medical societies: American Medical Association and American Osteopathic Association
Disclosure: Nothing to disclose.
Medical Editor
Hanumant Deshmukh, MD †, Former Chief of Cardiology, Veterans Affairs Medical Center; Former Associate Professor, Department of Medicine, Rosalind Franklin University of Medicine and Science
Disclosure: Nothing to disclose.
Pharmacy Editor
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
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Managing Editor
Steven J Compton, MD, FACC, FACP, Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals
Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, and Heart Rhythm Society
Disclosure: Nothing to disclose.
CME Editor
Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.
Chief Editor
Jeffrey N Rottman, MD, Professor of Medicine and Pharmacology, Director, Clinical Cardiac Electrophysiology Fellowship Program, Vanderbilt University School of Medicine; Chief, Department of Cardiology, Nashville Veterans Affairs Medical Center
Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association and North American Society of Pacing and Electrophysiology (NASPE)
Disclosure: Nothing to disclose.
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