Holiday heart syndrome

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Holiday heart syndrome
Afib ecg.jpg
Electrocardiographic image depicting atrial fibrillation (top, red arrow) and normal heart rhythm (bottom)
Specialty Cardiology
Symptoms Arrhythmia
Complications Mitochondrial dysfunction, valvular heart disease, oxidative damage, cell death, dilated cardiomyopathy, electrical vulnerability of the atrium, thrombosis, pneumonia, Cirrhosis, heart failure, and potentially death
Usual onsetUsually following heavy amounts of Alcohol consumption
DurationUsually 24 hours
CausesHigh amounts of ethanol consumption
Risk factors Drinking large quantities of alcohol, dehydration, high levels of stress
Diagnostic method Blood tests and Medical imaging
Differential diagnosis Alcohol use disorder, Dilated cardiomyopathy, Cirrhosis, Arrhythmia, Psychiatric disorders
TreatmentCardioversion
Prognosis If left untreated can have severe complications, and is possibly fatal
FrequencyUnclear

Holiday heart syndrome, also known as alcohol-induced atrial arrhythmias, is a syndrome defined by an irregular heartbeat and palpitations [1] associated with high levels of ethanol consumption. [2] [3] Holiday heart syndrome was discovered in 1978 when Philip Ettinger discovered the connection between arrhythmia and alcohol consumption. [4] It received its common name as it is associated with the binge drinking common during the holidays. [5] It is unclear how common this syndrome is. 5-10% of cases of atrial fibrillation may be related to this condition, but it could be as high 63%. [6]

Contents

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. [7] [8] 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. [9] Heavy consumption of alcohol may lead to an increased level of ethanol and metabolites such as acetaldehyde inside of the body. [10] [11] All of these factors can contribute to arrhythmia. [12]

Drinking large quantities of alcohol or caffeine, [13] [14] [15] eating fatty foods with salt, [16] heightened levels of stress, [17] [18] 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. [19] Usually patients with this disorder lack any family history or previous clinical evidence of cardiological problems. [5]

Symptoms and complications

The most common symptoms people with HHS have are heart palpitations and arrhythmia. [20] People usually present with atrial fibrillation; however, other forms of arrhythmia may be developed, such as atrial tachycardia, premature ventricular contraction, and atrial flutter. Patients with HHS also frequently report precordial pain, sweating, anxiety, shortness of breath, and syncope. Strokes and cardiac arrest can also occur in people with this syndrome. [5] People with holiday heart syndrome have a heightened risk of dilated cardiomyopathy, rhabdomyolysis, and acute kidney injury [21] and increased atrial vulnerability to external electrical stimulus under the influence. [22]

The heightened level of acetaldehyde this syndrome causes can result in mitochondrial dysfunction, valvular disease, oxidative damage, cell death, lowered effects of cardioprotective molecules, and an altered calcium transport and protein synthesis system. [5] If left untreated, it can result in thrombosis, pneumonia, cirrhosis, and heart failure. [6] [19] For most patients with HHS the syndrome only lasts 24 hours. However for 26% of people with this syndrome, they reexperience an episode of it within the next year. To treat patients with this condition cardioversion or other treatments for arrhythmia are used. [5]

See also

Related Research Articles

<span class="mw-page-title-main">Cardiology</span> Branch of medicine dealing with the heart

Cardiology is the study of the heart. Cardiology is a branch of medicine that deals with disorders of the heart and the cardiovascular system. The field includes medical diagnosis and treatment of congenital heart defects, coronary artery disease, heart failure, valvular heart disease, and electrophysiology. Physicians who specialize in this field of medicine are called cardiologists, a specialty of internal medicine. Pediatric cardiologists are pediatricians who specialize in cardiology. Physicians who specialize in cardiac surgery are called cardiothoracic surgeons or cardiac surgeons, a specialty of general surgery.

