Holiday Heart Syndrome 

In 1978, Philip Ettinger and coinvestigators coined the term holiday heart syndrome (HHS) as "an acute cardiac rhythm and/or conduction disturbance associated with heavy ethanol consumption in a person without other clinical evidence of heart disease..."[1] The initial recognition of the syndrome was a result of their study evaluating 32 separate dysrhythmic episodes in 24 patients who were admitted to the hospital for their condition.[1] These patients consumed alcohol heavily and regularly; in addition, they took part in a weekend or holiday drinking binge immediately prior to evaluation. In their series, the most common cardiac rhythm disturbances were supraventricular tachyarrhythmias and atrial fibrillation. Typically, this resolved rapidly with spontaneous recovery during subsequent abstinence from alcohol use.[1]

It is relevant to note that chronic consumption of large quantities of alcohol (In the context of this article, alcohol refers specifically to ethanol) has long been recognized to induce an alcoholic cardiomyopathy. Clinically similar to idiopathic dilated cardiomyopathy, alcoholic cardiomyopathy is a major form of secondary dilated cardiomyopathy in the western world. (See the Medscape Drugs and Diseases articles Alcoholic Cardiomyopathy and Dilated Cardiomyopathy.) With this change in cardiac structure and decline in function, there exists the substrate for atrial and ventricular arrhythmias.[2]  

In the modern era, the term HHS has primarily been used to refer to acute cardiac rhythm disturbances related to acute alcohol consumption (ie, binge drinking), regardless of the underlying cardiac disease.[3] This is supported by the fact that the effect of alcohol on the induction of arrhythmias is dose dependent, and it is independent of preexisting cardiovascular diseases or heart failure.[4]   Even modest alcohol intake can be identified as a trigger in some patients with paroxysmal atrial fibrillation.[3, 5]  Although less rigorously studied, it should be noted that other substances associated with binge drinking certainly may contribute. As such, similar reports have indicated that recreational use of marijuana may have corresponding effects.[6]

The most common rhythm disorder with HHS is atrial fibrillation.[7, 8] HHS should be considered as a diagnosis in patients without structural heart disease and with new-onset atrial fibrillation.[9]  

Several mechanisms are theorized to be responsible for the arrhythmogenicity of alcohol. They may be characterized into two broad groups: direct effects on the myocardium and alcohol's effect on traditional risk factors for atrial fibrillation.

With regard to direct effects on the atrial myocardium, alcohol causes a autonomic nervous system imbalance. Alcohol increases sympathetic nervous system (SNS) activity (and its related increased secretion of epinephrine and norepinephrine), with resultant effects including an increased release of calcium into the myocytes from the sarcoplasmic reticulum.[3, 10] Increased SNS activity is further evidenced by a marked increase in the incidence of sinus tachycardia and reduced respiratory sinus arrhythmia during acute alcohol intoxication.[11] Consequently, the parasympathetic nervous system (PNS) is activated as well, with an increased intermittent vagal tone, which has been shown to also shorten the atrial refractory period and preciptate atrial fibrillation.[10] Note that the risk of atrial fibrillation persists into the "hangover" and/or withdrawal phase, which corresponds with an increased sympathetic tone.[3]

Other direct effects on the myocardium are perhaps less well studied. They include the effects of alcohol's primary metabolite acetaldehyde, which is associated with local inflammation and oxidative stress.[10]  Alcohol itself can also directly decrease the myocyte 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 rabbits[12] and humans being similarly affected, whereas canine atria appear unaffected.[13]  Research indicates that cardiac cells exposed to ethanol doses of 0.1% or greater undergo extrusion of magnesium (Mg2+), possibly owing to ethanol oxidation by cytochrome P-450 2E1; whether this contributes to alcoholic cardiomyopathy is not known.[14, 15]

A more recent study revealed that binge alcohol consumption activates the stress kinase JNK (c-Jun N-terminal kinase) (JNK2), which subsequently phosphorylates (and activates) the CaMKII protein, thereby enhancing CaMKII-driven mishandling of sarcoplasmic reticulum calcium—which prompts aberrant calcium waves and enhances susceptibility to atrial arrhythmia.[8] Conversely, CaMKII inhibition eliminates binge alcohol-evoked arrhythmic activities.

