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Alcoholic Cardiomyopathy: Symptoms, Causes, and Treatment

By April 27, 2021January 2nd, 2025No Comments

alcoholic cardiomyopathy is especially dangerous because

For comparison, the mean annual beer consumption in Bavaria is nowadays estimated to be 145 l and in the rest of Germany around 100 l beer per person and year 24. Some of the adverse effects of heavy drinking can be reversed if you quit alcohol and adopt healthy lifestyle habits. Unfortunately, severe cases of alcoholic cardiomyopathy can lead to permanent damage and even death. If you or someone you know consumes large amounts of alcohol regularly, you should encourage them to try moderation or seek professional help to cut back or quit drinking. Thus, although there is a certain degree of consensus regarding the recommendation of full alcohol withdrawal in ACM, it is yet to be resolved whether moderate alcohol consumption is sufficient to achieve an improvement in the prognosis of these patients.

alcoholic cardiomyopathy is especially dangerous because

A Look At Alcoholic Cardiomyopathy: Causes & Treatment

Functionally high ethanol produces disruptions in the myocyte oxidative pattern and decreases in Complex I, II, and IV of the mitochondrial respiratory chain 100,109,110. As a reflection of this metabolic derangement, cytoplasmic lipid droplets and glycogen deposits appear. This ethanol misuse at high consumption rates causes a variety of health problems, ethanol Substance abuse being the sixth most relevant factor of global burden of disease and responsible for 5.3% of all deaths 5. Despite this clear epidemiological evidence of ethanol’s unsafe consumption and increased health risk, results of consumption policies are not effective enough. Therefore, the need to establish a more effective control on ethanol consumption has been repeatedly claimed 2.

  • 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.
  • Recent data favored a role for micro RNA, such as the involvement of miR-378a-5p in cardiomyocyte apoptosis and ACM development through ALDH2 gene suppression 120.
  • Echocardiography may reveal a mild or severe depression of cardiac function and ejection fraction or even show hypertrophy in the beginning 109.
  • Additionally, the accepted ACM definition does not take into account a patient’s sex or body mass index (BMI).
  • Patients may notice improvements in energy levels and well-being within a few weeks.
  • Further research is required to determine the definitive role of genetics on ACM pathophysiology.

Account

In contrast, chronic and excessive alcohol consumption could lead to progressive cardiac dysfunction and heart failure (HF)3. Along with signs of heart failure such as increased N-terminal pro-B-type natriuretic peptide, blood tests can provide hints suggesting chronic alcohol abuse. In 1887, Maguire reported on 2 patients with severe alcohol consumption who benefitted from abstinence. 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. In 1893, Graham Steell, well known for the Graham Steell murmur due to pulmonary regurgitation in pulmonary hypertension or in mitral stenosis, reported 25 cases in whom he recognized alcoholism as one of the causes of muscle failure of the heart. In his 1906 textbook The Study of the Pulse, William MacKenzie described cases of heart failure attributed to alcohol and first used the term “alcoholic heart disease” 26.

6. The Effect of Low-dose Ethanol on ACM

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. Virtual consultations allow you to receive personalized care, discuss symptoms, and adjust treatments without in-person visits, especially beneficial for those with mobility issues or living in remote areas. Patients may notice alcoholic cardiomyopathy is especially dangerous because improved heart function and reduced swelling within a few weeks, though regular blood tests are required to monitor potassium levels and kidney function. At Vertava Health, our treatment centers offer customizable treatment programs that include medical detox and behavioral therapy and other effective treatment services.

alcoholic cardiomyopathy is especially dangerous because

Cardiac magnetic resonance

It is more common https://ecosoberhouse.com/ in men, but women are also at risk, especially with long-term alcohol abuse. Early diagnosis and treatment can help slow the disease’s progression and improve quality of life. Cardiomyopathy itself is heart disease with several potential causes and risk factors that don’t involve alcohol but may be related to other heart conditions or health behaviors. The exact cause of cardiomyopathy, especially in younger adults and children, can be challenging to determine.

  • In valvular heart disease, it will show valve problems like narrowing or leaking, while in alcoholic cardiomyopathy, the heart valves are usually unaffected, but the heart muscle is weakened.
  • Pathologically, ethanol induces myocytolysis, apoptosis, and necrosis of myocytes, with repair mechanisms causing hypertrophy and interstitial fibrosis.
  • The swelling is often more pronounced in the ankles and feet and may worsen throughout the day, especially after prolonged standing or sitting.
  • Transplant-free survival after 7 years was worse among patients with ACM than among those with DCM (41% vs 53%).
  • In 1819 the Irish physician Dr. Samuel Black, who had a special interest in angina pectoris described what is probably the first commentary pertinent to the ”French Paradox“ 91.
  • In fact, there is an increasing consumption in particular groups, such as adolescents and young people 3,4.

5. The effects of Moderate Consumption of Ethanol and Binge-drinking

Studies that have assessed the prevalence of ACM among IDCM patients have found high alcohol consumption in 3.8% to 47% of DCM patients. The lowest prevalence of ACM among DCM (3.8%) was obtained from a series of 673 patients admitted to hospital consecutively due to HF in the state of Maryland27. This study included not only DCM, but also all causes of left ventricular dysfunction, including hypertensive heart disease, ischemic cardiomyopathy and heart valve disease.

alcoholic cardiomyopathy is especially dangerous because

Alcohol intake may also interfere with the drug and dietary treatment of hypertension. This altogether supports a causal relationship between alcohol consumption and a hypertensive state. The latest two papers to be published, unlike previous papers, reported worse outcomes for ACM patients compared to DCM patients. In the first of these studies, Fauchier et al11 studied 50 patients with ACM and 84 patients with DCM between 1986 and 1997. Although up to 81% of ACM patients received an ACEI, none received beta-blockers and the use of spironolactone was not specified, although it was probably quite low. Also, current common cardiac therapies such as ICD and CRT devices were not used because of the period when the study was conducted.

alcoholic cardiomyopathy is especially dangerous because

  • Various pathophysiological mechanisms have been postulated in the development of cardiomyopathy however one key factor undergoing active research is the role of genetic mutation and susceptibility to develop cardiomyopathy.
  • Markers such as ethyl sulphate, phosphatidyl ethanol, and fatty acid ethyl esters are not routinely done.
  • After a follow-up period of 47 mo, a significantly higher survival rate was observed among patients with DCM compared to patients with ACM.
  • This damage first induces diastolic dysfunction, which is initially subclinical and later clinically apparent 57.
  • A decrease in cardiac preload with diuretics and postload with angiotensin-converting-enzyme inhibitors or beta blockage agents allows for an improvement in signs of acute heart failure 19,131.

Heart myocytes are relatively resistant to the toxic effect of ethanol, developing a functional and structural compensatory mechanism able to minimize or repair the ethanol-induced myocyte damage 20,31,39. Structurally, hypertrophy of myocytes is seen in the early stages to avoid contractile depression 52,107,125. The heart output is progressively lower in a dose-dependent relationship with the lifetime accumulated total dose of alcohol consumed 38. Several growth factors and cardiomyokines exert an autocrine or paracrine effect that tries to compensate for this heart damage 119,133. Antioxidant, anti-inflammatory, anti-apoptotic, and antifibrogenic mechanisms try to avoid myocyte necrosis and heart fibrosis 14,30,58.

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