In spite of numerous studies, the sequence of events that occur in alcohol-induced myocardial damage is still highly controversial. Although some authors contend that the initial event is the appearance of hypertrophy, the majority accept that the core event is the loss of cardiomyocytes. The existence of a direct causal link between excessive alcohol consumption and the development of DCM is a controversial issue.

• Many cellular events, such as intrinsic myocyte dysfunction, which is characterized by changes in calcium homeostasis and regulation and decreased myofilament sensitivity, can come about due to oxidative stress.
• Heart remodeling is an adaptive mechanism, susceptible to being modified in ACM by the use of cardiomyokines (FGF21, Metrnl) and growth factors (IGF-1, Myostatin) 112,119.
• Growth factors and cardiomyokines are relevant molecules that may modify this process.
• New strategies to improve the natural course of ACM have been proposed as promising agents in this field 112,147.
• Acetaldehyde is produced at a lower quantity in the heart as compared to the liver, and systemic acetaldehyde does not achieve toxic heart concentrations 77.
• Several reports suggest that ethanol-induced decreases in myocardial protein synthesis may be mediated in part by decreased activity of an enzyme called mammalian (or mechanistic) target of rapamycin (mTOR) (Lang and Korzick 2014; Vary and Deiter 2005; Vary et al. 2008).
• The blood flow through the heart is slower than normal, especially when the heart is very enlarged (dilated).

A normal heart

She admitted to an eight-year history of the ingestion of more than 600 mL of vodka per day. Within the month before presentation, she had increased her alcohol intake by drinking a large glass of 70% ethanol per day. For tens of years, the literature has documented many clinical cases or small series of patients who have undergone a full recovery of ejection fraction and a good clinical evolution after a period of complete alcoholic abstinence.

5. Sarcomere Damage and Dysfunction in ACM

Data from animal models and human beings with a history of long-term drinking suggest that oxidative stress may be an early and initiating mechanism. Many cellular events, such as intrinsic myocyte dysfunction, characterized by changes in calcium homeostasis and regulation and decreased myofilament sensitivity, can come about due to oxidative stress. Excessive intake of alcohol may result in increased systemic blood pressure in a dose-response relationship, and this may contribute to chronic myocardial dysfunction. Patients who consume more than two drinks per day have a 1.5- to 2-fold increase in hypertension compared with persons who do not drink alcohol cardiomyopathy symptoms alcohol, and this effect is most prominent when the daily intake of alcohol exceeds five drinks. Because hypertension may directly contribute to left ventricular (LV) dysfunction, this may be a confounding comorbidity in persons who abuse alcohol, and it should be differentiated from pure forms of alcoholic cardiomyopathy. Electron microscopic studies (7,8) of biopsies from patients with alcohol-induced cardiomyopathy have shown evidence of damage to the myofibres, including separation of filaments and loss of striation.

Table 1. List of literature articles reviewed in this study.

This inability occurs despite adverse effects on the person’s health, occupation, or relationships. The heart’s LV attempts to compensate for this damage by enlarging to achieve a higher blood output. This eventually limits the heart’s ability to pump oxygen-rich blood around the body.

Clinical Review BoardAll Healthwise education is reviewed by a team that includes physicians, nurses, advanced practitioners, registered dieticians, and other healthcare professionals. Electrolyte abnormalities, including hypokalemia, hypomagnesemia, and hypophosphatemia, should be corrected promptly because of the risk of arrhythmia and sudden death. Chest radiographs usually show evidence of cardiac enlargement, pulmonary congestion, and pleural effusions. Richardson et al showed an elevation of creatine kinase, LDH, malic dehydrogenase, and alpha-hydroxybutyric dehydrogenase levels in endomyocardial biopsy specimens taken from 38 patients with DC. Other people are born with cardiomyopathy because of a gene passed on from a parent. Illustrations of a typical heart, as shown on the left, and a heart with hypertrophic cardiomyopathy.

This refers to the finding in the last century that moderate alcohol consumption could be the reason for the relatively low cardiovascular disease incidence in wine-drinking regions 92. Renaud and de Lorgeril 93 suggested that the inhibition of platelet reactivity by wine may be one explanation for protection from CAD in France. 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.

• Alcohol use was protective against CHD for subjects in most countries, except for people of South Asian ethnicity living in South Asia (India, Bangladesh, Nepal, Pakistan, and Sri Lanka).
• According to the American Heart Association (AHA) and other US-based guidelines, alcohol intake recommendations are provided to promote responsible drinking habits and maintain overall health.
• Previous studies were conducted on rats that are fed alcohol for about eight months.
• This review assembles and selects pertinent literature on the ambivalent relationship of ethanol and the cardiovascular system, including guidelines, meta-analyses, Cochrane reviews, original contributions, and data from the Marburg Cardiomyopathy registry.

Some of the potential cellular changes related to ethanol consumption reviewed above are illustrated in figure 5. More than one cellular event may be happening at the same time, and, as with other chronic health conditions, the relevant mechanisms may be synergistic and interrelated. Researchers have found evidence of mitochondrial dysfunction or impaired bioenergetics related to alcohol consumption. This is not surprising, because mitochondria are a major target for free-radical injury.

The percentage of apoptotic myocytes in ACM is relatively low but, in combination with a persistent decrease in myocyte proliferation, they may contribute to an absolute cell loss and decreased cardiac contractility 52,115. 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. Others have also found a significant decrease in intramitochondrial isocitrate dehydrogenase activity (20,24).