In another recent study involving isolated human atrial and murine atrial or ventricular cardiomyocytes, investigators indicated sarcoplasmic reticulum calcium leak as well as disordered excitation-contraction coupling as the basis for the arrhythmogenic and negative inotropic effects (reduced systolic calcium release) of acute ethanol exposure.[16] The investigators noted that production of reactive oxygen species (ROS) via nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2) and oxidative activation of CaMKII appeared have key roles in the mechanism of action.

Analysis of electrocardiograms (ECGs) performed following the resolution of arrhythmias in patients who have consumed a large quantity of alcohol shows significant prolongation of the PR, QRS, and QT intervals compared to that of patients who experienced arrhythmias in the absence of alcohol consumption.[1, 17]

The arrhythmogenicity of alcohol has also been examined in the electrophysiology (EP) laboratory. In a study that evaluated 14 patients with a history of significant alcohol consumption, initially, the atrial and ventricular extrastimulus technique induced nonsustained ventricular tachycardia in a patient, nonsustained atrial fibrillation in another patient, paired ventricular responses in a third patient, and no response in the remaining 11 patients.[18] 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.[18]  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.[2, 19]  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. Alcohol-induced atrioventricular block has been reported as a rare event that can occur at relatively low serum alcohol levels.[20] Investigators suggest that the mechanism for conduction slowing and block may be partly due to an exaggerated partial inhibition of calcium and, potentially, sodium currents in conductive tissue structures as result of elevated vagal tone. Impaired gap junction function may also play a role.[20]

With regard to alcohol's effect on traditional risk factors, one of the best studied is alcohol and its ability to exacerbate the severity of obstructive sleep apnea (OSA). OSA has clearly been associated with incident atrial fibrillation.[3] Alcohol consumption has been shown to increase the severity of sleep apnea, or the apnea-hypopnea index (AHI) through a variety of mechanisms.[21]  In addition, it is clear that alcohol consumption (perhaps via activation of the SNS), increases systolic and diastolic blood pressure.[22]  Furthermore, alcohol is also associated with worsening hypertension, obesity, and cardiomyopathy.[3] Although these risk factors are associated more with the long-term risk for development of atrial fibrillation, they are worth mentioning.

United States data

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.[23] Conversely, another study showed revealed 5%-10% of all new episodes of atrial fibrillation were attributable to alcohol use.[9]

The frequency of alcohol-related disturbance depends on the population studied. For example, when considering patients hospitalized for alcohol-related rhythm disturbances, atrial fibrillation and atrial flutter appear to be most common arrhythmias.[1, 3] When considering an otherwise healthy, asymptomatic outpatient population, sinus tachycardia appears to be the most common arrhythmia.[24]  

International data

The first large prospective study regarding arrhythmias and alchohol was performed in Munich at Octoberfest in 2015.[24] This study was unique when compared to prior studies in that the study population was an otherwise healthy outpatient population at a festival during acute alcohol consumption. The most common arrhythmia was sinus tachycardia (25.9%); atrial fibrillation (and/or atrial flutter) was seen in 0.8%. When all arrhythmias were considered together, an increasing blood alcohol concentration was associated with an increased incidence of arrhythmia.

The prognosis of holiday heart syndrome (HHS) depends on the presence of any underlying heart disease. Long-term alcohol use increases the risk of cardiomyopathy, arrhythmia, and chronic liver disease.

Note that although the majority (>90%) of cases of alcohol-related atrial fibrillation self-terminate, approximately 20%-30% will recur within 12 months.[11] When considering the type of atrial fibrillation, moderate to heavy alcohol consumption was the strongest risk factor for progression from paroxysmal atrial fibrillation to persistent atrial fibrillation.[25]

Morbidity/mortality

A study showed that males who consume more than 27 standard drinks per week have a higher risk of death, stroke, or systemic thromboembolism.[26] The same study demonstrated that females consuming over 20 standard drinks per week were at a higher risk of stroke or systemic thromboembolism.[26] However, contradictory evidence was seen in another study that demonstrated consumption of greater than 14 standard drinks per week was associated with a lower stroke risk.[3] This highlights the fact that the relationship between atrial fibrillation and thrombogenesis is still not well understood.

