The Effects of Ethanol on the Heart: Alcoholic Cardiomyopathy

Among the ACM patients, no differences between the patients in the death and survival groups were observed at baseline with respect to age, disease duration, smoking status, presence of syncope, heart rate, gender, and blood test results. The frequencies of a high New York Heart Association (NYHA; class III/IV) classification, atrial fibrillation (AF) and atrioventricular block were higher in the death group than those in the survival group. The QRS duration, LVEDD, and diameter of the right ventricle (RV) and left atrium (LA) were higher in the death group than those in the survival group, but the LVEF and blood pressure (systolic SBP or diastolic DBP) were lower in the death group than those in the survival group. Although some studies have detailed structural and functional damage in proportion to the amount of alcohol consumed during a patient’s lifetime24, a large majority of authors have discarded this theory21-23,25. Both the absence of a direct correlation and the theory of the existence of a threshold dose (above which some alcoholics develop ACM) require the presence of individual susceptibility to alcohol induced cardiac damage63.

ACKNOWLEDGMENTS

In addition, ethanol induces mitochondrial-dependent apoptosis pathways with Bax and caspase activation 101. Ethyl alcohol, also known as “ethanol” or usually just as “alcohol”, is the most consumed drug in human history 1. At present, its consumption rates are still very high, with a widespread worldwide distribution, in a global uncontrolled scenario with easy access 2. In fact, there is an increasing consumption in particular groups, such as adolescents and young people 3,4. Certain microscopic features may suggest damage secondary to alcohol causing cardiomyopathy. Commonly seen cellular structural alterations include changes in the mitochondrial reticulum, cluster formation of mitochondria and disappearance of alcoholic cardiomyopathy symptoms inter-mitochondrial junctions.

• However, no differences were found in these parameters between the sub-group of individuals who had been drinking for 5 to 14 years and the sub-group of individuals who had a drinking history of over 15 years.
• It’s important to be honest with your doctor about the extent of your alcohol use, including the number and amount of drinks you have each day.
• As the pathogenesis of AC is complex, specific treatments focus on different targets.

1. The Natural Course of ACM

This can cause heart inflammation, leading to an atypically fast heart rhythm, such as atrial fibrillation (AF). Until the second part of the 20th century, there was no scientific evidence on the direct and dose-dependent effect of ethanol on the heart as cause of ACM 6,38. This is a longstanding accumulated effect that usually appears when a subject has, in their lifetime, consumed more than 7 Kg of ethanol per Kg of body weight in men (equivalent to 60 drinks per month), and 5 Kg of ethanol per Kg of body weight in women (equivalent to 43 drinks per month) 19,46.

Acute vs. chronic

• Chronic alcohol consumption can cause multi-organ damage including myocardial dysfunction.
• In this respect, a higher prevalence of excessive alcohol consumption has been reported among individuals diagnosed with DCM than in the general population8.
• On physical examination, patients present with non-specific signs of congestive heart failure such as anorexia, generalized cachexia, muscular atrophy, weakness, peripheral edema, third spacing, hepatomegaly, and jugular venous distention.
• This induces a variety of effects, since more than 14 different sites in the myocyte can be affected by ethanol 19,98.
• We conducted our analysis on discharge data from the Healthcare Cost and Utilization Project‐Nationwide Inpatient Sample (HCUP‐NIS) from 2002 through 2014.
• It is important to note that the size and strength of different alcoholic beverages can vary, so these definitions serve as general guidelines.

Although there is beneficial potential in some patients, the coexistence of increased risk of cancer, neurological brain damage, and the high risk of ethanol addiction makes it necessary to discourage this low-dose consumption in the general population 19,41,45. Specific caution should be recommended regarding children or adolescents 4 and women 46, who are more susceptible to the damaging effects of ethanol at the same doses of consumption as men. Similarly, patients suffering from other ethanol-related diseases such as liver cirrhosis or brain atrophy should completely suppress their ethanol consumption 47,48.

Treatment

One of the few papers analysing genetic susceptibility in ACM was published by Fernández-Solà et al64 in 2002. He compared the prevalence of different polymorphisms of the angiotensin-converting enzyme gene in 30 ACM patients and in 27 alcoholics with normal ventricular function. Furthermore, 89% of the alcoholics with a DD genotype developed ACM, whereas only 13% of those with an II or ID genotype developed this condition. However, this individual susceptibility mediated by polymorphisms of the angiotensin-converting enzyme gene does not appear to be specific to ACM insofar as several diseases, including some that are not of a cardiologic origin, have been related to this genetic finding65.

• This test will assess the ejection fraction (EF), a measurement that expresses how much blood the LV pumps out with each contraction.
• The NIAAA provides an Alcohol Treatment Navigator, where people can learn about AUD treatments and access care and support networks locally.
• Although this figure may be sufficient to cause the structural alterations described above, we must stress that this value is arbitrary and is not based on robust experimental or epidemiological data; also, the average consumption of the individuals included in the research was always much greater9-12 .
• In order to maintain cardiac homeostasis, the removal of defective organelles and cell debris by autophagy is essential both in physiological and pathological conditions 115.

Data Availability

However, there is a clear personal susceptibility of this effect that creates a wide variability range and supposes significant inter-individual differences 50,66. In fact, ACM is considered to be the result of dosage and individual predisposition 32. Many changes can be observed including premature atrial or ventricular contractions, supraventricular tachycardias, atrioventricular blocks,  bundle branch blocks, QT prolongation, non-specific ST and T wave changes and abnormal Q waves. The key to diagnosis is a personal history of chronic heavy alcohol use and the absence of other etiologies. Enzymatic activity changes which are seen in the idiopathic cardiomyopathy including decreased activity of oxygen reduction mitochondrial enzymes, increased fatty acid uptake and increased lysosomal/microsomal enzyme activity can be seen.