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Holiday heart syndrome

Alcohol-associated arrhythmia condition

  • 3 min read
  • 2 chapters

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Through Syndrome, Ethanol and Circulatory system

Etiology

Cardiologists are unsure exactly what causes holiday heart syndrome. The ingestion of alcohol may slow down the cardiac conduction system, which is an important system for managing the circulatory system. It may also shorten the refractory period of the atrium. Another possibility is that alcohol consumption increases the level of catecholamines, which increased the level of P-waves, and therefore the risk of arrhythmia. Alcohol intake can also lead to a rise in plasma free fatty acids and an increase in the activity of the sympathetic nervous system. An ATP2A2 enhancer known as JNK2 may play a role. Alcohol may activate it, which can affect other proteins therefore increasing the risk of arrhythmia. Heavy consumption of alcohol may lead to an increased level of ethanol and metabolites such as acetaldehyde inside of the body. All of these factors can contribute to arrhythmia.

Drinking large quantities of alcohol or caffeine, eating fatty foods with salt, heightened levels of stress, and dehydration are all risk factors for the development of this syndrome. HHS can appear in people who do not usually drink. Often these people who rarely drink may engage in an episode of heavy alcohol consumption and develop it as soon as they drink, others contract it 12–36 hours following the time of intoxication. Usually patients with this disorder lack any family history or previous clinical evidence of cardiological problems. Studies suggest moderate drinking (5-7 drinks per week) may not increase the risk of atrial fibrillation compared to abstinence; however, consumption beyond this range is associated with a substantial increase in the risk of HHS, further supporting the greater risk that binge drinking poses to the development of this condition.

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