<span class="mw-page-title-main">Cardioversion</span> Conversion of a cardiac arrhythmia to a normal rhythm using an electrical shock or medications

Cardioversion is a medical procedure by which an abnormally fast heart rate (tachycardia) or other cardiac arrhythmia is converted to a normal rhythm using electricity or drugs. Synchronized electrical cardioversion uses a therapeutic dose of electric current to the heart at a specific moment in the cardiac cycle, restoring the activity of the electrical conduction system of the heart. Pharmacologic cardioversion, also called chemical cardioversion, uses antiarrhythmia medication instead of an electrical shock.

<span class="mw-page-title-main">Brugada syndrome</span> Heart conduction disease

Brugada syndrome (BrS) is a genetic disorder in which the electrical activity of the heart is abnormal due to channelopathy. It increases the risk of abnormal heart rhythms and sudden cardiac death. Those affected may have episodes of syncope. The abnormal heart rhythms seen in those with Brugada syndrome often occur at rest. They may be triggered by a fever.

<span class="mw-page-title-main">Tachycardia</span> Heart rate exceeding normal resting rate

Tachycardia, also called tachyarrhythmia, is a heart rate that exceeds the normal resting rate. In general, a resting heart rate over 100 beats per minute is accepted as tachycardia in adults. Heart rates above the resting rate may be normal or abnormal.

<span class="mw-page-title-main">Sinus node dysfunction</span> Medical condition

Sinus node dysfunction (SND), also known as sick sinus syndrome (SSS), is a group of abnormal heart rhythms (arrhythmias) usually caused by a malfunction of the sinus node, the heart's primary pacemaker. Tachycardia-bradycardia syndrome is a variant of sick sinus syndrome in which the arrhythmia alternates between fast and slow heart rates.

<span class="mw-page-title-main">Short QT syndrome</span> Medical condition

Short QT syndrome (SQT) is a very rare genetic disease of the electrical system of the heart, and is associated with an increased risk of abnormal heart rhythms and sudden cardiac death. The syndrome gets its name from a characteristic feature seen on an electrocardiogram (ECG) – a shortening of the QT interval. It is caused by mutations in genes encoding ion channels that shorten the cardiac action potential, and appears to be inherited in an autosomal dominant pattern. The condition is diagnosed using a 12-lead ECG. Short QT syndrome can be treated using an implantable cardioverter-defibrillator or medications including quinidine. Short QT syndrome was first described in 2000, and the first genetic mutation associated with the condition was identified in 2004.

<span class="mw-page-title-main">Amiodarone</span> Antiarrhythmic medication used for various types of irregular heartbeats

Amiodarone is an antiarrhythmic medication used to treat and prevent a number of types of cardiac dysrhythmias. This includes ventricular tachycardia (VT), ventricular fibrillation (VF), and wide complex tachycardia, as well as atrial fibrillation and paroxysmal supraventricular tachycardia. Evidence in cardiac arrest, however, is poor. It can be given by mouth, intravenously, or intraosseously. When used by mouth, it can take a few weeks for effects to begin.

<span class="mw-page-title-main">Catheter ablation</span> Removal or termination of an electrical pathway from parts of the heart

Catheter ablation is a procedure that uses radio-frequency energy or other sources to terminate or modify a faulty electrical pathway from sections of the heart of those who are prone to developing cardiac arrhythmias such as atrial fibrillation, atrial flutter and Wolff-Parkinson-White syndrome. If not controlled, such arrhythmias increase the risk of ventricular fibrillation and sudden cardiac arrest. The ablation procedure can be classified by energy source: radiofrequency ablation and cryoablation.

<span class="mw-page-title-main">Hypertensive heart disease</span> Medical condition

Hypertensive heart disease includes a number of complications of high blood pressure that affect the heart. While there are several definitions of hypertensive heart disease in the medical literature, the term is most widely used in the context of the International Classification of Diseases (ICD) coding categories. The definition includes heart failure and other cardiac complications of hypertension when a causal relationship between the heart disease and hypertension is stated or implied on the death certificate. In 2013 hypertensive heart disease resulted in 1.07 million deaths as compared with 630,000 deaths in 1990.

