Alcoholic Cardiomyopathy: Causes, Symptoms, and Diagnosis

Although the severity of histological alterations on endomyocardial biopsy correlates with the degree of heart failure in one of our studies, biopsy is not in common use for prognostic purposes 117. Even the recovery after abstinence of alcohol is hard to predict based on morphometric evaluation of endomyocardial biopsies 118. The first clinical recognition of ACM was performed by Hippocrates in Greece during the 4th century B.C. However, its modern clinical report was delayed until the 19th century, where specific ACM cases were clinically described in Germany and England 1.

Echocardiographic and haemodynamic studies in alcoholics

Oxidative stress and inflammation contribute to the death of heart muscle cells (cardiomyocytes) through a https://ecosoberhouse.com/article/wet-mush-brain-from-alcoholism-symptoms-and-dangers/ process called apoptosis. Ethanol is converted into acetaldehyde, a toxic substance, and free radicals during this process. Treatment for the disorder usually consists of complete cessation of alcohol use along with lifestyle changes that focus on heart health. In some cases, medication or a heart transplant may be the best treatment option.

Laboratory tests

Chronic ethanol exposure, in combination with other stress signals, provides a trigger for cardiac apoptosis through activation of the mitochondrial permeability transition pore by physiological calcium oscillations 111. This is because the ethanol molecule has a small size and is highly reactive, with many cell targets. 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. Ethanol-induced disruption of ribosomal protein synthesis also contributes to non-contractile protein depletion 104.

Mental Health Treatment

Doctors can measure your blood pressure and check for left ventricular hypertrophy on an echocardiogram. Consistently high blood pressure and thickened heart muscle suggest hypertensive heart disease, while alcoholic cardiomyopathy typically shows a weakened heart muscle. Fatigue is reported in about 60-70% of patients with alcoholic cardiomyopathy. It results from the heart’s inability alcoholism to pump enough blood to meet the body’s needs.

• It is a type of dilated cardiomyopathy since it involves dilation or enlargement of one of the heart’s chambers.
• ACM produces a progressive reduction in myocardial contractility and heart chamber dilatation, leading to heart failure episodes and arrhythmias.
• 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.
• Patients may notice improvements in energy levels and well-being within a few weeks.

Exercise stress tests or functional assessments may be conducted to assess how your heart reacts during periods of physical exertion and stress. Under certain conditions, cardiac catheterization procedures may be performed to assess blood flow and pressures. Overall weakness and tiredness are common, even with minimal physical exertion. The level of fatigue will increase with physical activity, but oftentimes, it doesn’t require much effort to feel significantly tired.

It has been said that ethanol is the “perfect drug” because of its pleasant effects but damaging long-term effect alcoholic cardiomyopathy 1,6. It is distributed worldwide, with easy social access, and is pleasant when consumed, with positive sensations of welfare, but its negative effects, which include depressive and damaging noxious health effects, are reserved for later. This dual effect creates an additional difficulty to achieve an effective control.

During the 20th century, the physiopathological basis for ACM was progressively established 6. At present, ACM is defined as a dilated cardiomyopathy of toxic origin with low left-ventricle ejection fraction, chamber dilatation, and progression to congestive heart failure 18,52,53. Excessive EtOH consumption is one of the main causes of non-ischemic dilated cardiomyopathy (CMP), representing around one-third of cases 30. In all ACM studies, inclusion of patients is based on patients’ self-reported alcohol drinking habits, which may lead to an underestimation of the prevalence of ACM together with problematic identification of patients who abstain and those who continue drinking.