Note that the incidence of atrial fibrillation, as a function of alcohol ingestion, clearly increases in a linear and dose-dependent fashion. A separate issue is that modest alcohol consumption has been shown to be beneficial. As such, there is a U-shaped curve relating to alcohol consumption and overall cardiovascular mortality.[3] Stated another way: With the available data, there is no dose of alcohol that should be considered "protective" for atrial fibrillation, whereas there is clearly a range of alcohol dosage that is protective with regard to overall cardiovascular disease.[3]

Patients with acute exposure to alcohol can present with a variety of symptoms.

To reiterate, when holiday heart syndrome (HHS) is considered, alcohol-induced atrial fibrillation is generally what is implied. With that in mind, palpitations are the most common symptom when a patient presents to the hospital for atrial fibrillation.[1, 3] These can be intermittent or persistent, depending on the presence or absence of a sustained arrhythmia and the ventricular response to atrial fibrillation. Patients with rapid ventricular responses can present with near syncopal symptoms, dyspnea on exertion, fatigue, weakness, or angina.

Patients with HHS often have a history of previous alcohol exposure. This often occurs as 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.

On physical examination, the patient with holiday heart syndrome 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 an "irregularly irregular" pulse. Mental status findings may be impaired, consistent with alcohol intoxication or hypotension if present.

Assess serum electrolyte levels, particularly potassium and magnesium, in all patients with acute arrhythmias. Hypomagnesemia and hypokalemia are common in alcoholics, particularly on presentation to the hospital.[32]

Twelve-lead electrocardiography (ECG) is essential to exclude other cardiac pathology such as ischemia, infarction, pulmonary embolism, or hypertrophy.

Echocardiography is the standard of care for assessment of cardiac chamber enlargement, left ventricular (LV) wall motion abnormalities, hypertrophy, valvular disease, and both systolic and diastolic dysfunction. In patients at risk for coronary artery disease, additional cardiac imaging (ie, perfusion imaging) may be required.

See the Medscape Drugs and Diseases topic Alcohol Toxicity.

Patients presenting to the emergency department with sustained tachyarrhythmia secondary to acute alcohol toxicity usually can be observed with electrocardiographic (ECG) monitoring. The three tenets of atrial fibrillation management are rate control, rhythm control, and stroke prevention. (This is well covered in the Medscape Drugs and Diseases topic Atrial Fibrillation. See also the Guidelines section for guidelines recommendations.)

Given the generally transient nature of alcohol-induced atrial fibrillation in the structurally normal heart, rate control and supportive care for alcohol intoxication is generally adequate. For rate control, treatment with an atrioventricular nodal blocking agent (eg, beta-blocker, calcium channel blocker) may be needed if the ventricular rate is rapid. If the duration of atrial fibrillation approaches 24-48 hours, cardioversion (pharmacologic or electrical) may be considered once the patient is medically optimized and the alcohol withdrawal period is complete. 

Most patients with known structural heart disease should be admitted for observation and further management if the arrhythmia persists.

Advise all patients against the excessive use of alcohol in the future and to refrain from use of stimulants. As discussed under the Pathophysiology and Prognosis sections, there is no "healthy" dose of alcohol for prevention of atrial fibrillation. The appearance of atrial fibrillation in patients in whom it is otherwise unexpected (eg, college students) should prompt a discussion of alcohol consumption and the possible cardiac and noncardiac consequences. Persons with alcoholism should be considered for transfer to facilities for detoxification/rehabilitation.

Consultations

Initial consultation of a local cardiologist is recommended. Eventually, the patient may also require the clinical care of an electrophysiologist (a specialist in the subspecialty of cardiology focused on electrical disease of the heart).

Diet

The use of alcohol in general is not recommended, specifically regarding risk of atrial fibrillation. As already noted in the Pathophysiology and Prognosis sections, there is no "healthy" dose of alcohol for prevention of atrial fibrillation. However, this should be balanced with the potential overall cardiovascular benefits with limited alcohol use. Intuitively, stimulants such as caffeine and over-the-counter medications should be avoided initially. However, note that caffeine consumption has not been clearly associated with an increased incidence of atrial fibrillation.[33]

Activity

Following alcohol-related arrhythmia, it is usually 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.

