In ACM, protein degradation with sarcomere disarray and contractile protein loss has been suggested to be a key point of autophagy induction 18. Different pathogenic hypotheses have been suggested, such as the pivotal role of acetaldehyde 122, the role of oxidative stress and stress signaling cascades 109, and the translocation of NFkB into the nucleus 106. The quantity of alcohol consumed daily and the duration of alcohol misuse are linked to the development of ACM, although the precise thresholds for causing cardiac dysfunction remain unknown. The risk of ACM significantly increases with alcohol intake exceeding 80 g per day for a minimum of five years 3. According to the American Heart Association (AHA) alcohol rehab and other US-based guidelines, alcohol intake recommendations are provided to promote responsible drinking habits and maintain overall health. The AHA suggests moderate alcohol consumption for those who choose to drink, defining moderation as up to one drink per day for women and up to two drinks per day for men.

NATURAL HISTORY OF ALCOHOLIC CARDIOMYOPATHY

Conversely, the 3 subjects recording a less satisfactory evolution had persisted in their consumption of alcohol. It should be noted that a moderate drinker included in this latter group showed an improvement of his ejection fraction. Finally, it is worth stressing that a large majority of studies on the physiopathology and prognosis of ACM were conducted some years ago, prior to the development of our current understanding regarding the role of genetics in DCM67. According to recent data, a genetic form of DCM could be present in up to 50% of idiopathic DCM cases, and other specific forms of DCM such as peripartum cardiomyopathy have been shown to have a genetic basis in a significant number of cases68.

AMOUNT OF ALCOHOL REQUIRED TO PRODUCE ACM

• This is because the ethanol molecule has a small size and is highly reactive, with many cell targets.
• Ethanol induces ACM in a dose-dependent manner, independently of nutrition, vitamin, or electrolyte disturbances.

In the ESC consensus document on the classification of cardiomyopathies, ACM is classified among the acquired forms of DCM19. The NIAAA provides an Alcohol Treatment alcoholic cardiomyopathy Navigator, where people can learn about AUD treatments and access care and support networks locally. According to the NIAAA, many people with AUD recover, although setbacks are common among those receiving treatment. Other deficiencies including nutritional such as thiamine or other toxic materials ingested may lead to additional concomitant complications.

4. Ethanol Disruption of Transients and SR Activation

Long-term alcohol abuse weakens and thins the heart muscle, affecting its ability to pump blood. When your heart can’t pump blood efficiently, the lack of blood flow disrupts all your body’s major functions. Pharmacologic therapy should include goal-directed heart failure therapy as used in idiopathic dilated cardiomyopathy with reduced ejection fraction. This includes a combination of beta-blockers, an angiotensin-converting enzyme inhibitor, diuretics, aldosterone receptor antagonist and angiotensin blocker-neprilysin inhibitor (if LVEF is less than or equal to 40%).

Distilled spirits, such as vodka, whiskey, rum, or tequila, are measured as 1.5 ounces (44 ml) per drink, with a typical ABV of around 40%. It is important to note that the size and strength of different alcoholic beverages can vary, so these definitions serve as general guidelines. It is always advisable to be mindful of individual tolerance and consume alcohol responsibly 4-6. The treatment of episodes of heart failure in ACM does not differ from that performed in idiopathic-dilated CMP 52,54. 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.

Pathologically, ethanol https://ecosoberhouse.com/ induces myocytolysis, apoptosis, and necrosis of myocytes, with repair mechanisms causing hypertrophy and interstitial fibrosis. Myocyte ethanol targets include changes in membrane composition, receptors, ion channels, intracellular Ca2+ transients, and structural proteins, and disrupt sarcomere contractility. Cardiac remodeling tries to compensate for this damage, establishing a balance between aggression and defense mechanisms.

Occidental Berberi is the term used for the clinical scenario caused by thiamine deficit, a situation commonly present in chronic alcohol misuse, and was attributed as the cause of ACM 68,69. Similarly, electrolyte (Na, K, Ca, Mg, P) deficiencies or disturbances may play a major role in cardiac function, and ethanol misuse may be related to them 52. Selenium deficit (Keshan disease in China) could also induce ACM in specific areas 70. Acute can be defined as large volume acute consumption of alcohol promotes myocardial inflammation leading to increased troponin concentration in serum, tachyarrhythmias including atrial fibrillation and rarely ventricular fibrillation.

• 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.
• Ethanol may produce the modification of sarcolemmal membrane L-type Ca2+ channels, leading to a decrease in transmembrane electrically induced Ca2+ transients 85,103,127.
• Investigative work up such as mean corpuscular volume (MCV), gamma-glutamyl-transpeptidase (GGT), elevated transaminases (AST, ALT) and elevated INR usually are seen in liver injury can be helpful as supportive evidence of alcohol use.1415.
• Since ACM is related to frequent perioperative events and high postoperative morbidity 139, detection and treatment of ACM is compulsory to avoid anesthetic and surgical complications 140.
• Despite the key clinical importance of alcohol as a cause of DCM, relatively few studies have investigated the effects of alcohol on the heart and the clinical characteristics of DCM caused by excessive alcohol consumption (known as alcoholic cardiomyopathy).
• Symptoms include gradual onset worsening shortness of breath, orthopnea/paroxysmal nocturnal dyspnea.
• On histological examination, various degrees of fibrosis, patchy areas of endocardial fibroelastosis, intramural blood clots and focal collections of swollen cells in both the epicardium and endocardium were found.

LIMITATIONS OF ACM STUDIES

Furthermore, the inclusion criteria for ACM were very strict and required a minimum consumption of 8 oz of alcohol (200 g or 20 standard units) each day for over 6 mo. In contrast, European studies focusing on the prevalence of ACM included only subjects diagnosed with DCM and applied the consumption threshold of 80 g/d for ≥ 5 years, finding an ACM prevalence of 23%-47% among idiopathic DCM patients9-12 (Figure 1). Askanas et al21 found a significant increase in the myocardial mass and of the pre-ejection periods in drinkers of over 12 oz of whisky (approximately 120 g of alcohol) compared to a control group of non-drinkers. 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. Kino et al22 found increased ventricular thickness when consumption exceeded 75 mL/d (60 g) of ethanol, and the increase was higher among those subjects who consumed over 125 mL/d (100 g), without specifying the duration of consumption.

• The quantity of alcohol consumed daily and the duration of alcohol misuse are linked to the development of ACM, although the precise thresholds for causing cardiac dysfunction remain unknown.
• Furthermore, they specified the definition of “one drink” offer clarity when it comes to alcohol consumption.
• The natural history and long-term prognosis studies of Gavazzi et al10 and Fauchier et al11 compared the evolution of ACM patients according to their degree of withdrawal.
• Specifically, ethanol disturbs the ryanodine Ca2+ release, the sarcomere Ca2+sensitivity 102,103, the excitation–contraction coupling and myofibrillary structure, and protein expression, decreasing heart contraction 86.
• The exact mechanism by which an increased adherence to the traditional Mediterranean diet exerts its favorable effects is not known.

It is important to note that these guidelines apply to healthy adults and should be adjusted for individuals with certain health conditions or those taking specific medications. In addition, the AHA advises against starting to drink alcohol solely for potential health benefits, as the risks can outweigh the advantages. It is crucial to exercise caution and be aware of individual tolerance and personal health circumstances when making decisions about alcohol consumption.