You are in: eMedicine Specialties > Cardiology > Cardiovascular Syndromes in Systemic Diseases Holiday Heart SyndromeArticle Last Updated: Sep 27, 2006AUTHOR AND EDITOR INFORMATIONSection 1 of 10
  Author: Adam S Budzikowski, MD, PhD, Assistant Professor of Medicine, Division of Cardiovascular Medicine - EP section, SUNY Downstate Adam S Budzikowski is a member of the following medical societies: American College of Cardiology and European Society of Cardiology 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; 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; Howard S Weiss, DO, Staff Physician, Department of Medicine, Winthrop University Hospital Editors: Hanumant Deshmukh, MD †, Former Chief of Cardiology, Veterans Affairs Medical Center; Former Associate Professor, Department of Medicine, Rosalind Franklin University of Medicine and Science; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Steven J Compton, MD, FACC, FACP, Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals; Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital; Leonard Ganz, MD, Associate Professor of Medicine, Temple University School of Medicine; Cardiac Electrophysiologist, Children's Hospital of Pittsburgh, University of Pittsburgh Medical Cent, West Penn Hospital Author and Editor Disclosure Synonyms and related keywords: holiday heart syndrome, alcohol-related paroxysmal atrial fibrillation, acute cardiac alcohol toxicity, arrhythmia, alcohol-related cardiomyopathy, idiopathic dilated cardiomyopathy, dysrhythmic episodes, acute cardiac rhythm disturbance, acute conduction disturbance, supraventricular tachyarrhythmia, binge, binge drinking INTRODUCTIONSection 2 of 10
  BackgroundIt has long been recognized that alcohol consumed in large quantities for many years can induce an alcoholic cardiomyopathy. Clinically identical to idiopathic dilated cardiomyopathy, alcoholic cardiomyopathy is the major form of secondary dilated cardiomyopathy in the Western world. With this change in cardiac structure and decline in function, there exists the substrate for atrial and ventricular arrhythmias. However, it is only within the past 20-25 years that the arrhythmogenic potential of short-term alcohol consumption in patients without clinically evident heart failure has been elucidated. 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. Holiday heart syndrome now most commonly refers to the association between alcohol use and rhythm disturbances, particularly supraventricular tachyarrhythmias in apparently healthy people. Recently, similar reports indicated that recreational use of marijuana may have similar effects. The most common rhythm disorder is atrial fibrillation, which usually converts to normal sinus rhythm within 24 hours. Holiday heart syndrome should be particularly considered as a diagnosis in patients without structural heart disease and with new-onset atrial fibrillation. 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. PathophysiologySeveral 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. 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 to patients who experienced arrhythmias in the absence of alcohol consumption. 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. 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. Although ventricular repolarization abnormalities on surface ECG were described, whether ventricular myocardium responds in a similar way 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. FrequencyUnited StatesThe 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. 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. InternationalWorldwide prevalence is not well documented. Prevalence is presumably increased in countries with higher rates of alcohol ingestion and alcoholism. Mortality/MorbidityRegular 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. RaceEvidence regarding race is unavailable. SexAn 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. AgeAlthough 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. CLINICALSection 3 of 10
HistoryPatients with acute exposure to alcohol can present with a variety of symptoms.
PhysicalOn 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. DIFFERENTIALSSection 4 of 10
Alcoholism Atrial Fibrillation Atrial Flutter Hyperthyroidism Paroxysmal Supraventricular Tachycardia Pulmonary Embolism
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| Drug Name | Metoprolol (Lopressor, Toprol XL) |
|---|---|
| Description | 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. |
| Adult Dose | 5 mg IV push q5min, not to exceed 3 doses; can be followed by 25 mg PO q6h |
| Pediatric Dose | Not established |
| Contraindications | Bradycardia; second- or third-degree heart block; significant pulmonary congestion; asthma; bronchospastic lung disease |
| 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 |
| Pregnancy | B - Usually safe but benefits must outweigh the risks. |
| 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 |
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.
| Drug Name | Verapamil (Calan, Covera-HS, Verelan) |
|---|---|
| Description | Can diminish PVCs associated with perfusion therapy and decrease the risk of ventricular fibrillation and ventricular tachycardia. |
| Adult Dose | 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 Dose | Not recommended |
| Contraindications | Documented hypersensitivity; severe CHF, sick sinus syndrome or second- or third-degree AV block, and hypotension (<90 mm Hg systolic) |
| 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 |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| 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 |
| Drug Name | Diltiazem (Cardizem CD, Dilacor, Tiazac) |
|---|---|
| Description | 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. |
| Adult Dose | 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 Dose | Not recommended |
| Contraindications | Documented hypersensitivity; severe CHF, sick sinus syndrome, second- or third-degree AV block, and hypotension (<90 mm Hg systolic) |
| 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 |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Caution in impaired renal or hepatic function; may increase LFT levels, and hepatic injury may occur |
| Drug Name | Digoxin (Lanoxin, Lanoxicaps) |
|---|---|
| Description | 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. |
| Adult Dose | 0.75-1.25 mg/d PO in divided doses (0.25 mg q4h x 4) |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; beriberi heart disease, idiopathic hypertrophic subaortic stenosis, constrictive pericarditis, and carotid sinus syndrome |
| 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 |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| 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 |
Holiday Heart Syndrome excerpt
Article Last Updated: Sep 27, 2006
