Alcoholic Cardiomyopathy: Causes, Symptoms, and Diagnosis

The trace amounts of arsenic have not been comparable to the arsenic-in-beer endemic in Manchester but may still reach up to 10-times the amount admitted for arsenic in drinking water in the European Union and the US. 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. Due to page limitations, we recognize that we have not included all the excellent scientific work completed in the area of alcohol and the cardiovascular system. The main symptoms are chest pain and breathlessness, similar to those of a heart attack. Some people who experience significant emotional or physical stress, such as bereavement or major surgery, go on to experience a temporary heart problem.

• In endomyocardial biopsies of alcoholics up to 30 % of patients were found to exhibit sparse lymphocytic infiltrates with myocyte degeneration and focal necrosis and increased HLA (human leukocyte antigen) or ICAM (intercellular adhesion molecule) expression (Fig. 3; [16, 84]).
• Although anticoagulation may be of benefit to patients with profound LV dysfunction and atrial fibrillation, the risks must be weighed heavily in this patient population.
• Under the latter conditions, autophagy via degradation of macromolecular intracellular constituents becomes important in generating and recycling carbons and amino acids.
• Often, when a doctor suspects cardiomyopathy, they will order an echocardiogram.
• For many decades, ACM has been considered one of the main causes of left ventricular dysfunction in developed countries.

2. Is ethanol the Real Cause of ACM

• Ethanol-induced myocyte apoptosis may be regulated by growth factors [117,118] and cardiomyokines [119].
• The first study, which specifically focused on the amount of alcohol necessary to cause ACM, was conducted by Koide et al[20] in 1975.
• They may admit drinking at social events but not the abuse in the first contact.
• Notably, in patients with a history of chronic alcohol consumption complicated by significant myocardial dysfunction and chronic malnutrition, re-feeding syndrome may increase the cardiac dysfunction.

Similarly, electrolyte (Na, K, Ca, Mg, P) deficiencies or disturbances may play a major role in cardiac function, and ethanol misuse may be related to them [52]. Selenium deficit (Keshan disease in China) could also induce ACM in specific areas [70]. This ethanol misuse at high consumption rates causes a alcoholic cardiomyopathy symptoms 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.

Cardiac Effects of Alcohol

Further research is required to determine the definitive role of genetics on ACM pathophysiology. Furthermore, Fernández-Solá et al[30], when analysing a population of alcoholics, found a higher prevalence of DCM in alcoholics than among the general population. Specifically, among alcoholics they found a prevalence of DCM of 0.43% in women and 0.25% in men, whereas the described prevalence of DCM in the general population is 0.03% to 0.05%[18,19]. Finally, it should be noted that McKenna and co-workers, in one of the most frequently cited papers in the ACM field, reported an incidence of 40% in 100 individuals suffering from idiopathic DCM, but in this case the consumption threshold used was only g/d[8].

Coronary artery disease and atherosclerosis

In the mid-1960s, another unexpected heart failure epidemic among chronic, heavy beer drinkers occurred in two cities in the USA, in Quebec, Canada, and in Belgium. It was characterized by congestive heart failure, pericardial effusion, and an elevated hemoglobin concentration. The explanation proved to be the addition of small amounts of cobalt chloride. Cobalt was used as a foam stabilizer by certain breweries in Canada and in the USA. Cobalt poisoning and alcohol together acted synergistically in these patients. As the syndrome could be attributed to the toxicity of this trace element, the additive was prohibited thereafter.

Acknowledgements

Electron microscopy reveals mitochondrial enlargement and disorganization, dilatation of the sarcoplasmic reticulum, fat and glycogen deposition, and dilatation of the intercalating discs. Chronic alcohol consumption can cause multi-organ damage including myocardial dysfunction. There are no specific targeted histological or immunological biomarkers for the diagnosis of alcohol-induced cardiomyopathy.

Basic studies on molecular mechanisms of myocardial damage

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]. Ethanol-induced disruption of ribosomal protein synthesis also contributes to non-contractile protein depletion [104]. Several aspects of mitochondrial function, including respiratory complex activities and mitochondrial-dependent oxidative damage and apoptosis, are also induced by ethanol [26,100]. Myocyte cytoskeletal structure [21], connexin channel communication, and desmosomal contacts are affected by ethanol, causing structural cell instability [105]. Ethanol may induce changes in nuclear regulation of transcription with a dose-dependent translocation of NFkB into the nucleus [106]. The resulting effect in those multiple sites may be additive and synergistic, increasing the final damage [20,52] (Figure 1).

Is there an immediate risk of alcohol intake?

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].

This treatment carefully alters the diseased heart tissue that causes the heart rhythm problems. You’ll also be at greater risk of developing a heart infection (endocarditis). Blood flow from the heart may be reduced or restricted (called obstructive hypertrophic https://ecosoberhouse.com/ cardiomyopathy). Hypertrophic cardiomyopathy is the most common cause of sudden unexpected death in childhood and in young athletes. The heart chambers are reduced in size so they cannot hold much blood, and the walls cannot relax properly and may stiffen.