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] Aditya Ganti M.B.B.S. [3]

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. 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 common cause of holiday heart syndrome is excessive alcohol consumption. The incidence and prevalence of holiday heart syndrome is unclear due to conflicting evidence. 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. Patients with HHS often have a history of previous alcohol exposure. If diagnosed early and treated with alcohol cessation, the prognosis for holiday heart disease is good as the disease is reversible. Patients with acute exposure to alcohol can present with a variety of symptoms. Holiday heart syndrome is considered, alcohol-induced atrial fibrillation. 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. 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. 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.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.[1]

Historical Perspective

The term was coined by Ettinger et al in 1978.[2][3]

Pathophysiology

  • 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.
  • 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.
  • On a microscopic level, patients with Holiday heart have visible changes to the structure of the mitochondrial reticulum in the myocytes.

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

Epidemiology and Demographics

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

Natural History, Complications, and Prognosis

Natural History

Complications

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

Physical Examination

Laboratory Findings

  • 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.

References

  1. Nissen MB, Lemberg L (1984). "The "holiday heart" syndrome". Heart & Lung : the Journal of Critical Care. 13 (1): 89–92. PMID 6559190. Unknown parameter |month= ignored (help)
  2. Ettinger PO, Wu CF, De La Cruz C, Weisse AB, Ahmed SS, Regan TJ (1978). "Arrhythmias and the "Holiday Heart": alcohol-associated cardiac rhythm disorders". Am. Heart J. 95 (5): 555–62. doi:10.1016/0002-8703(78)90296-X. PMID 636996. Unknown parameter |month= ignored (help)
  3. Luck JC, Engel TR (1983). "Arrhythmias and social drinking". Annals of Internal Medicine. 98 (2): 253. PMID 6824262. Unknown parameter |month= ignored (help)
  4. Bhardwaj P, Chaudhury S (January 1996). "HOLIDAY HEART SYNDROME: A Case Report". Med J Armed Forces India. 52 (1): 61–62. doi:10.1016/S0377-1237(17)30840-7. PMC 5530300. PMID 28769342.
  5. Koskinen P, Kupari M, Leinonen H, Luomanmäki K (May 1987). "Alcohol and new onset atrial fibrillation: a case-control study of a current series". Br Heart J. 57 (5): 468–73. doi:10.1136/hrt.57.5.468. PMC 1277202. PMID 3593617.

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