Conferintele Green Report

The natural course of ACM is mainly related to the degree of persistence in alcohol consumption and the individual biological adaptive response [2,20,41,56,81]. Ethanol abstinence allows for recovery in the majority of cases, including in those with previous severe depression of LV EF [81,88,135]. The term alcoholic cardiomyopathy (ACM) has been widely used to describe a specific heart muscle disease found in individuals with a history of long-term heavy alcohol (ethanol) consumption. Data from human and animal studies have revealed that within the myocardium, a number of adverse histological, cellular, and structural changes occur in response to and over the course of long-term heavy alcohol consumption. The most important unresolved question, however, relates to the primary injury/mechanism by which ethanol stimulates or initiates this array of adverse changes within the myocardium.

New Methods for Analyzing Alcohol Consumption and Stroke-Related Outcomes

It is unknown whether individual susceptibility would be related to increased vulnerability at the myocardial level and/or to impaired alcohol metabolism. Unfortunately Lazarević et al[23], as in most of these studies, systematically excluded patients with a history of heart disease or with HF symptoms. It is therefore possible that most of these studies may have also consistently omitted most alcohol abusers in whom alcohol had already caused significant ventricular dysfunction. In alcoholic cardiomyopathy is especially dangerous because their autopsies, he described finding dilated cavities of the heart and fatty degeneration of the ventricular walls[14]. This ethanol misuse at high consumption rates causes a variety of health problems, ethanol 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.

Long-term Effects

• In these patients, only early and absolute abstinence of alcohol can reverse myocardial dysfunction [56, 57, 126] which in a historic study by McDonald and Burch was achieved with prolonged bedrest for several months without further access to alcoholic beverages.
• Further research is required to determine the definitive role of genetics on ACM pathophysiology.
• Until the second part of the 20th century, there was no scientific evidence on the direct and dose-dependent effect of ethanol on the heart as cause of ACM [6,38].
• 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.
• As women typically have a lower BMI than men, a similar amount of alcohol would reach a woman’s heart after consuming smaller quantities of alcohol.

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). There are several plasma biomarkers of oxidative stress, such as 8-isoprostane (34). In a nonhuman primate model (cynomolgus and rhesus monkeys) following 12 months of alcohol consumption (3.3 ± 0.2 g/kg alcohol/day), Cheng et al. found marked increases in plasma 8-isoprostane levels in animals consuming alcohol (124.8 ± 11 pg/ml) compared to controls (28 ± 5.1 pg/ml) (46). Results from another meta-analysis of 12 cohort studies found a similar dose–response relationship between alcohol consumption and HTN for males. A J-shaped relationship for females showed protective effects at or below consumption levels of 15 g/day (Taylor et al. 2009).

Signs and symptoms

Under the latter conditions, autophagy via degradation of macromolecular intracellular constituents becomes important in generating and recycling carbons and amino acids. 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 https://ecosoberhouse.com/ atrogin-1/MuRF-1 (70). Investigators have used a variety of noninvasive tests to evaluate the acute effects of alcohol consumption on myocardial function and hemodynamics in healthy humans. As with isolated animal heart experiments, some investigators have found that acute alcohol exposure (blood alcohol levels 40 to 110 mg%) depresses myocardial systolic function in humans (Delgado et al. 1975; Lang et al. 1985; Timmis et al. 1975). For example, in one study, the ejection fraction decreased by 4 percent after alcohol consumption (Delgado et al. 1975).

Coronary artery disease and atherosclerosis

In the Miró study, alcohol drinkers also had been receiving pharmacologic treatments such as beta-adrenergic blocking agents that reduce blood pressure and also may have antioxidant effects. Mechanisms related to the positive and adverse effects of alcohol on cardiovascular conditions, such as coronary heart disease and stroke as well as cardiomyopathy. Different mechanisms may be in effect depending on the dose, duration, and pattern of alcohol consumption.

Enhancing Healthcare Team Outcomes

Recently, Lang and Korzick (65) reported that 20 weeks of alcohol consumption in female Fischer 344 rats increased myocardial atrogin-1 and MuRF1 expression (e.g., messenger ribonucleic acid levels). In this same study, investigators found increased markers of autophagy, such as LC3B and autophagy-related gene 7 proteins and tumor necrosis factor α, along with a reduction in mTOR activity. Autophagy is a catabolic mechanism carried out by lysosomes and is important for the degradation of unnecessary or damaged intracellular proteins, therefore keeping the cell healthy. This mechanism is also important for cell and organism survival during stress and nutrient deprivation.

• More recently, Lazarevic found a modest increase in end-systolic and diastolic left ventricular volumes and a subsequent thickening of the posterior wall in a cohort of alcoholics consuming at least 80 g during 5 years[23]; however, no differences in systolic function were observed.
• Alcoholic cardiomyopathy (ACM) is a disease in which the long-term consumption of alcohol leads to heart failure.[1] ACM is a type of dilated cardiomyopathy.
• Still, medical professionals have not identified a specific alcohol level toxic to heart cells.
• 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 DCM[67].
• He divided this cohort into two groups according to the evolution of the ejection fraction during 36 mo in which no deaths were recorded.

Derangements in Fatty Acid Metabolism and Transport

They also had lower levels of circulating inflammatory markers, such as C-terminal proendothelin-1 and pentraxin-3 (Cosmi et al. 2015). Several studies and meta-analyses have been conducted to determine the relationship between alcohol consumption and the risk of developing heart failure in healthy subjects, as well as in those with a history of MI or CHD. Studies also have examined the “safety” of alcoholic beverage consumption in subjects with heart failure. Several reports indicate that alcohol first exerts a seemingly positive effect, followed by a more negative impact (i.e., it is biphasic) on the endothelial–nitric oxide–generating system. Endothelial dysfunction is an early indicator of blood vessel damage and atherosclerosis, as well as a strong prognostic factor for future CV events (Deanfield et al. 2007; Ras et al. 2013). Low-to-moderate levels of alcohol consumption may initially improve endothelial function, whereas high daily levels and binge drinking may impair it.