Alcohol and Arrhythmias

Wong, Christopher X.; Tu, Samuel J.; Marcus, Gregory M

doi:10.1016/j.jacep.2022.10.023

Cited by 9 publications

(6 citation statements)

References 88 publications

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“…The role of acute alcohol consumption in arrhythmia highly depends on the dose and these effects are not well understood. Excessive alcohol intake may lead to sudden cardiac death, whereas moderate alcohol intake may have anti-arrhythmic properties [ 66 , 67 ].…”

Section: Resultsmentioning

confidence: 99%

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Cardiovascular Risks of Simultaneous Use of Alcohol and Cocaine—A Systematic Review

van Amsterdam,

Gresnigt,

van den Brink

2024

JCM

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Background: The simultaneous use of cocaine and alcohol is highly prevalent and is associated with high numbers of emergency department admissions, primarily due to cardiovascular complications. Aims: To answer the question of whether the co-use of cocaine and alcohol increases the cardiovascular risk compared to the use of cocaine alone. Method: A systematic review of human studies comparing the cardiovascular risk of co-used cocaine and alcohol with the use of cocaine alone. Results: Despite a higher myocardial workload induced by the co-use of cocaine and alcohol and the potentiation of cocaine’s cardiovascular effects by alcohol, the findings on the risk and severity of cardiovascular symptoms due to combined use are inconsistent. However, the co-use of cocaine and alcohol clearly leads to higher mortality. Interestingly, the presence of cocaethylene, a unique metabolite generated only via a pharmacokinetic interaction between alcohol and cocaine, carries an 18- to 25-fold increase over the absence of cocaethylene (cocaine-alone users) in the risk of sudden death and is associated with myocardial injury and cardiac arrest, probably due to the inhibition of cardiac ion channels by cocaethylene. Conclusion: Despite the inconsistency in some of the results, it is concluded that the co-use of cocaine and alcohol poses an additional risk of cardiovascular fatalities compared to the use of cocaine alone.

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Section: Resultsmentioning

confidence: 99%

“…Alcohol itself shows little direct cardiovascular effects [ 30 ], which rules out an additive cardiotoxic effect of alcohol when combined with cocaine. Moreover, various studies have observed a small protective acute effect of alcohol on cardiovascular events, including AMI and cardiac arrhythmia [ 67 , 83 , 84 , 85 ].…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular Risks of Simultaneous Use of Alcohol and Cocaine—A Systematic Review

van Amsterdam,

Gresnigt,

van den Brink

2024

JCM

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“…Of modifiable risk factors, smoking status, less physical activity, and a larger waist‐to‐hip ratio were all associated with a higher PVC burden 12,13 . While there have been extensive studies documenting the association of alcohol consumption with atrial fibrillation and sudden cardiac death, there is currently very little evidence to suggest that alcohol consumption has a meaningful impact on PVC burden 14 …”

Section: Predictors Of Pvc Burdenmentioning

confidence: 99%

“…12,13 While there have been extensive studies documenting the association of alcohol consumption with atrial fibrillation and sudden cardiac death, there is currently very little evidence to suggest that alcohol consumption has a meaningful impact on PVC burden. 14 The understanding of caffeine's role in predicting PVC burden has been less straightforward. Conventional wisdom suggested that caffeine consumption increases arrhythmias, and the multi-society guidelines for supraventricular tachycardias and ventricular arrhythmias recommended limiting caffeine consumption to avoid arrhythmias.…”

Section: Predictors Of Pvc Burdenmentioning

confidence: 99%

Predictors and possible mechanisms of premature ventricular contraction induced cardiomyopathy

Pundi,

Marcus

2023

Cardiovasc electrophysiol

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Premature ventricular complexes (PVCs) are encountered frequently in clinical practice. While PVCs may have various causes, a small number of individuals with PVCs develop cardiomyopathy in the absence of other potential etiologies. When correctly identified, patients with PVC‐incuded cardiomyopathy can have dramatic improvement of their cardiomyopathy with treatment of their PVCs. In this focused review, we discuss potential predictors of PVC‐induced cardiomyopathy, including PVC frequency, PVC characteristics, and modifiable patient risk factors. We also review some proposed mechanisms of PVC‐induced cardiomyopathy and conclude with future directions for research and clinical practice.

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“…According to the National Institute of Alcohol Abuse and Alcoholism (NIAAA), alcohol use disorder (AUD) is "a chronic relapsing brain disorder characterized by an impaired ability to stop or control alcohol use despite adverse social, occupational, or health consequences". At the 46th Research Society of Alcoholism-which was held from 24-28 June 2023 in Bellevue, USA-Dr. George F. Koob, Director of the NIAAA, mentioned during his opening lecture that acute and chronic alcohol consumption not only affects the brain, by causing cognitive and neurological disorders [10,11], but also affects every organ of the body, leading to arrhythmia, cardiovascular disease, hepatitis, and pancreatitis, and especially gut dysbiosis [12][13][14][15][16][17]. Binge alcohol consumption is characterized by 3-5 drinks in a short time of 2-3 h, whereas chronic alcohol consumption is considered as the daily intake of alcohol for several weeks [18].…”

Section: Introductionmentioning

confidence: 99%

Alcohol and the Brain–Gut Axis: The Involvement of Microglia and Enteric Glia in the Process of Neuro-Enteric Inflammation

Khan,

Chang

2023

Cells

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Binge or chronic alcohol consumption causes neuroinflammation and leads to alcohol use disorder (AUD). AUD not only affects the central nervous system (CNS) but also leads to pathologies in the peripheral and enteric nervous systems (ENS). Thus, understanding the mechanism of the immune signaling to target the effector molecules in the signaling pathway is necessary to alleviate AUD. Growing evidence shows that excessive alcohol consumption can activate neuroimmune cells, including microglia, and change the status of neurotransmitters, affecting the neuroimmune system. Microglia, like peripheral macrophages, are an integral part of the immune defense and represent the reticuloendothelial system in the CNS. Microglia constantly survey the CNS to scavenge the neuronal debris. These cells also protect parenchymal cells in the brain and spinal cord by repairing nerve circuits to keep the nervous system healthy against infectious and stress-derived agents. In an activated state, they become highly dynamic and mobile and can modulate the levels of neurotransmitters in the CNS. In several ways, microglia, enteric glial cells, and macrophages are similar in terms of causing inflammation. Microglia also express most of the receptors that are constitutively present in macrophages. Several receptors on microglia respond to the inflammatory signals that arise from danger-associated molecular patterns (DAMPs), pathogen-associated molecular patterns (PAMPs), endotoxins (e.g., lipopolysaccharides), and stress-causing molecules (e.g., alcohol). Therefore, this review article presents the latest findings, describing the roles of microglia and enteric glial cells in the brain and gut, respectively, and their association with neurotransmitters, neurotrophic factors, and receptors under the influence of binge and chronic alcohol use, and AUD.

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Alcohol and Arrhythmias

Cited by 9 publications

References 88 publications

Cardiovascular Risks of Simultaneous Use of Alcohol and Cocaine—A Systematic Review

Cardiovascular Risks of Simultaneous Use of Alcohol and Cocaine—A Systematic Review

Predictors and possible mechanisms of premature ventricular contraction induced cardiomyopathy

Alcohol and the Brain–Gut Axis: The Involvement of Microglia and Enteric Glia in the Process of Neuro-Enteric Inflammation

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