Holiday heart syndrome

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2]

Overview

Holiday heart syndrome is an irregular heartbeat pattern presented in individuals who are otherwise healthy. It can be the result of stress, dehydration, and drinking. Usually this syndrome is associated with binge drinking. However, it may also occur in patients who usually drink little or no alcohol.

Historical Perspective

The term was coined by Ettinger et al in 1978.

Pathophysiology

• Holiday heart syndrome is defined as "arrhythmias of the heart, sometimes apparent after a vacation or weekend away from work, following excessive alcoholconsumption; usually transient".
• Irregular heartbeats are very serious and result mostly from supraventricular tachycardias.
• If palpitations continue for longer than a few hours patients should seek medical attention.
• Atrial fibrillation is the most common arrhythmia in holiday heart syndrome and can result in very serious consequences such as stroke, but a variety of changes in the intervals and morphology of the EKG may occur (irregular series of QRS complexes and absent p waves).
• Other frequently observed arrhythmias include atrial flutter, atrial tachycardia, junctional tachycardia, multiple APC's, multiple PVC's and ventricular tachycardia.
• In patients with new onset atrial fibrillation and no overt pre-existing heart disease, holiday heart syndrome should be considered as a part of differential diagnosis.

Pathophysiology

• 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.
• 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.
• 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.
• Note that the risk of atrial fibrillation persists into the "hangover" and/or withdrawal phase, which corresponds with an increased sympathetic tone.
• 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.
  •  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 and humans being similarly affected, whereas canine atria appear unaffected.
• 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.
• Conversely, CaMKII inhibition eliminates binge alcohol-evoked arrhythmic activities.
• 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.
• Although ventricular repolarization abnormalities on surface ECG were described, whether ventricular myocardium responds similarly to ethanol is uncertain.

Epidemiology and Demographics

• The frequency with which cardiac arrhythmias can be attributed to alcohol use is unclear owing to differing data.
• Holiday heart syndrome commonly affects individuals younger than 65 years of age.

Causes

The most common cause of holiday heart syndrome is excessive alcohol consumption. Other associated causes that might aggravate the disease include elevated stress levels and dehydration.

Differentiating Holiday Heart Syndrome from Other Diseases

Holiday heart syndrome must be differentiated from

• Alcoholism
• Arrhythmia
• Cirrhotic cardiomyopathy
• Dilated cardiomyopathy
• Psychiatric problems

Epidemiology and Demographics

• The incidence and prevalence of holiday heart syndrome is unclear due to conflicting evidence.

Natural History, Complications, and Prognosis

Natural History

• If left untreated, it may culminate in severe cardiomyopathy, valvular disease, and ultimately death. Some patients may develop end-stage liver disease which also has a poor prognosis.

Complications

• Complications of the holiday heart syndrome include:
  • New or worsening heart failure
  • Life-threatening arrhythmias
  • Community-acquired pneumonia
  • Thromboembolism
  • Death

Prognosis

• If diagnosed early and treated with alcohol cessation, the prognosis for holiday heart disease is good as the disease is reversible.

Diagnosis

History and Symptoms

• Patients with HHS often have a history of previous alcohol exposure.
• A history of alcoholism should alert physicians to concomitant illnesses such as alcohol-related cardiomyopathy and chronic liver disease.

Symptoms

• Patients with acute exposure to alcohol can present with a variety of symptoms.
• Holiday heart syndrome is considered, alcohol-induced atrial fibrillation.
• Palpitations are the most common symptom when a patient presents to the hospital for atrial fibrillation.
• 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.

Physical Examination

• 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.

Laboratory Findings

• The following laboratory findings can help in diagnosis of holiday heart syndrome.
  • Complete blood count may show macrocytic anemia via an elevated mean corpuscular volume.
  • Sometimes an elevated white blood cell count may be seen as alcoholics have decreased immunity and tend to get sick more often.
  • Complete metabolic panel may show 2:1 aspartate aminotransferase (AST) to alanine aminotransferase (ALT) ratio.
  • Magnesium and thiamine are commonly low in alcoholics.
  • Urine tests also exist including ethyl glucuronide and ethyl sulfate , which are both biomarkers signifying the breakdown of alcohol.
  • Gamma-glutamyl transferase may be high in these patients.
  • Another blood test to identify alcohol use is phosphatidyl ethanol (PEth), a marker.
  • This is typically measured in blood and can indicate moderate to heavy drinking.
  • Carbohydrate-deficient transferrin is useful to identify patients who have relapsed following a period of abstinence.

• Twelve-lead electrocardiography (ECG) is essential to exclude other cardiac pathology such as ischemia, infarction, pulmonary embolism, or hypertrophy.
• A chest x-ray may show cardiomegaly.
• An echocardiogram should be performed to evaluate for any structural abnormalities and to assess cardiac function.
• 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.
• Liver disease is often a feature holiday heart syndrome as alcohol damages the liver. Therefore, ultrasound of the liver may reveal liver cirrhosis.

Treatment

The mainstay of treatment for holiday heart syndrome depends on the patients vitals at the time of presentation.

• If the patient is unstable and has atrial fibrillation, cardioversion is the recommendation.
• If the patient is stable, the therapeutic indication is for arrhythmia treatment.
  • Complete alcohol cessation was needed to see a reversal of the disease process,
  • The patient must be encouraged to join alcoholics anonymous (AA) and other support groups.
• Patients presenting to the emergency department with sustained tachyarrhythmia secondary to acute alcohol toxicity usually can be observed with electrocardiographic monitoring.