SCN5A Protein-coding gene in the species Homo sapiens

Sodium channel protein type 5 subunit alpha, also known as NaV1.5 is an integral membrane protein and tetrodotoxin-resistant voltage-gated sodium channel subunit. NaV1.5 is found primarily in cardiac muscle, where it mediates the fast influx of Na+-ions (INa) across the cell membrane, resulting in the fast depolarization phase of the cardiac action potential. As such, it plays a major role in impulse propagation through the heart. A vast number of cardiac diseases is associated with mutations in NaV1.5 (see paragraph genetics). SCN5A is the gene that encodes the cardiac sodium channel NaV1.5.

<span class="mw-page-title-main">MYL7</span> Protein-coding gene in the species Homo sapiens

Atrial Light Chain-2 (ALC-2) also known as Myosin regulatory light chain 2, atrial isoform (MLC2a) is a protein that in humans is encoded by the MYL7 gene. ALC-2 expression is restricted to cardiac muscle atria in healthy individuals, where it functions to modulate cardiac development and contractility. In human diseases, including hypertrophic cardiomyopathy, dilated cardiomyopathy, ischemic cardiomyopathy and others, ALC-2 expression is altered.

<span class="mw-page-title-main">Pilsicainide</span> Chemical compound

Pilsicainide (INN) is an antiarrhythmic agent. It is marketed in Japan as サンリズム (Sunrythm). It was developed by Suntory Holdings Limited and first released in 1991. The JAN applies to the hydrochloride salt, pilsicainide hydrochloride.

<span class="mw-page-title-main">Ankyrin-2</span> Protein-coding gene in the species Homo sapiens

Ankyrin-2, also known as Ankyrin-B, and Brain ankyrin, is a protein which in humans is encoded by the ANK2 gene. Ankyrin-2 is ubiquitously expressed, but shows high expression in cardiac muscle. Ankyrin-2 plays an essential role in the localization and membrane stabilization of ion transporters and ion channels in cardiomyocytes, as well as in costamere structures. Mutations in ANK2 cause a dominantly-inherited, cardiac arrhythmia syndrome known as long QT syndrome 4 as well as sick sinus syndrome; mutations have also been associated to a lesser degree with hypertrophic cardiomyopathy. Alterations in ankyrin-2 expression levels are observed in human heart failure.

<span class="mw-page-title-main">Michel Haïssaguerre</span>

Michel Haïssaguerre is a French cardiologist and electrophysiologist. His investigations have been the basis for development of new markers and therapies for atrial and ventricular fibrillation.

<span class="mw-page-title-main">Atrial fibrillation</span> Irregular beating of the atria of the heart

Atrial fibrillation is an abnormal heart rhythm (arrhythmia) characterized by rapid and irregular beating of the atrial chambers of the heart. It often begins as short periods of abnormal beating, which become longer or continuous over time. It may also start as other forms of arrhythmia such as atrial flutter that then transform into AF.

<span class="mw-page-title-main">KCNE5</span> Protein-coding gene in the species Homo sapiens

KCNE1-like also known as KCNE1L is a protein that in humans is encoded by the KCNE1L gene.

<span class="mw-page-title-main">Arrhythmia</span> Group of medical conditions characterized by irregular heartbeat

Arrhythmias, also known as cardiac arrhythmias, heart arrhythmias, or dysrhythmias, are irregularities in the heartbeat, including when it is too fast or too slow. A resting heart rate that is too fast – above 100 beats per minute in adults – is called tachycardia, and a resting heart rate that is too slow – below 60 beats per minute – is called bradycardia. Some types of arrhythmias have no symptoms. Symptoms, when present, may include palpitations or feeling a pause between heartbeats. In more serious cases, there may be lightheadedness, passing out, shortness of breath, chest pain, or decreased level of consciousness. While most cases of arrhythmia are not serious, some predispose a person to complications such as stroke or heart failure. Others may result in sudden death.