Guideline contributor: Noel G Boyle, MB, BCh, MD, PhD, Professor of Medicine, UCLA Cardiac Arrhythmia Center, Ronald Reagan UCLA Medical Center.

The most recent American Heart Association/American College of Cardiology/Heart Rhythm Society (AHA/ACC/HRS) guidelines regarding atrial fibrillation (AF) can be found at: http://circ.ahajournals.org/content/130/23/e199

Atrial fibrillation classification

In 2014, the AHA/ACC/HRS released updated guidelines for the management of patients with AF. These guidelines supersede the AF guideline published in 2006 and updated in 2011. The guidelines provide the following revised classification schema, based on duration of episodes[30]

• Paroxysmal AF: Episodes of AF that terminate spontaneously or with intervention within 7 days; may recur with variable frequency

• Persistent AF: Episodes of continuous AF that last more than 7 days and do not self-terminate

• Long-standing persistent AF: Episodes of continuous AF that last more than 12 months

• Permanent AF: Applies when a joint physician/patient decision has been made to accept the presence of AF and stop further attempts to restore and/or maintain sinus rhythm (as this represents clinical acceptance rather than an inherent pathophysiological attribute of AF, it is understood that acceptance of AF may change as symptoms, efficacy of interventions, and patient/physician preferences evolve)

• Nonvalvular AF: AF in the absence of rheumatic mitral valve disease, a prosthetic heart valve, or mitral valve repair

It is further noted that episodes often increase in frequency and duration over time. In addition, the term “lone AF” to identify AF in typically younger patients without structural heart disease, hypertension, or diabetes mellitus is deemed potentially confusing and should not be used to guide treatment decisions.[30]

The European Society of Cardiology (ESC) utilizes a similar classification schema published in its 2010 guidelines. The ESC included one additional characterization, silent AF (asymptomatic), which can manifest as AF-related complications such as ischemic stroke or tachycardiomyopathy, or is diagnosed incidentally on electrocardiography (ECG). Any form of AF may be silent or asymptomatic.[34]

Guidelines have been issued by the following organizations for prevention of stroke in atrial fibrillation (AF) patients:

• 2014 American Heart Association/American College of Cardiology/Heart Rhythm Society (AHA/ACC/HRS) ^[30]
• 2012 European Society of Cardiology (ESC) ^[31]
• 2014 American Academy of Neurology (AAN) ^[35]
• 2012 American College of Chest Physicians (ACCP) ^[36]

All major guidelines note that one of the major management decisions in AF is determining the risk of stroke and the appropriate anticoagulation regimen for low-, intermediate-, and high-risk patients. For each anticoagulant, the benefit in terms of stroke reduction must be weighed against the risk of serious bleeding, with the risk-benefit ratio generally considered not advantageous in low-risk patients with AF. Thus, the guidelines stress that clinical judgment and patient preferences should play a major role in shared decision making.[30, 31, 35, 36]

The CHADS2 score (Cardiac failure, Hypertension, Age >75 years, Diabetes, prior Stroke or TIA [transient ischemic attack] or Thromboembolism [doubled]) is the most widely used algorithm to determine yearly thromboembolic risk. Two points are assigned for a history of stroke or TIA, and 1 point is given for age older than 75 years or a history of hypertension, diabetes, or heart failure.[37]

The ACCP bases its recommendations for antithrombotic therapy in patients with nonvalvular atrial fibrillation (NVAF) on the CHADS2 score, as follows[36] :

• CHADS ₂ score = 0 (low risk): No antithrombotic therapy
• CHADS ₂ score ≥1 (intermediate or high risk): Oral antithrombotic therapy

However, the 2014 AHA/ACC/HRS and 2012 updated ESC guidelines both recommend that the CHADS2 score be replaced with the more comprehensive CHA2DS2-VASc score (Congestive heart failure, Hypertension, Age ≥75 years [doubled], Diabetes mellitus, Prior Stroke or TIA or thromboembolism [doubled], Vascular disease, Age 65 to 74 years, Sex category).[30, 31] In this scoring system, points are assigned as follows[38] :

