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 a clinical presentation of irregular heartbeat pattern, in individuals who are otherwise healthy. It can be the result of stress, dehydration, and drinking. The most common cause of this syndrome is excessive alcohol consumption. Usually associated with binge drinking, it has also been documented in patients who are not heavy alcohol drinkers. 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 use in large quantities, leads to cardiac structural and cellular changes through a buildup of ethanol and its metabolites. The incidence and prevalence of holiday heart syndrome is unclear due to conflicting evidence. 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. If diagnosed early and treated with measures such as 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 also known as alcohol-induced atrial fibrillation. The finding on physical examination are characteristic, patients show features of alcohol intoxication and their breath smells of alcohol. There could be changes in the mental status, as the person is intoxicated and sometimes hypotensive. 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 pathologies like 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 the cardiac status and function. Echocardiography is the standard diagnostic method 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. For unstable patients with atrial fibrillation, cardioversion is the recommended treatment. 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 thus remains unresolved.
  • It may be due to the direct myotoxic effects of alcohol or the indirect effects caused by its metabolism.
  • The most accepted theory is that chronic ethanol consumption in large quantity, leads to cardiac structural and cellular changes through the accumulation of ethanol and its metabolites.
  • These metabolites cause oxidative damage, mitochondrial dysfunction, cell death, lower the effects of cardio-protective molecules, alter protein synthesis and impair calcium transport.The most common metabolite responsible for these changes is acetaldehyde, which is produced by the liver by a chemical reaction with alcohol dehydrogenase. It is believed to cause arrhythmias by increasing the systemic and intra-myocardial catecholamines (epinephrine and norepinephrine), thus causing the imbalance in the autonomic nervous system.
  • It also causes the activation of the Parasympathetic Nervous System, thus causing increased vagal tone and slowing the refractory period of atrium. This high risk of electrical disturbance in the Holiday heart syndrome, is just like dilated cardiomyopathy.
  • On a microscopic level, patients with Holiday heart have visible changes to the structure of the mitochondrial reticulum in the myocytes.
  • Apart from the electrical similarity with dilated cardiomyopathy, the gross changes seen at the tissue level are similar in a patient with Holiday heart syndrome.
  • The most common arrhythmia seen in patients with Holiday heart syndrome is Atrial fibrillation, followed by atrial flutter and premature ventricular contractions.

Causes

The most common cause of holiday heart syndrome is excessive alcohol consumption. The risk is further accentuated by binge drinking episodes by people who already have a chronic drinking background. 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

  • On physical examination, the patient with holiday heart syndrome may show signs of alcohol intoxication and strong odor of alcohol in their breath.[5]

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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