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Holiday Heart Syndrome

Holiday Heart Syndrome

Article Author:
Kristen Brown
Article Author:
Varun Yelamanchili
Article Editor:
Akshay Goel
8/16/2020 10:40:39 AM
For CME on this topic:
Holiday Heart Syndrome CME
PubMed Link:
Holiday Heart Syndrome


The Holiday heart syndrome is a common cause of cardiac disease predominantly in the United States of America. The Holiday heart syndrome, also referred to as alcohol-induced atrial arrhythmias, is characterized by an acute cardiac rhythm and/or conduction disturbance associated with heavy ethanol consumption in a person without other clinical evidence of heart disease. The most important aspect of holiday heart syndrome is that it is reversible. Recovery of cardiac function occurs through early diagnosis and complete cessation of alcohol use. This chapter will discuss holiday heart syndrome in detail including etiology, epidemiology, pathophysiology, histopathology, history and physical, recommended tests, treatment, and potential complications.


Excessive alcohol consumption along with elevated stress levels and dehydration appears to be the cause of Holiday heart syndrome. 


The frequency of Holiday heart syndrome is unclear due to conflicting evidence. One study revealed that 5%-10% of all new episodes of atrial fibrillation were attributable to alcohol use.[1] Conversely, another showed alcohol as the causative agent in 35% of cases of new-onset atrial fibrillation and 63% of cases in patients younger than 65 years.[2]


The pathophysiology of Holiday heart syndrome, or alcohol-induced arrhythmia, is complex, and therefore not completely understood. The most commonly accepted therapy is that chronic ethanol heavy use leads to cardiac structural and cellular changes through a buildup of ethanol and its metabolites. The most commonly researched metabolite is acetaldehyde, produced by the liver by a chemical reaction with alcohol dehydrogenase. It along with other substances is thought to cause oxidative damage, mitochondrial dysfunction, cell death, lower the effects of cardioprotective molecules, alter protein synthesis and calcium transport.[3][4][5] As with dilated cardiomyopathy, there is a higher risk of electrical disturbance in the Holiday heart syndrome. Atrial fibrillation is the most frequently seen arrhythmia in Holiday heart syndrome. 


The gross changes seen in a tissue sample in a patient with Holiday heart syndrome are non-specific and frankly very similar to other causes of dilated cardiomyopathy. One study showed that alcoholic cardiomyopathy had a statistically significant reduction in myocytes compared to other cardiomyopathies. That same study revealed that the LV had the greatest of variation in myocytes between the two groups. Interestingly, no statistical difference existed regarding the amount of fibrosis.[6] On a microscopic level, patients with Holiday heart have visible changes to the structure of the mitochondrial reticulum in the myocytes.[7]

History and Physical

A diagnosis of Holiday heart syndrome derives from a good history and physical examination, the history being the more significant aspect. Healthcare providers have to exercise tact to solicit the patient's alcohol history, especially since not all patients are willing to divulge this information. The other part of the puzzle is ruling out any other potential causes of the presenting symptoms. Ensuring the patient doesn't already have a diagnosis that would explain the symptoms is essential. The physical exam is more straightforward. The cardiac exam may reveal an atrial arrhythmia. It is important to note that some atrial arrhythmias are intermittent and may not be present on examination. Repeat cardiac examination may be necessary if there is suspicious of this diagnosis. Additionally, signs and symptoms of heart failure may be present depending on the extent and duration of the disease. 


Routine laboratory tests may reveal evidence suggestive of alcohol use. For example, complete blood count (CBC) may show macrocytic anemia via an elevated mean corpuscular volume (MCV). Sometimes an elevated white blood cell count (WBC) may be seen as alcoholics have decreased immunity and tend to get sick more often. Complete metabolic panel (CMP) may show 2:1 aspartate aminotransferase (AST) to alanine aminotransferase (ALT) ratio. One may also show diffuse elevation in liver function tests (LFTs). Magnesium and thiamine are commonly low in alcoholics. One of the most straightforward tests to remember and order is the blood alcohol level, which of course will be positive if the patient has alcohol in their system. Urine tests also exist including ethyl glucuronide (EtG) and ethyl sulfate (EtS), which are both biomarkers signifying the breakdown of alcohol. If the patient doesn't have alcohol in their system, there are still several other tests that may aid in the diagnosis. Gamma-glutamyl transferase (GGT) 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 (CDT) is useful to identify patients who have relapsed following a period of abstinence.

