Pharmacology of ethanol.

Electrophysiologic properties of alcohol in man

Alcohol and the heart

Background In some patients, above-average alcohol consumption before occurrence of atrial fibrillation (AF) in terms of a "holiday heart syndrome" (HHS) can be determined. There is evidence that long before development of apparent alcohol-induced cardiomyopathy, above-average alcohol consumption generates an arrhythmogenic substrate which abets the onset of AF. Changes of atrial current densities in terms of an electrical remodeling after sustained short-term ethanol infusion in rabbits as a potential part of HHS pathophysiology were examined in this study. Methods Rabbits of the ethanol group (EG) received sustained short-term intravenous alcohol infusion for 120 hours (during infusion period, blood alcohol level did not fall below 158 mg/dl), whereas NaCl 0.9% was infused in the placebo group (PG). Using patch clamp technique in whole-cell mode, atrial current densities were measured and compared between both groups. Results Ethanol infusion did not alter current densities of I(to) [58.7 +/- 5.0 pA/pF (PG, n = 20 cells) vs. 53.9 +/- 5.0 pA/pF (EG, n = 24)], I(sus) [11.3 +/- 1.4 pA/pF (PG, n = 20) vs. 10.2 +/- 1.0 pA/pF (EG, n = 24)], and I(K1) [-1.6 +/- 0.3 pA/pF (PG, n = 17) vs. -2.0 +/- 0.3 pA/pF (EG, n = 22)]. However, alcohol infusion resulted in a remarkable reduction of I(Ca,L) current densities [-28.4 +/- 1.8 pA/pF (PG, n = 20) vs. -15.2 +/- 1.4 pA/pF (EG, n = 22)] and I(Na) [-75.4 +/- 3.6 pA/pF (PG, n = 17) vs. -35.4 +/- 4.4 pA/pF (EG, n = 21)], respectively. Conclusion Sustained short-term ethanol infusion in rabbits alters atrial current densities. HHS might be favored by alcohol-induced atrial electrical remodeling.

Alcohol-Induced Electrical Remodeling: Effects of Sustained Short-Term Ethanol Infusion on Ion Currents in Rabbit Atrium

The etiology of arrhythmias including atrial fibrillation is multifactorial. Most arrhythmias are associated with comorbid illnesses like hypertension, diabetes, thyroid disease, or advanced age. Although it is tempting to blame a stimulant like caffeine as a trigger for arrhythmias, the literature does not support this idea. There is no real benefit to having patients with arrhythmias limit their caffeine intake. Caffeine is a vasoactive substance that also may promote the release of norepinephrine and epinephrine. However, acute ingestion of caffeine (as coffee or tea) does not cause atrial fibrillation. Even patients suffering a myocardial infarction do not have an increased incidence of ventricular or other arrhythmias after ingesting several cups of coffee. Large epidemiologic studies have also failed to find a connection between the amount of coffee/caffeine used and the development of arrhythmias. As such, it does not make sense to suggest that patients with palpitations, paroxysmal atrial fibrillation, or supraventricular tachycardia, abstain from caffeine use. Energy drinks are a new phenomenon on the beverage market, with 30–50 % of young adults and teens using them regularly. Energy drinks are loaded with caffeine, sugar, and other chemicals that can stimulate the cardiac system. There is an increasing body of mainly anecdotal case reports describing arrhythmias or even sudden death triggered by exercise plus using energy drinks. Clearly, there must be more study in this area, but it is wise to either limit or avoid their use in patients with arrhythmias. Moderate to heavy alcohol use seems to be associated with the development of atrial fibrillation. The term “holiday heart” was coined back in 1978, to describe patients who had atrial fibrillation following binge alcohol use. Thus, it is reasonable to recommend to patients with arrhythmias that they limit their alcohol use, although unfortunately this treatment will likely not completely resolve their arrhythmia.

/pdf/recommendations-regarding-dietary-intake-and-caffeine-and-ako8plnr4b.pdf

Recommendations Regarding Dietary Intake and Caffeine and Alcohol Consumption in Patients With Cardiac Arrhythmias: What Do You Tell Your Patients To Do or Not To Do?

Isolated isometric ventricular muscle of frogs and cats was studied. Perfusing solutions were played directly on the muscle to permit rapid exchange of the extracellular space. Developed force and maximal rate of rise of force were measured in all studies and action potentials (AP) were recorded in some. For both species low concentrations of ethanol (75 degrees mg/l) potentiate contraction. Higher concentrations ( greater than or equal to 750 mg/l) depress contraction progressively with increasing concentration. Concentrations which depress contraction, e.g., 3-4.5 gm/l, usually shorten AP duration. The shortening of AP duration can occur even though contractile force does not fall and, conversely, force may fall while AP duration is unaffected. When 10 mM caffeine is added to the perfusate of either species, AP duration is prolonged and contraction is potentiated. If both ethanol (4.5 gm/l) and 10 mM caffeine are added simultaneously to the perfusate, there is a rapid (within 4 beats) increase in AP duration and an initial depression of contraction, followed by a further increase in AP duration and a significant potentiation of contraction. The steady state contraction is less than with caffeine alone. These preliminary studies suggest that ethanol may depress contraction both by shortening AP duration and by a direct effect upon the contractile apparatus.

The action of ethanol upon the action potential and contraction of ventricular muscle.

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The action of ethanol upon the action potential and contraction of ventricular muscle.