• Congestive heart failure (CHF): 1 point
• Hypertension: 1 point
• Age ≥75 years: 2 points
• Diabetes: 1 point
• Stroke, TIA, or thromboembolism history: 2 points
• Vascular disease (myocardial infarction [MI], peripheral arterial disease, aortic plaque): 1 point
• Age 65-74 years: 1 point
• Sex category (female sex): 1 point

The AHA/ACC/HRS further recommends that antithrombotic therapy should be based on the risk of thromboembolism irrespective of whether the AF pattern is paroxysmal, persistent or permanent.[30]

In 2014, the American Heart Association (AHA) also issued joint guidelines with the American Stroke Association (ASA) for the primary prevention of stroke, which included specific recommendations for stroke prevention in patients with AF. The main advantage of the CHA2DS2-VASc score (range, 0-9) is that it provides significantly improved risk prediction for individuals at low to moderate risk compared with the CHADS2 (scores of 0 or 1), particularly for elderly women.[39]

The AHA/ACC/HRS recommendations for antithrombotic therapy in patients with AF, based on CHA2DS2-VASc scores, are as follows[30] :

• NVAF and CHA ₂DS ₂-VASc score = 0: No antithrombotic therapy
• NVAF and CHA ₂DS ₂-VASc score = 1: No antithrombotic therapy or oral antithrombotic therapy
• Prior stroke, TIA or CHA ₂DS ₂-VASc Score ≥2: Oral antithrombotic therapy

The ESC offers varying recommendations for patients with AF based on CHA2DS2-VASc scores, as follows[31] :

• CHA ₂DS ₂-VASc score = 0: No antithrombotic therapy
• CHA ₂DS ₂-VASc score = 1: Oral anticoagulants
• CHA ₂DS ₂-VASc score ≥2: Oral anticoagulants

The shift from the CHADS2 score to the CHA2DS2-VASc score has not been without controversy. The number of patients eligible for oral anticoagulant therapy in the United States is estimated to increase by nearly 1 million, raising concerns about the associated increase in bleeding complications. An analysis by O’Brien and colleagues concluded that using the 2014 AHA/ACC/HRS recommendations to guide the management of AF would result in 98.5% of patients 65 years of age and older and 97.7% of women with AF receiving a definitive recommendation for oral anticoagulant therapy.[40]

The 2014 AAN revised guidelines for stroke prevention in NVAF recommend use of risk stratification to aid in clinical decision making, but do not recommend the use of any specific tool. Furthermore, the guidelines caution against use of strictly interpreted thresholds as definitive indicators for which patients require anticoagulation therapy. Additional recommendations for patient selection included the following[35] :

• Anticoagulation therapy should be offered to all patients with NVAF and a history of ischemic attack or stroke
• Anticoagulation therapy should not be offered to patients with NVAF who lack additional risk factors; these patients may be offered aspirin therapy or no antithrombotic therapy

The major guidelines vary considerably in their recommendations for antithrombotic therapy. See the table below.

Table. Antithrombotic Therapy Recommendations for Atrial Fibrillation (Open Table in a new window)

The 2014 American Heart Association (AHA)/American College of Cardiology (ACC)/Heart Rhythm Society (HRS) guidelines include the following recommendations for control of ventricular rate in patients with atrial fibrillation (AF)[30] :

• Beta-blockers or non-dihydropyridine calcium channel blockers are first-line agents for paroxysmal, persistent or permanent AF.

• Intravenous (IV) beta-blockers or non-dihydropyridine calcium channel blockers may be used to slow ventricular heart rate in an acute setting in patients without preexcitation; in hemodynamically unstable patients, electrical cardioversion is indicated.

• Consider IV amiodarone for rate control in critically ill patients without preexcitation if the condition limits the use of beta-blockers or calcium channel blockers.

• In patients with AF symptoms during activity, assess heart rate control during exertion, adjusting drug treatment as needed.

• Heart rate control (defined as < 80 bpm at rest) may be considered for less symptomatic patients with AF; a more lenient rate-control strategy (< 110 bpm at rest) is reasonable when patients remain asymptomatic and left ventricular (LV) systolic function is preserved.

• In patients with inadequate ventricular rate control despite drug therapy, atrioventricular (AV) nodal ablation and pacemaker implantation may be considered.

