Bottoms up: The effects of moderate use of alcohol and cardiac arrhythmia

There is a growing and worrisome understanding that moderate alcohol use may be more cardiotoxic than many of use were fully aware. There are studies that link alcohol to cardiac arrhythmias including atrial fibrillation – an irregular heart beat that is known to increase the risk of stroke and other cardioembolic events.  What is the cause of cardiac arrhythmias from the use of liquor? Atrial fibrillation is caused by ectopy that create a second node (or cluster of cells) of abnormal electrical activity that compete with the sinoatrial node – the pacemaker in the right atrium in the heart. The atria actually undergoes a physical change called atrial remodeling when secondary nodes compete for primary pacer node in the atria. There can be only one primary node.  The result of this triggers a rapid, irregular rhythm and puts one at risk for cardioembolic stroke and other potential cardiovascular risks like remodeling.

This is a surprising, but not new reality, in the setting of my regular physical exams and cardiology consultations where I have openly and honestly over-estimated my consumption of alcohol by indicating that: “I should probably quit”. My physicians were nonplussed and seemed unconcerned. For all I knew, a glass of red wine daily kept heart disease at bay.and built red blood cells.  At the rehabilitation hospital where I consult and provide assessment and biofeedback, we see dozens of cases of patients suffering from the health-related impact of A-fib. Of course, most of these are for reasons other than alcohol abuse but a fair number of our admissions are there as a result of the effects of alcohol such as liver cirrhosis, delirium, obstructive sleep apnea, diabetes, obesity, and acute renal disease. We treat the liver transplants sent from the UMASS Transplantation Service although these are not entirely the result of alcohol-related disorders.

“From a pathophysiological perspective, alcohol may exhibit direct effects on arrhythmogenesis as observed in the “holiday heart syndrome”. The holiday heart syndrome related to the binge drinking during times of celebration like from Thanksgiving through New Years. Many people call for a “dry January” as a way of drying out and feeling better after weeks of holiday cheer. Acute alcohol consumption also induces autonomic imbalance reflected by sinus tachycardia, predisposing to arrhythmia.”  Electrolyte disturbance and alterations of the acid-base balance are further pro-arrhythmic triggers. In truth, there are many co-occuring medical complexities like obstructive sleep apnea, hypertention, obesity, and diabetes mellitus that contribute to the cardiogenic changes or remodeling from alcohol. Chronic alcohol consumption is known to be correlated with changes in cardiac structure and function including cardiomyopathy. Alcohol binge drinking or the “holiday heart syndrome” is well characterized in the literature. However, more modest levels of alcohol intake on a regular basis may also increase the risk of AFib from the increase of cardiotoxic effects of oxidative stress and inflammation triggered by hypoxia associated with sleep apnea and hypertension during apneic episodes as well as vascular events from ischemia due to thrombus or blood clot in a vessel in the heart. 

The sympathetic system activates the bodies internal survival mechanism by raising the threat level needed to fight or to flee. It is almost instantaneous. The fight/flight mechanism exists in all animals having an evolutionary value needed for survival and defense against potential prey.  Michael Sefton

When you pull the curtain back from the totality of the impact of alcohol on the nervous system that we must think about the sympathetic storm and the fight-flight responses that belie changes in heart functioning. One can see that studies show, following small to moderate amounts of ethanol, P-wave duration was prolonged in the control group with no history of AF, suggesting that alcohol directly slows interatrial conduction in all according to Steinbigler et al, 2003. This means the the depolarization and repolarization of the electrical activity in the heart which is key to the squeeze needed to move blood through the body and its vital organs can be altered. The evidence of elevated risk from thromboembolic events in the setting of atrial fibrillation, cerebral vascular events, and mortality is well understood and often ignored. Anticoagulation clinics have seemingly sprouted up on every street corner next to liquor stores and smoke shops.

Voskoboinik, A et al. (2016)

Methods that reduce autonomic innervation or outflow have been shown to reduce the incidence of spontaneous or induced atrial arrhythmias.26 The latter studies suggest that neuromodulation may be helpful in controlling AF. See Chen et al. (2014) for a review of the relationship between the autonomic nervous system and the pathophysiology of AF and the potential benefit and limitations of neuromodulation in the management of this arrhythmia. I am hopeful that the neuroregulation derived from EEG biofeedback may be a mitigating treatment for both autonomic dysfunction and greater self-regulation and abstinence. The role of the autonomic nervous system in atrial fibrillation is multifactorial with alcohol induces atriogenic changes among them, including script and the potential for cardiac remodeling. “Autonomic nervous system activation can induce significant and heterogeneous changes of atrial electrophysiology and induce atrial tachyarrhythmias, including atrial tachycardia and atrial fibrillation (AF).” The importance of the autonomic nervous system in atrial arrhythmogenesis is also supported by circadian variation in the incidence of symptomatic AF in humans in Chen et al., 2014. I am working on a protocol using biofeedback and mindfulness to mitigate the autonomic underpinnings of arrhythmias. There is a literature for using neurofeedback for reducing the craving for alcohol that may be matched with paced breathing and heart rate variability which can activate parasympathetic pathways and modify baroreceptor response and its multifactorial impact on health.

References

Center for Behavioral Health Statistics and Quality. Behavioral Health Trends in the United States: Results From the 2014 National Survey on Drug Use and Health (HHS Publication No. SMA 15-4927, NSDUH Series H-50). Available at: http://www.samhsa.gov/data. Accessed January 25, 2021

Steinbigler, P Haberl, R. König, B. et al. (2003) P-wave signal averaging identifies patients prone to alcohol-induced paroxysmal atrial fibrillationAm J Cardiol, 91, pp. 491-494

Voskoboinik, A et al. (2016). Alcohol and Atrial Fibrillation: A Sobering Review. J of Amer College of Cardiology, Volume 68, Issue 23, 13 December 2016, Pages 2567-2576.

O’Keefe, J, DiNicolantonio, D.J. Alcohol and Atrial Fibrillation Journal of the American College of Cardiology, Volume 69, Issue 20, 23 May 2017, Pages 2578

Chen, P, Chen, L, Fishbein, M, Lin, S-F, and Nattel, S (2014). Role of the Autonomic Nervous System in Atrial Fibrillation: pathophysiology and therapy. Circulation Research, Volume 114, Issue 9, 25, Pages 1500-1515

Viskin S, Golovner M, Malov N, Fish R, Alroy I, Vila Y, Laniado S, Kaplinsky E, Roth A. (1999). Circadian variation of symptomatic paroxysmal atrial fibrillation. Data from almost 10,000 episodes. Eur Heart Journal; 20:1429–1434.

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