Electrocardiogram (ECG) or cardiac monitoring reveals an atrial arrhythmia. A chest x-ray may show cardiomegaly. An echocardiogram should be performed to evaluate for any structural abnormalities and to assess cardiac function. Liver disease is often a feature Holiday heart syndrome as alcohol damages the liver. Therefore, ultrasound of the liver may reveal liver cirrhosis. 

Treatment / Management

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. It is important to note that medical therapy does not improve this disease absent alcohol cessation or moderation. The previous thinking was that complete alcohol cessation was needed to see a reversal of the disease process, but recent studies have shown that as long as alcohol intake reduces to less than 80 mg per day, it may result in reversible cardiac changes. The patient must be encouraged to join alcoholics anonymous (AA) and other support groups. 

Differential Diagnosis

Differential diagnosis includes the following:

  • alcoholism
  • arrhythmia
  • cirrhotic cardiomyopathy
  • dilated cardiomyopathy
  • psychiatric problems


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

  • New or worsening heart failure 
  • Life-threatening arrhythmias
  • Community-acquired pneumonia
  • Thromboembolism
  • Death


The patient should obtain referrals to Alcoholics Anonymous or a similar support group, psychiatrist, psychologist, and depending on the extent of the disease, a cardiologist. 

Deterrence and Patient Education

Healthcare providers must educate their patient on the effects of alcohol misuse. Although alcoholics may have many other problems beyond what appears on the surface, Holiday heart syndrome typically presents with several other problems, including financial hardship, family stress, work stress, and even drug use. It is essential to identify the source of alcohol use and recommend discontinuation. Many patients may be reluctant to quit alcohol because to them alcohol is a means to escape an underlying bigger problem. 

Pearls and Other Issues

The biggest pitfall to the diagnosis of Holiday heart syndrome is that there is no definitive diagnostic test. Therefore, one can never be entirely sure that holiday heart syndrome is, in fact, the diagnosis and responsible for the atrial arrhythmias. Prevention of the disease is straightforward and requires avoidance of excessive alcohol use.

Enhancing Healthcare Team Outcomes

Managing holiday heart syndrome requires an interprofessional team of healthcare professionals that includes a nurse, laboratory technologist, pharmacist and a number of physicians in different specialties including psychiatry and cardiology. Without proper management the morbidity and mortality from holiday heart syndrome are high. The moment the triage nurse has admitted  a patient with an arrhythmia and excessive alcohol use, the emergency department clinician is responsible for coordinating the care which includes the following:

  • Ordering alcohol levels in blood and urine, or other metabolites
  • Monitor the patient for signs and symptoms of respiratory depression, suicidal ideations, signs, and symptoms of heart failure, and alcohol withdrawal
  • Monitor and replete thiamine before giving glucose in alcoholics to avoid neurologic deficits
  • Consult with the pharmacist about the initiation of CIWA protocol in at-risk individuals
  • Consult with a pharmacist about starting a benzodiazepine if tremor or seizure history is present
  • Consult with a nutritionist if the patient appears malnourished
  • Consult with a toxicologist and nephrologist on further management, which may include dialysis
  • Consult with the cardiologist regarding arrhythmia management
  • Consult with the intensivist about ICU care and monitoring while in hospital
  • Review medication reconciliation as many drugs interact with alcohol

The management of holiday heart syndrome does not stop in the emergency department. Once the patient is stabilized, one has to determine how and why the patient ingested large amounts of alcohol. Consult with a mental health counselor if this was an intentional act and assess risk factors for-self harm. [Level 1] Further, the possibility of addiction and withdrawal symptoms is a consideration. Only by working as an interprofessional team can the morbidity of alcohol ingestion be decreased. [Level 5]


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[3] Figueredo VM,Chang KC,Baker AJ,Camacho SA, Chronic alcohol-induced changes in cardiac contractility are not due to changes in the cytosolic Ca2 transient. The American journal of physiology. 1998 Jul     [PubMed PMID: 9688904]
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