お得情報屋

Some of these papers have also described the recovery of LVEF in many subjects after a period of alcohol withdrawal[15-17]. In this review, we evaluate the available evidence linking alcohol consumption with HF and DCM. In the course of ethanol-induced cardiac damage, one of the more relevant findings is that ethanol exerts its deleterious effects on cardiac myocytes https://ecosoberhouse.com/ at multiples sites (membrane, receptors, mitochondria, ribosomes, sarcolemma, DNA, or cytoskeleton) [18,19,98] (Table 1). One of the characteristics that makes ethanol harmful is its systemic toxic effect on the human body [10,11]. It has been described as having some kind of effect in all human body organs either in acute or chronic consumption [11,12].

International Patients

For comparison, the mean annual beer consumption in Bavaria is nowadays estimated to be 145 l and in the rest of Germany around 100 l beer per person and year [24]. A literature review using the PubMed database with the search terms ‘alcoholic cardiomyopathy’, ‘alcoholic heart disease’, was conducted up to January 2017. The literature search was limited to publications written in the English language. To avoid alcoholic cardiomyopathy, abstain from alcohol or drink in moderation.

Clinical work-up for alcoholic cardiomyopathy

In addition, ethanol has a widespread diffusion because of the potential for distribution though biological membranes, achieving targets not only in the membrane receptors and channels but also in endocellular particles and at the same nuclear compartment [29,99,100]. This induces a variety of effects, since more than 14 different sites in the myocyte can be affected by ethanol [19,98]. Specifically, ethanol disturbs the ryanodine Ca2+ release, the sarcomere Ca2+sensitivity [102,103], the excitation–contraction coupling and myofibrillary structure, and protein expression, decreasing heart contraction [86].

• Incidence of alcoholic cardiomyopathy ranges from 1-2% of all heavy alcohol users.
• The major risk factor for developing ACM is chronic alcohol use; however, there is no cutoff value for the amount of alcohol consumption that would lead to the development of ACM.
• Thus, CCM has been introduced as an new entity separate of the cirrhosis etiology.
• Although analytical markers of alcohol consumption, such as average erythrocyte volume and serum gamma-glutamyltranspeptidase levels, could be an aid to establish abstinence or persistence of alcohol intake in patients, the quantity of alcohol intake is dependent on the patients’ report.
• In this study, the only independent predictor of cardiac death was alcohol abstinence.

Ways to stay healthy

At a pathological level, sarcomere Z-line distortion and disruption of the sarcomere pattern leads to myocytolysis [107,129]. Myocytolysis is evident through focal myofiber dissolution, cell vacuolization, and fiber disarray [19] (Figure 2). The sarcomere complex is early affected by ethanol, decreasing the titin content, a protein that is responsible for sarcomere relaxation and LV distensibility [130].

Diagnosing ACM still relies on exclusion criteria, similar to alcoholic liver disease, as excessive alcohol consumption is observed in up to 40% of DCM patients. In a national inpatient sample study, some authors have reported ACM to be most common in white males aged between 45 and 59 [2]. ACM is a type of heart disease that develops due to chronic alcohol consumption. Incidence of alcoholic cardiomyopathy ranges from 1-2% of all heavy alcohol users. It is estimated, approximately 21-36% of all non-ischemic cardiomyopathies are attributed to alcohol.

Outlook, Diagnosis & Treatment Options

This fact has been assessed with echocardiographic monitoring in women consuming high doses of ethanol both in the subclinical period of disease [46] as well as in the clinical period when congestive heart failure appears [95]. At the experimental level, some gender differences also are evident in functional proteomic analysis, with sex-dependent differences in structural and energy-producing myocardial proteins in a rat model of alcoholic cardiomyopathy [96]. The biological reason for this gender difference is based on different ethanol absorption rates, distribution pattern, and metabolism in women compared to men [52]. Therefore, efforts to prevent ACM development in women should be specifically addressed [97]. During pregnancy, ethanol consumption should be clearly discouraged because of the possibility of fetal alcohol syndrome or the development of other congenital heart diseases [97]. Apoptosis occurs mainly as a consequence of lipid peroxidation and oxidative stress in various body organs.

Get the latest heart transplant-related health

Control of these alcohol-related systemic diseases, as well as the strict control of the presence of other heart risk factors (tobacco, cocaine, arterial hypertension, diabetes mellitus, or anemia) contributes to ACM improvement [10,20,23,37,52]. Atrial fibrillation should be controlled with chronotropic drugs such as digoxin or diltiazem and anticoagulant treatment to avoid arterial embolisms [60,145]. The cardiovascular system is, after the liver and gastrointestinal system, the second most affected system by global ethanol toxicity [1,33,34].

How is this condition treated, and can it be cured?

Alcoholic cardiomyopathy can present with signs and symptoms of congestive heart failure. Symptoms include gradual onset worsening shortness of breath, orthopnea/paroxysmal nocturnal dyspnea. Palpitations and syncopal episodes can occur due to tachyarrhythmias seen in alcoholic cardiomyopathy. Since cardiac myocytes are excitable cells, and ethanol may easily damage this excitation–contraction mechanism, disruption of this coupling mechanism is involved in the ACM pathogenic process [19,58].

• 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].
• The effect is much like how a rubber band or spring weakens when stretched too much.
• Subjects with a shorter period of alcohol abuse, from 5 to 10 years, had a significant increase in left ventricular diameter and volume compared to the control group.
• In contrast, beta-blockers, similar to aldosterone inhibitors, however beneficial they may be, have thus far not yielded sufficient data on their efficacy in relation to this disease.
• The first paper to assess the natural history and long-term prognosis of ACM was published by McDonald et al[69] in 1971.

Forensic Pathology Related to Cardiovascular Toxicity