<span class="mw-page-title-main">Cardiac transient outward potassium current</span> Ion current

The cardiac transient outward potassium current (referred to as Ito1 or Ito ) is one of the ion currents across the cell membrane of heart muscle cells. It is the main contributing current during the repolarizing phase 1 of the cardiac action potential. It is a result of the movement of positively charged potassium (K+) ions from the intracellular to the extracellular space. Ito1 is complemented with Ito2 resulting from Cl− ions to form the transient outward current Ito.

<span class="mw-page-title-main">Topera Medical</span>

Topera, Inc. is a cardiac arrhythmia mapping company for targeting catheter ablation company launched in San Diego, California and specializes in mapping electrical signals of the heart. Topera's headquarters are located in Palo Alto, California. The company uses 3D analysis and mapping to detect the sources of atrial fibrillation, atrial flutter, and atrial tachycardia and ventricular tachycardia to identify targets for catheter ablation.

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References

  1. ↑ Jain, Anubhav; Yelamanchili, Varun S.; Brown, Kristen N.; Goel, Akshay (2024), "Holiday Heart Syndrome", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   30725870 , retrieved 2024-02-15
  2. ↑ "Holiday heart syndrome – definition". Biology-Online.org.
  3. ↑ Rosenthal L, Stokken GT, Smith RH, Daubert JP, Weiss HS, Budzikowski AS (17 October 2021). Talavera F, Compton SJ, Dizon JM (eds.). "Holiday Heart Syndrome: Background, Pathophysiology, Epidemiology". Medscape.
  4. ↑ Ettinger PO, Wu CF, De La Cruz C, Weisse AB, Ahmed SS, Regan TJ (May 1978). "Arrhythmias and the "Holiday Heart": alcohol-associated cardiac rhythm disorders". American Heart Journal. 95 (5): 555–562. doi:10.1016/0002-8703(78)90296-x. PMID   636996.
  5. 1 2 3 4 5 Tonelo D, Providência R, Gonçalves L (August 2013). "Holiday heart syndrome revisited after 34 years". Arquivos Brasileiros de Cardiologia. 101 (2): 183–189. doi:10.5935/abc.20130153. PMC   3998158 . PMID   24030078.
  6. 1 2 Brown KN, Yelamanchili VS, Goel A (2022). "Holiday Heart Syndrome". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID   30725870 . Retrieved 2022-08-26.
  7. ↑ Brunner S, Winter R, Werzer C, von Stülpnagel L, Clasen I, Hameder A, et al. (June 2021). "Impact of acute ethanol intake on cardiac autonomic regulation". Scientific Reports. 11 (1): 13255. Bibcode:2021NatSR..1113255B. doi:10.1038/s41598-021-92767-y. PMC   8225621 . PMID   34168256.
  8. ↑ Balbão CE, de Paola AA, Fenelon G (February 2009). "Effects of alcohol on atrial fibrillation: myths and truths". Therapeutic Advances in Cardiovascular Disease. 3 (1): 53–63. doi: 10.1177/1753944708096380 . PMID   19124390. S2CID   27879551.
  9. ↑ Yan J, Thomson JK, Zhao W, Gao X, Huang F, Chen B, et al. (April 2018). "Role of Stress Kinase JNK in Binge Alcohol-Evoked Atrial Arrhythmia". Journal of the American College of Cardiology. 71 (13): 1459–1470. doi:10.1016/j.jacc.2018.01.060. PMC   5903584 . PMID   29598867.
