Heart Risks and Chronic Alcohol Abuse: Understanding Alcoholic Cardiomyopathy
These include damaging factors such as acetaldehyde or ROS, cardiac fibrosis, or apoptosis. 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. S3 gallop sound along with apical pansystolic murmur due to mitral regurgitation is often heard. 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. Many medications can help in cases of alcohol-induced cardiomyopathy, treating the symptoms that happen because of this condition.
- The trace amounts of arsenic have not been comparable to the arsenic-in-beer endemic in Manchester but may still reach up to 10-times the amount admitted for arsenic in drinking water in the European Union and the US.
- In the 16th century Paracelsus Theophrastus Bombastus from Hohenheim used this term for distilled liquor and called it alcohol [15].
- Furthermore, Fernández-Solá et al[30], when analysing a population of alcoholics, found a higher prevalence of DCM in alcoholics than among the general population.
- Because of this, their origin could be multifactorial and linked both to the alcohol molecule and to its main metabolite, acetaldehyde.
- The Scd-1 gene encodes for stearoyl-CoA desaturase 1, an enzyme that catalyzes the rate-limiting step in mono-unsaturated fatty acid synthesis.
Current Therapies for ACM
- Overall, your healthcare provider is the best source of information and answers when it comes to your recovery.
- Chronic alcohol consumption can disrupt blood pressure regulation and fluid balance in the body, adding strain to the heart.
- A 1- and 4-year follow-up study of 55 men with alcoholism showed that abstinence and controlled drinking of up to 60 g/day (4 drinks) resulted in comparable improvement in left ventricular (LV) ejection fraction.
- Individuals who have a history of heavy alcohol consumption, even if they have since reduced or stopped drinking, may still have the potential to develop alcoholic cardiomyopathy as a consequence of their past alcohol abuse.
Often, when a doctor suspects cardiomyopathy, they will order an echocardiogram. This test will assess the ejection fraction (EF), a measurement that expresses how much blood the LV pumps out with each contraction. Once doctors have found this, they will look for the cause of the weakened heart. Cardiotoxicity refers to heart damage that occurs in response to certain drugs, such as alcohol. The mainstay of management is providing support, resources including but not limited to alcoholic anonymous and encouragement for alcohol abstinence and address underlying stressors if any which requires assistance from nursing staff and pharmacy. Some studies have suggested that even moderation of alcohol consumption similar outcomes as compared to abstinence.
Alcoholic Cardiomyopathy and Your Health
That also may involve supportive care that will help prevent — or at least reduce the impact of — any alcohol withdrawal symptoms. Supportive care for withdrawal is especially important because some of its symptoms can be severe or even life-threatening. A healthcare alcoholic cardiomyopathy is especially dangerous because provider can also connect you with available resources and refer you to other specialists and experts who can help you reduce or stop your alcohol intake. Alcohol-induced cardiomyopathy is a condition where consuming too much alcohol damages your heart.
- Using a mass spectrometric-based proteomic analysis, Fogle et al. examined the effects of 16 weeks of ethanol consumption on rat cardiac muscle protein expression (45).
- Alcohol-induced cardiomyopathy primarily affects individuals who engage in chronic, excessive, and long-term alcohol consumption.
- ACM weakens the heart’s ability to pump blood effectively, leading to heart failure.
- In 1890, Strümpell listed alcoholism as a cause of cardiac dilatation and hypertrophy, as did Sir William Osler in 1892 in his textbook Principles and Practices of Medicine.
- The authors examined the prevalence of cardiomegaly by means of chest x-rays and related it to alcohol consumption among a consecutive series of Japanese males of working age.
Echocardiographic and haemodynamic studies in alcoholics
In the study by Gavazzi et al[10], ACM patients who continued drinking exhibited worse transplant-free survival rates after 7 years than those who stopped drinking alcohol (27% vs 45%)[10]. From the data provided in the available ACM studies, it appears that patients who received an ACEI globally showed improved prognosis. In contrast, https://ecosoberhouse.com/ beta-blockers, similar to aldosterone inhibitors, however beneficial they may be, have thus far not yielded sufficient data on their efficacy in relation to this disease. In the second study, Gavazzi led a multicentre study in which, from 1986 to 1995, 79 patients with ACM and 259 patients with DCM were recruited[10].
What tests will be done to diagnose this condition?
The population was divided into 3 groups according to their intake volume during the follow-up period. At the end of the first year, no differences were found among the non-drinkers, who improved by 13.1%, and among those who reduced consumption to g/d (with an average improvement of 12.2%). Conversely, those whose consumption remained in excess of 80 g/d showed an average decline of 3.8% in their ejection fraction. Unfortunately Lazarević et al[23], as in most of these studies, systematically excluded patients with a history of heart disease or with HF symptoms.
Alcoholic cardiomyopathy (ACM) is a disease in which the long-term consumption of alcohol leads to heart failure.[1] ACM is a type of dilated cardiomyopathy. Prompt treatment can help prevent the disease from getting worse and developing into a more serious condition, such as congestive heart failure (CHF). Others have examined the potential effects of micronutrient deficiencies (such as zinc) on ethanol-induced changes in the heart. Wang et al. found evidence of ethanol-induced changes in mitochondrial structure that were more pronounced in a metallothionein knock-out mouse model compared to wild-type mouse (80). Metallothionein binds zinc within the cell and is important for overall zinc homeostasis. In that study, zinc supplementation suppressed some of the ethanol-induced changes in both the metallothionein knock-out mouse model and wild-type; however, ethanol-induced mitochondrial swelling and disorganization remained in both mouse groups.
- The latest two papers to be published, unlike previous papers, reported worse outcomes for ACM patients compared to DCM patients.
- Long-term alcohol abuse weakens and thins the heart muscle, affecting its ability to pump blood.
- Recently, Lang and Korzick (65) reported that 20 weeks of alcohol consumption in female Fischer 344 rats increased myocardial atrogin-1 and MuRF1 expression (e.g., messenger ribonucleic acid levels).
- In 1884, the pathologist and veterinarian Otto von Bollinger (Fig. 2a) described the “Munich beer heart” with fibrosis, hypertrophy, and fatty degeneration in postmortem cardiac tissue of alcoholics who consumed an estimated average of 432 liters of beer per year (Fig. 2b; [23]).
Alcohol Metabolism & Acetaldehyde Formation
Furthermore, it is now evident that mitochondria function in networks and that when mitochondria become damaged their function can possibly restored by fusion with neighboring mitochondria (55). Also, others have suggested that, in data from animal models of alcoholism, there is an interaction between chronic ethanol consumption and caloric deprivation in eliciting alterations in myocardial energy metabolism (58). Many of the studies reviewed in this section were published more than 15 years ago and used measurements of respiratory states (1-IV) and respiratory control index ratios. These studies were performed in experimental conditions in which there may be multiple mitochondrial deficits and therefore need to be interpreted with caution.
