Alcoholic cardiomyopathy: The result of dosage and individual predisposition

The excessive intake of alcohol weakens the heart muscle, leading to an enlarged and less efficient heart. Over time, this weakening can cause heart failure and other serious cardiovascular issues. Hypertension due to alcohol may be a confounding comorbidity in that it may contribute to LV dysfunction; therefore, LV dysfunction due to hypertension must be differentiated from pure AC. 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.

Lifestyle Risk Factors

Renaud and de Lorgeril 93 suggested that the inhibition of platelet reactivity by wine may be one explanation for protection from CAD in France. 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.

Laboratory tests

Unfortunately, all the available reports were completed at a time when a majority of the current heart failure therapies were not available (Table 1). Caution for anticoagulation is warranted due to the problems of noncompliance, trauma, and overdosage especially in hepatic dysfunction. Acetaldehyde is a potent oxidant and, as such, increases oxidative stress, leading to the formation of oxygen radicals, with subsequent endothelial and tissue dysfunction. Mitochondria play an essential role in cellular metabolism, and disruption of their function can have profound effects on the entire cell. The myocyte mitochondria in the hearts of persons exposed to alcohol are clearly abnormal in drug addiction treatment structure, and many believe that this may be an important factor in the development of AC. Alcoholic cardiomyopathy is a specific cause of heart failure, so the two share many symptoms, such as shortness of breath, fatigue, and leg swelling.

5. Sarcomere Damage and Dysfunction in ACM

Patients with alcoholic cardiomyopathy, therefore, usually present with symptoms of heart failure, i. Echocardiography may reveal a mild or severe depression of cardiac function and ejection fraction or even show hypertrophy in the beginning 109. Heart failure symptoms may be due to early diastolic or to later systolic dysfunction. At later stages, due to atrial fibrillation, thrombi are not uncommon in the dilated atria.

Although some studies have detailed structural and functional damage in proportion to the amount of alcohol consumed during a patient’s lifetime24, a large majority of authors have discarded this theory21-23,25. Both the absence of a direct correlation and the theory of the existence of a threshold dose (above which some alcoholics develop ACM) require the presence of individual susceptibility to alcohol induced cardiac damage63. It is unknown whether individual susceptibility would be related to increased vulnerability at the myocardial level and/or to impaired alcohol metabolism. Myocardial impairment following chronic excessive alcohol intake has been evaluated using echocardiographic and haemodynamic measurements in a significant number of reports.

Most common causes of Takotsubo cardiomyopathy

Among patients who continued drinking heavily, transplant-free survival was significantly worse than in non-drinkers (27% vs 45%). 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. Cardiac MRI may be helpful in the differential diagnosis to hypertrophic cardiomyopathy, storage diseases, and inflammatory cardiomyopathy. Early diagnosis and complete cessation of alcohol can sometimes reverse heart damage. In extreme cases, surgical options such as heart transplantation may be considered.

As the heart’s function declines, patients may also experience shortness of breath at rest. Alcoholic cardiomyopathy is a form of dilated cardiomyopathy, where the heart’s chambers enlarge and weaken due to alcohol’s toxic effects on the heart muscle. Over time, the heart struggles to pump blood efficiently, leading to symptoms like shortness of breath, fatigue, and leg swelling. If what is alcoholic cardiomyopathy untreated, it can progress to heart failure, a life-threatening condition requiring immediate medical attention. 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.

The myth: Cardiomyopathy affects only your cardiovascular system.

However, heart failure can stem from many causes, including ischemic heart disease, hypertensive heart disease, and valvular heart disease. A persistent cough is present in about 20-30% of patients with alcoholic cardiomyopathy. This symptom is often due to fluid buildup in the lungs (pulmonary congestion) as the heart’s ability to pump blood declines.

Alcoholic Cardiomyopathy: What Are The Symptoms, And How Is It Diagnosed And Treated?

To identify the causative agent of AC, investigators administered ethanol to rats pretreated with inhibitors of ethanol metabolism. Use of ethanol alone or ethanol with an alcohol dehydrogenase inhibitor resulted in a 25% decrease in protein synthesis. When the rats were given an inhibitor of https://ecosoberhouse.com/ acetaldehyde dehydrogenase to increase levels of the ethanol metabolite acetaldehyde, an 80% decrease in protein synthesis occurred.

Links to NCBI Databases

• This leads to fluid buildup in the lungs, known as pulmonary congestion, making it difficult to breathe, especially during physical activity or when lying down.
• Elevated pressures suggest pulmonary hypertension, while alcoholic cardiomyopathy would show a weakened heart muscle on an echocardiogram without elevated lung pressures.
• In a world-wide setting, alcohol use disorders show similarities in developed countries, where alcohol is cheap and readily available 8.
• They found that 2 of the 6 individuals (33%) whose alcohol consumption exceeded 125 mL/d had cardiomegaly.

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. Ethanol may produce the modification of sarcolemmal membrane L-type Ca2+ channels, leading to a decrease in transmembrane electrically induced Ca2+ transients 85,103,127. One of the most relevant targets of ethanol in the membrane is the disruption of membrane receptor composition and activities 86.