• AV nodal ablation should not be performed without prior attempts to achieve rate control with medications.

• Non-dihydropyridine calcium channel blockers are contraindicated in decompensated heart failure.

• With preexcitation syndrome and AF, non-dihydropyridine calcium channel blockers, digoxin, and IV amiodarone are contraindicated.

• Dronedarone should not be used in patients with permanent AF or class III or IV heart failure.

The American Heart Association (AHA)/2014 American College of Cardiology (ACC)/Heart Rhythm Society (HRS) guidelines provide the following recommendations regarding cardioversion of atrial fibrillation (AF)[30] :

• AF of ≥48 hours’ duration, or when the duration is unknown: Warfarin anticoagulation (international normalized ratio [INR] 2-3) for at least 3 weeks before and 4 weeks after cardioversion, regardless of the CHA2DS2-VASc score and the cardioversion method (electrical or pharmacological) used; anticoagulation with dabigatran, rivaroxaban, or apixaban is also reasonable

• AF of ≥48 hours’ duration, or when the duration is unknown, requiring immediate cardioversion for hemodynamic instability: Anticoagulation should be administered as soon as possible and continued for 4 weeks after cardioversion

• AF with high risk of stroke and < 48 hours’ duration: Administration of IV heparin or low molecular weight heparin (LMWH), factor Xa inhibitor, or direct thrombin inhibitor as soon as possible before and immediately after cardioversion, followed by long-term anticoagulation therapy

• AF with low risk of stroke and < 48 hours’ duration: Administration of either IV heparin or LMWH, factor Xa or direct thrombin inhibitor or no antithrombotic therapy may be considered for cardioversion, without the need for postcardioversion oral anticoagulation therapy

• For AF of any duration, long-term anticoagulation therapy should be based on the patient’s stroke risk profile

• AF or atrial flutter of ≥48 hours’ duration: For conversion of AF of ≤7 days, agents with proven efficacy include flecainide, ibutilide, propafenone and, to a lesser degree, amiodarone

• For conversion of AF lasting 7-90 days, agents with proven efficacy include amiodarone, ibutilide, flecainide, and propafenone

• For conversion of AF lasting more than 90 days, oral propafenone, amiodarone, and dofetilide have been shown to be effective at converting persistent AF to normal sinus rhythm

• Propafenone or flecainide in addition to a beta-blockers or non-dihydropyridine calcium channel antagonists is reasonable for termination of AF outside the hospital, once this treatment has been observed to be safe in a monitored setting for selected patients (“pill-in-the-pocket”)

• Dofetilide therapy should not be initiated out of hospital because of the risk of torsade de pointes

• Direct current cardioversion (DCC) is indicated when rapid ventricular rate does not respond promptly to medications in patients with AF and ongoing myocardial ischemia, hypotension or heart failure

• Immediate DCC in preexcitation with rapid tachycardia or hemodynamic instability

NOTE: Repeated cardioversions may be undertaken in patients with persistent AF, provided that sinus rhythm can be maintained for a clinically meaningful period between cardioversion procedures; severity of AF symptoms and patient preference should be considered before initiation of a strategy requiring serial cardioversions

In general, the European Society of Cardiology (ESC) recommendations for cardioversion concur with the AHA/ACC/HRS guidelines. Many of the differences between the guidelines involve the use of vernakalant, which was approved for use in European Union in 2010 but has not been approved by the US Food and Drug Administration. Additional and/or variant ESC recommendations include the following[31] :

• In the absence of structural heart disease, IV flecainide, propafenone, ibutilide, or vernakalant
• In patients with risk factors for stroke or AF recurrence, oral anticoagulant therapy should be continued lifelong, irrespective of the apparent maintenance of sinus rhythm following cardioversion
• In patients with AF ≤7 days and moderate structural heart disease, IV vernakalant may be considered
• Vernakalant should be used with caution in patients with NYHA class I–II heart failure

The ESC guidelines note that vernakalant is contraindicated in patients with any of the following:

• Hypotension (systolic blood pressure < 100 mm Hg)
• Recent (30 days) acute coronary syndrome
• New York Heart Association (NYHA) class III and IV heart failure
• Severe aortic stenosis
• QT interval prolongation (uncorrected QT >440 ms)

