Holiday Heart Syndrome Treatment & Management: Medical Care, Diet and Activity

Sections

Treatment

Medical Care

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.

Guidelines

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Hald EM, Enga KF, Lochen ML, et al. Venous thromboembolism increases the risk of atrial fibrillation: the Tromso study. J Am Heart Assoc. 2014 Jan 2. 3 (1):e000483. [Medline].
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Table. Antithrombotic Therapy Recommendations for Atrial Fibrillation

Table. Antithrombotic Therapy Recommendations for Atrial Fibrillation

Issuing Organization	Year	Patient Groups	Antithrombotic Therapy
American Heart Association/American College of Cardiology/ Heart Rhythm Society (AHA/ACC/HRS)^[30]	2014	AF with mechanical heart valve With prior stroke, TIA or CHA ₂DS ₂-VASc score ≥2 NVAF and CHA ₂DS ₂-VASc score ≥2 NVAF with CHA ₂DS ₂-VASc score ≥2 and end-stage CKD or on hemodialysis NVAF with CHA ₂DS ₂-VASc score ≥2 and moderate to severe CKD All patients	Warfarin therapy; target INR, 2.0-3.0 or 2.5-3.5 based on type and location of prosthesis Bridging therapy with unfractionated heparin or LMWH for patients undergoing procedures that require interruption of warfarin. Decisions on bridging therapy should balance the risks of stroke and bleeding. Oral anticoagulants: Warfarin (INR 2.0-3.0), dabigatran, apixaban, or rivaroxaban Warfarin (INR 2.0-3.0); if unable to maintain a therapeutic INR level with warfarin, use of a direct thrombin or factor Xa inhibitor (dabigatran, rivaroxaban, or apixaban) Warfarin (INR 2.0-3.0); direct thrombin or factor Xa inhibitors are not recommended Reduced doses of direct thrombin or factor Xa inhibitors may be considered (eg, dabigatran, rivaroxaban, apixaban), but safety and efficacy have not been established In patients receiving warfarin, the INR should be determined at least weekly during initiation of antithrombotic therapy and at least monthly when anticoagulation (INR in range) is stable Periodic reevaluation of the need and choice of anti-thrombotic therapy to reassess stroke and bleeding risks
American Heart Association/American Stroke Association (AHA/ASA)^[39]	2014	Valvular AF/ CHA ₂DS ₂-VASc score ≥2 NVAF// CHA ₂DS ₂-VASc score ≥2 and low risk for hemorrhagic complications NVAF, CHA ₂DS ₂-VASc score = 1, and low risk for hemorrhagic complications	Warfarin therapy; target INR, 2.0-3.0 Oral anticoagulant (warfarin, dabigatran, apixaban, or rivaroxaban) individualized based on patient risk factors (particularly risk for intracranial hemorrhage), cost, tolerability, patient preference, potential for drug interactions, and other clinical characteristics. No antithrombotic therapy, anticoagulant therapy, or aspirin therapy may be considered
American Academy of Neurology (AAN)^[35]	2014	NVAF and history of TIA or stroke; age >75 years, if no history of unprovoked bleeding or intracranial hemorrhage; patients with dementia or occasional falls; however in patients with moderate to severe dementia or frequent falls, risk-benefit ratio is uncertain Patients at moderate stroke risk in developing countries where newer anticoagulants are unavailable	Warfarin, target INR 2.0 to 3.0 Dabigatran, rivaroxaban, or apixaban (preferred) if at high risk for intracranial bleeding or unable to submit to frequent periodic INR testing Apixaban, if at increased risk for gastrointestinal bleeding Triflusal 600 mg/day plus moderate-intensity anticoagulation (INR 1.25–2.0) with acenocoumarol is likely more effective than acenocoumarol alone at the higher INR (2.0-3.0)
American College of Chest Physicians (ACCP)^[36]	2012	NVAF intermediate risk (CHADS₂ score = 1) or high risk (CHADS₂score ≥2)	Oral anticoagulants: dabigatran 150 mg BID preferred over warfarin (target INR range, 2.0-3.0) Patients who are unsuitable for or choose not to take an oral anticoagulant (for reasons other than concerns about major bleeding): combination therapy with aspirin and clopidogrel
European Society of Cardiology (ESC)^[31]	2012	CHA ₂DS ₂-VASc score = 0, and females aged < 65 years with CHA ₂DS ₂-VASc score = 1 CHA ₂DS ₂-VASc score = 1 CHA ₂DS ₂-VASc score ≥2 All patients Patients who refuse oral anticoagulants	No antithrombotic therapy Oral anticoagulants: Warfarin (INR 2.0-3.0) or dabigatran or rivaroxaban or apixaban based on assessment of risk of bleeding Oral anticoagulants: Dabigatran or rivaroxaban or apixaban preferred over warfarin (INR 2.0-3.0) When dabigatran is considered, 150 mg BID preferred; 110 mg BID is preferred for ages ≥80 years, concomitant use of interacting drugs, high bleeding risk or moderate renal impairment When rivaroxaban is considered, 20 mg OD preferred; 15 mg OD is preferred for those with high bleeding risk or moderate renal impairment Baseline and subsequent annual assessment of renal function (by CrCl) is recommended in patients following initiation of any novel oral anticoagulant (dabigatran, rivaroxaban, and apixaban), and 2-3 times per year in those with moderate renal impairment; novel oral anticoagulants are not recommended in patients with severe renal impairment (CrCl < 30 mL/min) Antiplatelet therapy should be considered, using combination therapy with aspirin 75–100 mg plus clopidogrel 75 mg daily (where there is a low risk of bleeding) or—less effectively—aspirin 75–325 mg daily
Note: Edoxaban was approved by the FDA in January 2015 for use as an oral anticoagulant in atrial fibrillation. AF = atrial fibrillation; BID = twice daily; CKD = chronic kidney disease; CrCl = creatinine clearance; INR = international normalized ratio; LMWH = low-molecular-weight heparin; NVAF = nonvalvular atrial fibrillation; OD = before bedtime; TIA = transient ischemic attack.

