Holiday heart syndrome: Difference between revisions

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==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.
==Historical Perspective==
The term holiday heart syndrome was coined by Ettinger et al in 1978.<ref>{{cite journal |author=Ettinger PO, Wu CF, De La Cruz C, Weisse AB, Ahmed SS, Regan TJ |title=Arrhythmias and the "Holiday Heart": alcohol-associated cardiac rhythm disorders |journal=Am. Heart J. |volume=95 |issue=5 |pages=555–62 |year=1978 |month=May |pmid=636996 |doi=10.1016/0002-8703(78)90296-X}}</ref><ref name="pmid68242622">{{cite journal |author=Luck JC, Engel TR |title=Arrhythmias and social drinking |journal=[[Annals of Internal Medicine]] |volume=98 |issue=2 |pages=253 |year=1983 |month=February |pmid=6824262 |doi= |url=}}</ref>
==Pathophysiology==
* Holiday heart syndrome is defined as "[[arrhythmias]] of the [[heart]], sometimes apparent after a [[vacation]] or weekend away from work, following excessive [[alcohol]]consumption; usually transient". <ref name="pmid8805002">{{cite journal |author=Menz V, Grimm W, Hoffmann J, Maisch B |title=Alcohol and rhythm disturbance: the holiday heart syndrome |journal=[[Herz]]|volume=21 |issue=4 |pages=227–31 |year=1996 |month=August |pmid=8805002 |doi= |url=}}</ref>
* Irregular heartbeats are very serious and result mostly from [[supraventricular tachycardia]]s.
* If palpitations continue for longer than a few hours patients should seek medical attention.
* [[Atrial fibrillation]] is the most common arrhythmia in holiday heart syndrome and can result in very serious consequences such as [[stroke]], but a variety of changes in the intervals and morphology of the [[EKG]] may occur (irregular series of QRS complexes and absent p waves).
* Other frequently observed arrhythmias include [[atrial flutter]], [[atrial tachycardia]], [[junctional tachycardia]], multiple APC's, multiple [[PVC]]'s and [[ventricular tachycardia]]. <ref name="pmid15875505">{{cite journal |author=Alboni P, Gianfranchi L, Pacchioni F, Pedaci M |title=Antiarrhythmic drugs in patients with recurrent atrial fibrillation: where are we? |journal=[[Italian Heart Journal : Official Journal of the Italian Federation of Cardiology]] |volume=6 |issue=3 |pages=169–74 |year=2005 |month=March |pmid=15875505 |doi= |url=}}</ref><ref name="pmid6824246">{{cite journal |author=Greenspon AJ, Schaal SF |title=The "holiday heart": electrophysiologic studies of alcohol effects in alcoholics |journal=[[Annals of Internal Medicine]] |volume=98 |issue=2 |pages=135–9 |year=1983 |month=February |pmid=6824246 |doi= |url=}}</ref>
* In patients with new onset atrial fibrillation and no overt pre-existing heart disease, holiday heart syndrome should be considered as a part of differential diagnosis.
=== Pathophysiology ===
* Several mechanisms are theorized to be responsible for the arrhythmogenicity of alcohol.
* They may be characterized into two broad groups: direct effects on the myocardium and alcohol's effect on traditional risk factors for atrial fibrillation.
* With regard to direct effects on the atrial myocardium, alcohol causes a autonomic nervous system imbalance.
* Alcohol increases sympathetic nervous system (SNS) activity (and its related increased secretion of epinephrine and norepinephrine), with resultant effects including an increased release of calcium into the myocytes from the sarcoplasmic reticulum.
* Increased SNS activity is further evidenced by a marked increase in the incidence of sinus tachycardia and reduced respiratory sinus arrhythmia during acute alcohol intoxication.
* Consequently, the parasympathetic nervous system (PNS) is activated as well, with an increased intermittent vagal tone, which has been shown to also shorten the atrial refractory period and preciptate atrial fibrillation.
* Note that the risk of atrial fibrillation persists into the "hangover" and/or withdrawal phase, which corresponds with an increased sympathetic tone.
* Other direct effects on the myocardium are perhaps less well studied.
** They include the effects of alcohol's primary metabolite acetaldehyde, which is associated with local inflammation and oxidative stress.
**  Alcohol itself can also directly decrease the myocyte sodium current and can affect intracellular pH, ether causing acidosis with low doses or alkalosis with higher doses. Interestingly, these effects may be species specific, with rabbits and humans being similarly affected, whereas canine atria appear unaffected.
* Binge alcohol consumption activates the stress kinase JNK (c-Jun N-terminal kinase) (JNK2), which subsequently phosphorylates (and activates) the CaMKII protein, thereby enhancing CaMKII-driven mishandling of sarcoplasmic reticulum calcium—which prompts aberrant calcium waves and enhances susceptibility to atrial arrhythmia.
* Conversely, CaMKII inhibition eliminates binge alcohol-evoked arrhythmic activities.
* Analysis of electrocardiograms (ECGs) performed following the resolution of arrhythmias in patients who have consumed a large quantity of alcohol shows significant prolongation of the PR, QRS, and QT intervals compared to that of patients who experienced arrhythmias in the absence of alcohol consumption.
* Although ventricular repolarization abnormalities on surface ECG were described, whether ventricular myocardium responds similarly to ethanol is uncertain.
== Epidemiology and Demographics ==
* The frequency with which cardiac arrhythmias can be attributed to alcohol use is unclear owing to differing data.
*Holiday heart syndrome commonly affects individuals younger than 65 years of age.
<br />
==Overview==
==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 diseases|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 heart rhythms|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 [[Cardiac arrhythmia|arrhythmia]] treatment.<ref name="pmid6559190">{{cite journal |author=Nissen MB, Lemberg L |title=The "holiday heart" syndrome |journal=[[Heart & Lung : the Journal of Critical Care]] |volume=13 |issue=1 |pages=89–92 |year=1984 |month=January |pmid=6559190 |doi= |url=}}</ref>
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 diseases|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 heart rhythms|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 [[Cardiac arrhythmia|arrhythmia]] treatment.<ref name="pmid6559190">{{cite journal |author=Nissen MB, Lemberg L |title=The "holiday heart" syndrome |journal=[[Heart & Lung : the Journal of Critical Care]] |volume=13 |issue=1 |pages=89–92 |year=1984 |month=January |pmid=6559190 |doi= |url=}}</ref>

Revision as of 00:53, 8 April 2020

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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]

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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