The 2014 American College of Cardiology (ACC)/American Heart Association (AHA)/Heart Rhythm Society (HRS) guidelines include the following recommendations for the prevention of atrial fibrillation (AF) and maintenance of sinus rhythm[30] :

• Precipitating or reversible causes of AF should be treated before initiation of antiarrhythmic drug therapy; antiarrhythmic drug therapy can be considered for treatment of tachycardia-induced cardiomyopathy

• Antiarrhythmic drugs include amiodarone, dofetilide, dronedarone, flecainide, propafenone, and sotalol; drug selection should be based on underlying heart disease and comorbidities

• Consider risks, including proarrhythmia, before initiating antiarrhythmic drug treatment

• Amiodarone should be used only after consideration of its potential toxicities and risks, and when other agents have failed or are contraindicated

• Discontinue antiarrhythmic drugs, including dronedarone, when AF becomes permanent

• Dronedarone is contraindicated for treatment of AF in patients with New York Heart Association (NYHA) class III and IV heart failure or patients who have had an episode of decompensated heart failure in the past 4 weeks

The European Society of Cardiology recommendations for maintenance of sinus rhythm are similar to those in the AHA/ACC/HRS.[31]

Both the 2014 American Heart Association (AHA)/American College of Cardiology (ACC)/Heart Rhythm Society (HRS) and 2012 European Society of Cardiology (ESC) updated guidelines suggest a more prominent role for radiofrequency ablation in the treatment of atrial fibrillation (AF), including its use as first-line therapy in recurrent symptomatic paroxysmal or persistent AF.[30, 31]

According to AHA/ACC/HRS guidelines, AF catheter ablation is contraindicated for patients who cannot be treated with anticoagulant therapy during and after the procedure and should not be performed with the sole intent of eliminating the need for anticoagulation.[30]

Symptoms of acute alcohol toxicity generally resolve spontaneously, and management is largely supportive (ie, intravenous [IV] hydration and correction of electrolyte derangements). Arrhythmia monitoring and observation are sufficient 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 beta-blockers or nondihydropyridine calcium channel blockers (CCBs) is appropriate. Digoxin is a third-line option; chronic therapy with this drug is rarely indicated. Patients who are hemodynamically unstable should be treated with direct-current cardioversion.

As discussed earlier under Prognosis, although the majority (>90%) of cases of alcohol-related atrial fibrillation self-terminate, approximately 20%-30% will recur within 12 months.[11] When considering the type of atrial fibrillation, moderate to heavy alcohol consumption has been demonstrated to be the strongest risk factor for progression from paroxysmal atrial fibrillation to persistent atrial fibrillation.[25]

As discussed under Diagnostic Considerations, although long-term anticoagulation is indicated for patients with paroxysmal, persistent, or permanent atrial fibrillation plus risk factors for stroke or systemic thromboembolism, it may be prudent to be cautious about anticoagulating patients with expected acute alcohol toxicity, especially if there is a history of possible trauma. Unless high-risk features are present (ie, prior stroke, mechanical heart valve, or other indication for anticoagulation) a reasonable approach may be to allow the patient to recover from the acute episode, and then initiate anticoagulation once they are clinically stable.

Note that when considering initiating anticoagulation, the most recent American College of Cardiology/American Heart Association (ACC/AHA) guidelines do not specifically consider "reversible" causes as a reason to forgo anticoagulation for stroke risk reduction. That is, a single episode of atrial fibrillation may result in a significant change in a patient's medical regimen for the forseeable future.[30]  In this scenario, anticoagulation would be initiated after a patient-physician discussion regarding the risks and benefits of anticoagulation. Integral to this discussion is calculation of both the CHA2DS2VASc (Cardiac failure, Hypertension, Age >75 years [doubled], Diabetes, prior Stroke or TIA [transient ischemic attack] or thromboembolism [doubled], Vascular disease, Age 65-75 years, Sex category) score and the HAS-BLED (Hypertension, Abnormal renal/liver function, Stroke, Bleeding history or predisposition, Labile INR [international normalized ratio], Elderly, Drugs/alcohol concomitantly (https://www.chadsvasc.org/) score.[30, 31]

Because atrial fibrillation with rapid ventricular response (RVR) is the primary acute concern with holiday heart syndrome (HHS), commonly used medications for heart rate control are outlined in the next sections. (Also see the Guidelines section, under Rate Control.) Although there is no clear consensus about what heart rate should be targeted, a goal based on symptoms is reasonable (eg, A heart rate < 85 beats per minute is reasonable in a symptomatic patient, whereas a more lenient heart rate goal is reasonable in an asymptomatic patient.) Other antiarrhythmic medications and anticoagulants are outside the scope of this article. Information regarding these ageents can be found here.