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Author

Lawrence Rosenthal, MD, PhD, FACC, FHRS Associate Professor of Medicine, Director, Section of Cardiac Pacing and Electrophysiology, Director of EP Fellowship Program, Division of Cardiovascular Disease, University of Massachusetts Memorial Medical Center

Lawrence Rosenthal, MD, PhD, FACC, FHRS is a member of the following medical societies: American College of Cardiology, Massachusetts Medical Society, American Heart Association

Disclosure: Nothing to disclose.

Coauthor(s)

Glenn T Stokken, MD Fellow in Cardiac Electrophysiology, Department of Cardiology, University of Massachusetts Medical School

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Steven J Compton, MD, FACC, FACP, FHRS Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

Steven J Compton, MD, FACC, FACP, FHRS is a member of the following medical societies: American College of Physicians, American Heart Association, American Medical Association, Heart Rhythm Society, Alaska State Medical Association, American College of Cardiology

Disclosure: Nothing to disclose.

Chief Editor

Jose M Dizon, MD Associate Professor of Clinical Medicine, Clinical Electrophysiology Laboratory, Division of Cardiology, Columbia University College of Physicians and Surgeons; Assistant Attending Physician, Department of Medicine, C\New York-Presbyterian/Columbia University Medical Center

Jose M Dizon, MD is a member of the following medical societies: American College of Cardiology, Heart Rhythm Society

Disclosure: Nothing to disclose.

Additional Contributors

Richard H Smith, MD Director of Echocardiography, Long Island Heart Associates

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, American Medical Association

Disclosure: Nothing to disclose.

James P Daubert, MD Professor of Medicine, Cardiology Division, Duke University School of Medicine

James P Daubert, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, Heart Rhythm Society

Disclosure: Partner received equity interest from Medtronic for none; Received honoraria from Boston Scientific for speaking and teaching; Received consulting fee from CV Therapeutics for consulting; Received consulting fee from Cryocor for consulting.

Howard S Weiss, DO Associate Medical Director, St Peter's Hospital Sleep Center

Howard S Weiss, DO is a member of the following medical societies: American Medical Association, American Osteopathic Association

Disclosure: Nothing to disclose.

Adam S Budzikowski, MD, PhD, FHRS Assistant Professor of Medicine, Division of Cardiovascular Medicine, Electrophysiology Section, State University of New York Downstate Medical Center, University Hospital of Brooklyn

Adam S Budzikowski, MD, PhD, FHRS is a member of the following medical societies: European Society of Cardiology, Heart Rhythm Society

Disclosure: Received consulting fee from Boston Scientific for speaking and teaching; Received honoraria from St. Jude Medical for speaking and teaching; Received honoraria from Zoll for speaking and teaching.

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