Holiday heart syndrome

Revision as of 15:39, 29 January 2020 by Aditya Ganti (talk | contribs) (Pathophysiology)
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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. [1]

Historical Perspective

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

Pathophysiology

  • Holiday heart syndrome is defined as "arrhythmias of the heart, sometimes apparent after a vacation or weekend away from work, following excessive alcoholconsumption; usually transient". [4]
  • Irregular heartbeats are very serious and result mostly from supraventricular tachycardias.
  • 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. [5][6]
  • 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.

Treatment

All symptoms usually resolve themselves within 24 hours. Specific anti-arrhythmic therapy is not warranted.

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. Menz V, Grimm W, Hoffmann J, Maisch B (1996). "Alcohol and rhythm disturbance: the holiday heart syndrome". Herz. 21 (4): 227–31. PMID 8805002. Unknown parameter |month= ignored (help)
  5. Alboni P, Gianfranchi L, Pacchioni F, Pedaci M (2005). "Antiarrhythmic drugs in patients with recurrent atrial fibrillation: where are we?". Italian Heart Journal : Official Journal of the Italian Federation of Cardiology. 6 (3): 169–74. PMID 15875505. Unknown parameter |month= ignored (help)
  6. Greenspon AJ, Schaal SF (1983). "The "holiday heart": electrophysiologic studies of alcohol effects in alcoholics". Annals of Internal Medicine. 98 (2): 135–9. PMID 6824246. Unknown parameter |month= ignored (help)



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