Alcohols Effects on the Cardiovascular System

Pathologically, ethanol 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 alcohol rehab and defense mechanisms.

AMOUNT OF ALCOHOL REQUIRED TO PRODUCE ACM

Their results achieved 90% accuracy in defining a history of alcohol abuse for patients positive in at least four of these parameters (Table 1). Because the clinical signs can be gathered during a physical exam, and the questions administered in the medical history seem unrelated to alcohol abuse, it is more likely that valid information will be obtained 24. An alternative approach utilizes biochemical assays to differentiate individuals with ACM from other cardiomyopathies Wang et al. (1989). 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.

Genetic factors

In fact, ACM is considered to be the result of dosage and individual predisposition 32. Before recognizing that ethanol itself is the etiological factor of ACM, different theories and hypotheses emerged 1,66. It was suspected that malnutrition, frequently related to chronic alcohol misuse, was the origin of ACM 6,67. However, it has been evidenced that ACM may develop in the absence of protein or caloric malnutrition 38. However, nutritional factors may worsen the natural course of ACM and should be avoided 18,19.

Direct toxic effect of ethanol

Finally, it should be noted that a large majority of studies on the long-term prognosis of ACM used the cut-off point of 80 g/d for a minimum of 5 years to consider alcohol as the cause of DCM. New therapeutic strategies for AC are being developed with the support of animal models. These include damaging factors alcoholic cardiomyopathy such as acetaldehyde or ROS, cardiac fibrosis, or apoptosis.

Beriberi heart disease

Most often, low-risk or moderate drinking has been defined as 1 to 2 standard drinks per day and heavy alcohol consumption as 4 or more standard drinks per day. However, ascertaining the exact alcohol consumption threshold for determining both the benefit and risk has been challenging, and threshold levels continue to differ across studies. Interestingly, Wu et al. using carotid pulse measurements, observed a gender dependent effect in preclinical ACM (asymptomatic ACM)—that is, female patients displayed no deviation in carotid pulse measurements values for either PEP or LVET while males did 36. In contrast, Kupari et al. reported that alcoholic women presented with reduced ejection fraction 37. These studies suggest that in patients presenting with no clinical signs of heart disease, impaired diastolic function may serve as an early sign =https://ecosoberhouse.com/ of ACM, while systolic dysfunction may represent move metn along the continuum towards failure. The presence of cardiac abnormalities in the asymptomatic alcoholic exemplifies the importance for clinicians to conduct an extensive examination when presented with an individual with a history of ethanol abuse.

• If a person regularly drinks more alcohol than experts recommend, they can speak with a doctor about cutting back.
• Along with signs of heart failure such as increased N-terminal pro-B-type natriuretic peptide, blood tests can provide hints suggesting chronic alcohol abuse.
• Depression of LV ejection fraction (EF) is the hallmark of this period that also occurs with a reduction in LV shortening fraction, increase in LV diameter, and mass indices that may be measured by echocardiography or cardiac MR spectroscopy 40,52.

However, in this context, experimental in vitro studies using cardiomyocytes have shown that alcohol depresses the contractile capacity of the myocardium, regardless of the sympathetic tone and the haemodynamic conditions36. Alcohol-induced cardiomyopathy remains a relevant health problem, for which the mainstay of treatment is alcohol abstinence. In recent years, basic and clinical research has shed light on its pathogenesis, which includes direct toxic effects of alcohol on the myocardium, oxidative stress, mitochondrial dysfunction, and genetic susceptibility.

Alcoholic Cardiomyopathy: Multigenic Changes Underlie Cardiovascular Dysfunction

However, the consensus among medical professionals is that the drawbacks of alcohol far outweigh any of its suggested benefits. To date, none of the ACM studies have proposed a treatment for ACM other than that recommended for DCM in current HF guidelines. Further research is required to determine the definitive role of genetics on ACM pathophysiology. Despite these features, the structural changes do not seem to be specific, furthermore, they are not qualitatively different from those found in idiopathic DCM and they do not allow us to differentiate between the two conditions44. It also appears that the changes emerging in ACM patients only differ from idiopathic DCM in quantitative terms, with histological changes being more striking in idiopathic DCM than in ACM44.

The second phase was due to mitochondrial generation of oxidants that induce mitochondrial DNA (mtDNA) damage that destabilizes the mitochondrial complexes as well as interfering with their formation 75-77,96,111,113. At this time it is unknown if the combination of these changes have a greater effect on the myocardial conduction system compared to the cardiomyocytes, or that the much smaller number of cells in the conduction system makes them more vulnerable. Irrespective of the mechanisms of the pathology, AF is a significant concern in the management of alcoholics. Future studies with a strict classification of non-drinkers and drinkers will help clarify whether complete abstinence is mandatory for ACM patients. In the interim it seems appropriate to continue discouraging any alcohol consumption in these patients, as it would be difficult for them to maintain a limited alcohol intake considering their history of alcohol dependence and abuse. Guillo et al17 in 1997 described the evolution of 9 ACM patients who had been admitted.

Heartache in a Bottle: Understanding Alcoholic Cardiomyopathy

New strategies to improve the natural course of ACM have been proposed as promising agents in this field 112,147. Since ethanol has multiple cell targets with different pathological mechanisms implicated, those different strategies to directly target alcohol-induced heart damage are only partially effective and can only be used as support medication in a multidisciplinary approach 112. They try to control myocardial remodeling to avoid the progression of myocyte hypertrophy 39,148 or fibrosis 149 and ventricle dysfunction and dilatation, as well as to increase the degree of myocyte regeneration 150. Recently, new cardiomyokines (FGF21, Metrnl) and several growth factors (myostatin, IGF-1, leptin, ghrelin, miRNA, and ROCKs inhibitors) have been described as being able to regulate cardiac plasticity and decrease cardiac damage, improving cardiac repair mechanisms 112,119. They aim to control oxidative damage, myocyte hypertrophy, interstitial fibrosis, and persistent apoptosis.

In contrast to control mice, the IGF-1–expressing animals exhibited no evidence of changes in expression of antioxidant enzymes (i.e., superoxide dismutase-1) or any decreases in contractile function after 16 weeks of ethanol consumption. The findings suggest a protective effect of overexpression of IGF-1 in the transgenic animals (Zhang et al. 2014). Evidence of oxidative stress is found after short periods of alcohol consumption (2 to 18 weeks), at least in animal models. These data suggest that antioxidant defense mechanisms that attempt to protect the heart against oxidative damage appear to be initiated soon after drinking alcohol. Also, as noted below, data from other studies demonstrate the protective role of administered antioxidants, such as a synthetic compound that mimics the native superoxide dismutase enzyme, called a superoxide dismutase mimetic.