Class Summary

Beta-blockers (also known as beta-antagonists) function via sympatholytic effects. The beta-1 adrenoreceptor is the adrenoreceptor responsible for myocardial effects. Thus, beta-1 selective agents are generally preferred if possible to avoid off-target effects. In general, they are the treatment of choice in the setting of acute myocardial ischemia or left ventricular systolic dysfunction.

Metoprolol (Lopressor, Toprol XL)

Metoprolol is a beta-1 selective (ie, cardioselective) beta-blocker that may be given IV or PO for acute rate control.

Metoprolol is not avaliable as an infusion. Thus, once rate controlled, the patient must be switched to scheduled IV or PO doses.

Esmolol (Brevibloc)

Esmolol is another cardioselective beta-blocker. It is administered as an IV bolus with maintenance infusion. Its main clinical utility is its short half-life (9 minutes, with a clinical hemodynamic effect commonly quoted at 10-30 minutes).

Class Summary

In specialized conducting and automatic cells in the heart, calcium is involved in the generation of the action potential. Calcium channel blockers inhibit the movement of calcium ions across the cell membrane, thus depressing both impulse formation (automaticity) and conduction velocity.

Diltiazem (Cardizem CD, Dilacor, Tiazac)

Diltiazem has a relatively balanced effect on both the myocardium as well as the peripheral vasculature. Similar to verapamil, this agent should be used with caution whenever left ventricular systolic dysfunction is present.

Diltiazem may be given as an IV bolus or as an infusion.

Verapamil (Calan, Covera-HS, Verelan)

Verapamil is the most cardioselective of the calcium channel blockers, with minimal effect on the peripheral vasculature. It should be used with caution whenever left ventricular systolic dysfunction is present.

Verapamil may be given as an IV bolus or as an infusion. In general, verapamil infusions are used less commonly when compared with use of diltiazem.

Class Summary

Cardiac glycosides have direct and indirect cardiac effects. Their direct effect is in inhibiting the membrane sodium-potassium (Na+-K+) pump, raising intracellular levels of sodium and leading to an accumulation of intracellular calcium. This in turn increases cardiac contractility. Their indirect effect is in enhancing vagal tone.

Digoxin (Lanoxin, Lanoxicaps)

Digoxin's effects on atrioventricular nodal conduction are mediated via increased vagal tone. It is also characterized by positive inotropic effects on the myocardium via inhibition of the sodium-potassium ATPase, and the resultant increase in intracellular calcium. Digoxin has fallen out of favor in relatively recent years over concerns of proarrhythmias, drug-drug-interactions, and variable effects on overall long-term mortality depending on the population studied. In general, it should only be used for rate control in the presence of heart failure with reduced ejection fraction.

Class Summary

Class III antiarrhythmic agents inhibit adrenergic stimulation; affect sodium, potassium, and calcium channels; markedly prolong action potential and repolarization; and decrease atrioventricular conduction and sinus node function.

Amiodarone (Cordarone, Nexterone, Pacerone)

Amiodarone is perhaps the most effective of all the antiarrhythmic drugs. It has effects in all four of the Vaughn Williams antiarrhythmic classes. In general, however, amiodarone should not be a first-line agent. When used for acute rate control in the acute setting, only IV amiodarone is practical. It is useful for rate control when heart failure or hypotension are present, as amiodarone tends to cause less hypotension than beta-blockers and calcium channel blockers.  

NOTE: There is a theoretical concern for cardioversion with amiodarone which must be considered if selecting this drug.  

In this particular context of alcohol-induced atrial fibrillation, keep in mind that amiodarone is also associated with many adverse effects, one of which is hepatotoxicity.