  10. ↑ Sutanto H, Cluitmans MJ, Dobrev D, Volders PG, Bébarová M, Heijman J (September 2020). "Acute effects of alcohol on cardiac electrophysiology and arrhythmogenesis: Insights from multiscale in silico analyses". Journal of Molecular and Cellular Cardiology. 146: 69–83. doi: 10.1016/j.yjmcc.2020.07.007 . PMID   32710981. S2CID   220773275.
  11. ↑ Mustroph J, Wagemann O, Lebek S, Tarnowski D, Ackermann J, Drzymalski M, et al. (March 2018). "SR Ca2+-leak and disordered excitation-contraction coupling as the basis for arrhythmogenic and negative inotropic effects of acute ethanol exposure". Journal of Molecular and Cellular Cardiology. 116: 81–90. doi: 10.1016/j.yjmcc.2018.02.002 . PMID   29410242.
  12. ↑ Falcone AM, Schussler JM (October 2009). "Sudden atrial fibrillation associated with acute alcohol ingestion and cor triatriatum". Proceedings. 22 (4): 335–336. doi:10.1080/08998280.2009.11928550. PMC   2760166 . PMID   19865505.
  13. ↑ Wang Y, Morishima M, Li D, Takahashi N, Saikawa T, Nattel S, Ono K (October 2020). "Binge Alcohol Exposure Triggers Atrial Fibrillation Through T-Type Ca2+ Channel Upregulation via Protein Kinase C (PKC) / Glycogen Synthesis Kinase 3β (GSK3β) / Nuclear Factor of Activated T-Cells (NFAT) Signaling – An Experimental Account of Holiday Heart Syndrome". Circulation Journal. 84 (11): 1931–1940. doi: 10.1253/circj.CJ-20-0288 . PMID   33028764. S2CID   225072772.
  14. ↑ Bhardwaj P, Chaudhury S (January 1996). "HOLIDAY HEART SYNDROME: A Case Report". Medical Journal, Armed Forces India. 52 (1): 61–62. doi:10.1016/S0377-1237(17)30840-7. PMC   5530300 . PMID   28769342.
  15. ↑ Rosenberg MA, Mukamal KJ (2012). "The Estimated Risk of Atrial Fibrillation Related to Alcohol Consumption". Journal of Atrial Fibrillation. 5 (1): 424. doi:10.4022/jafib.424 (inactive 31 January 2024). PMC   5153079 . PMID   28496744.{{cite journal}}: CS1 maint: DOI inactive as of January 2024 (link)
  16. ↑ "Learn the symptoms of Holiday Heart Syndrome and how to prevent it". www.baystatehealth.org. Retrieved 2022-08-26.
  17. ↑ LaMotte S (2019-12-12). "'Holiday heart syndrome': What is it and how to avoid it". CNN. Retrieved 2022-08-26.
  18. ↑ Yang M, Barrios J, Yan J, Zhao W, Yuan S, Dong E, Ai X (February 2021). "Causal roles of stress kinase JNK2 in DNA methylation and binge alcohol withdrawal-evoked behavioral deficits". Pharmacological Research. 164: 105375. doi:10.1016/j.phrs.2020.105375. PMC   7867628 . PMID   33316384.
  19. 1 2 Voskoboinik A, Prabhu S, Ling LH, Kalman JM, Kistler PM (December 2016). "Alcohol and Atrial Fibrillation: A Sobering Review". Journal of the American College of Cardiology. 68 (23): 2567–2576. doi: 10.1016/j.jacc.2016.08.074 . PMID   27931615. S2CID   205581782.
  20. ↑ "What to Know About Holiday Heart Syndrome". Cleveland Clinic. 2021-12-03. Retrieved 2022-08-26.
  21. ↑ Ul Abideen Z, Abbas SF, Farooq M, Rasheed A, Ali F (December 2016). "Acute Abdominal Aorta Thrombosis and Ischemic Rhabdomyolysis Secondary to Severe Alcohol Intoxication". Cureus. 8 (12): e905. doi: 10.7759/cureus.905 . PMC   5207781 . PMID   28083449.
  22. ↑ Engel TR, Luck JC (March 1983). "Effect of whiskey on atrial vulnerability and "holiday heart"". Journal of the American College of Cardiology. 1 (3): 816–818. doi: 10.1016/S0735-1097(83)80195-8 . PMID   6826972.

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