Some studies have suggested that a genetic vulnerability exists to the myocardial effects of alcohol consumption. Individuals with certain mitochondrial deoxyribonucleic acid (DNA) mutations and angiotensin-converting enzyme (ACE) genotypes (DD genotype) may be particularly susceptible to the damaging effects of alcohol. The natural history and long-term prognosis studies of Gavazzi et al[10] and Fauchier et al[11] compared alcoholic cardiomyopathy the evolution of ACM patients according to their degree of withdrawal. These authors found a relationship between the reduction or cessation of alcohol consumption and higher survival rates without a heart transplant. 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.

• Consumption of other drugs such as cocaine or tobacco may interact with ethanol and potentiate the final ethanol-related cardiac damage [22,72].
• Others have found an increased level of fatty acid ethyl esters in the alcoholic heart, which can attach to the mitochondria and disrupt mitochondria respiratory function (32).
• As early as in 1915, Lian [45] reported in middle-aged French servicemen during the first world war that heavy drinking could lead to hypertension.
• Among patients who continued drinking heavily, transplant-free survival was significantly worse than in non-drinkers (27% vs 45%).

Decreases in mTOR activation may play a role in reduced myocardial protein synthesis, ventricular wall thinning, and dilation. Some adverse BP-related mechanisms that may be triggered by alcohol include changes in intracellular calcium levels, baroreflex control, and heart rate and activation of other neurohormonal systems besides the RAAS, such as the sympathetic nervous system (Marchi et al. 2014). The way in which alcohol consumption has been measured and categorized varies, sometimes making it challenging to compare data among studies. More studies today report alcohol consumption in terms of either “drinks” or grams/units of ethanol per day or week, and alcohol consumption is measured by self-report.

How should I change my diet if I have this condition?

As the syndrome could be attributed to the toxicity of this trace element, the additive was prohibited thereafter. Ethanol-induced changes may be related to oxidative or non-oxidative pathways of ethanol metabolism. More than one mechanism may be activated that lead to the multitude of ethanol-induced changes in cellular proteins and cell function. As reviewed in text, data from pharmacologic and transgeneic approaches, have revealed an important role for oxidative stress and the hormone, angiotensin II. There are several plasma biomarkers of oxidative stress, such as 8-isoprostane (34).

In addition to inducing apoptosis, ethanol inhibits the effect of anti-apoptotic molecules such as BCL-2 [101]. Ethanol-induced myocyte apoptosis may be regulated by growth factors [117,118] and cardiomyokines [119]. 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].

EFFECTS OF ALCOHOL WITHDRAWAL

However, there is evidence that there is enhanced autophagy in certain cardiac pathological conditions such as heart failure, cardiomyopathy, and cardiac hypertrophy, conditions in which there are increased levels of angiotensin II (69). Interestingly, angiotensin II administration induces skeletal muscle atrophy in rodents, and mechanisms include increased expression of the E3 ligases atrogin-1/MuRF-1 (70). Excessive alcohol consumption represents one of the main causes of non-ischemic dilated cardiomyopathy. Alcoholic cardiomyopathy is characterized by dilation and impaired contraction of one or both myocardial ventricles. Several pathophysiological mechanisms have been proposed at the basis of alcohol-induced damage, most of which are still object of research.

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].

Quantity of Alcohol Intake in Cardiac Disease

In patients for whom open-heart is too dangerous, such as among older seniors, experts may recommend a procedure called an alcohol septal ablation. This involves injecting a small amount of alcohol into the heart, which can shrink the thickened muscle and improve blood flow. Clinical observation confirmed that several days to weeks of drinking show higher and weeks of abstinence lower pressures. Alcohol intake may also interfere with the drug and dietary treatment of hypertension.

Different levels of daily wine consumption (i.e., sometimes, 1 to 2 glasses/day, and ≥3 glasses/day) had no effect on fatal or nonfatal outcomes (e.g., hospitalization for a CV event). Subjects who drank wine more often, however, were less likely to have symptoms of depression and more likely to have a better perception of health status. They also had lower levels of circulating inflammatory markers, such as C-terminal proendothelin-1 and pentraxin-3 (Cosmi et al. 2015).