Alcoholic cardiomyopathy: Treatments, outlook, and more

Dysregulated excessive autophagy, together with other factors such as oxidative stress, neurohormonal activation, and altered fatty acid metabolism, contributes to cardiac structural and functional damage following alcoholism. This influences the maintenance of cardiac geometry and contractile function, increasing the development of ACM [121]. In ACM, protein degradation with sarcomere disarray and contractile protein loss has been suggested to be a key point of autophagy induction [18].

Acknowledgments

After myocyte apoptosis or necrosis, the heart tries to repair and regenerate this tissue damage [39,123], but the heart regenerative capacity is low as a result of the ethanol aggressive damage and develops ineffective repair mechanisms such as progressive fibrosis [124,125]. In fact, ethanol itself decreases the myocyte regeneration capacity and increases the fibrogenic process [52,126]. alcoholic cardiomyopathy is especially dangerous because Subendocardial and interstitial fibrosis progressively appear in the course of ACM, usually in advanced stages [52,56]. More than 30% of the myocyte ventricular fraction can be replaced by fibrotic tissue, thus decreasing the heart elasticity and contractile capacity [64] (Figure 2). Some cardiomyokines, such as FGF21, may regulate this process of alcohol-induced cardiac fibrosis [119].

Alcohol Consumption and Total Stroke Incidence and Prevalence

• Finally, it should be noted that McKenna and co-workers, in one of the most frequently cited papers in the ACM field, reported an incidence of 40% in 100 individuals suffering from idiopathic DCM, but in this case the consumption threshold used was only g/d[8].
• Recently, apoptosis and necrosis have been also attributed to autophagy in ACM [18].
• The ryanodine L-type Ca2+ receptor at the sarcoplasmic reticulum (SR) is also significantly affected by ethanol in a dose-dependent manner [86,102].

Muscular weakness may also be present because of the effect of alcohol on muscles (alcoholic myopathy). They commonly include fatigue, shortness of breath, and swelling of the legs and feet. Anyone with concerns about alcohol consumption or heart health https://ecosoberhouse.com/ needs to consult a doctor for further advice and guidance. Alcoholic cardiomyopathy affects the heart’s ability to pump oxygen-rich blood around the body. This can cause various symptoms, including shortness of breath, fluid retention, and fainting.

1. Oxidative and Energy Disturbances in ACM

• In spite of the high prevalence of excessive alcohol consumption and of its consideration as one of the main causes of DCM, only a small number of studies have analysed the long-term natural history of ACM.
• Selenium deficit (Keshan disease in China) could also induce ACM in specific areas [70].
• Excessive EtOH consumption is one of the main causes of non-ischemic dilated cardiomyopathy (CMP), representing around one-third of cases [30].
• Most heavy drinkers remain asymptomatic in the earlier stages of disease progression, and many never develop the familiar clinical manifestations that typify heart failure.
• However, during the time that these haemodynamic changes appeared, some researchers identified a possible decrease in the ejection fraction and other parameters related to systolic function[32-39].

Infection or other stressful events also can lead to immune-triggered platelet production, a condition called rebound thrombocytosis, which may occur immediately after withdrawal from both heavy and one-time heavy (binge) drinking (Numminen et al. 1996). Although highly individualized and dose dependent, alcohol use also can increase bleeding time (i.e., taking longer to develop a clot)(Salem and Laposata 2005). Acute or chronic right heart failure leads to elevation of liver enzymes most likely due to liver congestion, whereas  cirrhosis due to cardiac disease is infrequent.

Basic studies on molecular mechanisms of myocardial damage

LIMITATIONS OF ACM STUDIES

• In Munich, the annual consumption of beer reached 245 l per capita and year in the last quarter of the 19th century.
• Experts do not know what quantity of alcohol a person needs to consume to develop ACM.
• Specifically in the United States, ACM was declared the leading cause of non-ischemic DCM[7]; a fact related to the high consumption of alcoholic beverages worldwide, which is particularly elevated in Western countries[26] .
• Alterations in protein physiology/content can also be due to accelerated protein degradation.
• 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.
• ACM produces a progressive reduction in myocardial contractility and heart chamber dilatation, leading to heart failure episodes and arrhythmias.