Heartache in a Bottle: Understanding Alcoholic Cardiomyopathy

Frequently, a relative decrease occurs in systolic blood pressure because of reduced cardiac output and increased diastolic blood pressure due to peripheral vasoconstriction, resulting in a decrease in the pulse pressure. A 1- and 4-year follow-up study of 55 men with alcoholism showed that abstinence and controlled drinking of up to 60 https://ecosoberhouse.com/ g/day (4 drinks) resulted in comparable improvement in LV ejection fraction. Ten patients who continued to drink higher amounts of alcohol all died during the follow-up period. 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 acetaldehyde dehydrogenase to increase levels of the ethanol metabolite acetaldehyde, an 80% decrease in protein synthesis occurred.

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Alterations in protein physiology/content can also be due to accelerated protein degradation. In skeletal muscle, ubiquitin E3 ligases, such as atrogin-1 and muscle RING Finger 1 (MuRF1), accelerate protein breakdown and lead to muscle atrophy (67,68). Recently, Lang and Korzick (65) reported that 20 weeks of alcohol consumption in female Fischer 344 rats increased myocardial atrogin-1 and MuRF1 expression (e.g., messenger ribonucleic acid levels). In this same study, investigators found increased markers of autophagy, such as LC3B and autophagy-related gene 7 proteins and tumor necrosis factor α, along with a reduction in mTOR activity. Autophagy is a catabolic mechanism carried out by lysosomes and is important for the degradation of unnecessary or damaged intracellular proteins, therefore keeping the cell healthy.

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Genetic testing may be recommended if there’s a family history of dilated cardiomyopathy. An echocardiogram can reveal enlarged heart chambers in both conditions, but alcohol-related liver damage or a history of heavy drinking points more toward alcoholic cardiomyopathy. 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. Clinical overview, pathogenesis, treatment and prognosis of alcoholic cardiomyopathy. DCM, dilated cardiomyopathy; alcoholic cardiomyopathy is especially dangerous because HF, heart failure; HFrEF, heart failure with reduced ejection fraction; HTx, heart transplant; LVEDD, left ventricular end-diastolic diameter; LVEF, left ventricular ejection fraction; SD, standard deviation.

Are there long term effects of Alcoholic Cardiomyopathy (Alcohol-related Heart Damage)?

A study in a rat model using an alcohol dehydrogenase transgene that results in elevated levels of acetaldehyde demonstrated a change in calcium metabolism at the intracellular level and a decrease in peak shortening and shortening velocity. This was interpreted by the authors as suggesting that acetaldehyde plays a key role in the cardiac dysfunction seen after alcohol intake. Others have suggested that an acute decrease in mitochondrial glutathione content may play a part in mitochondrial damage and implicate oxidative stress as a contributor to this process. 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.

• In the 1950s, evidence began to emerge that supported the idea of a direct toxic myocardial effect of alcohol, and research during the last few decades has been particularly productive in characterizing the disease entity of alcoholic cardiomyopathy (AC).
• Additional studies included 24-hour ECG monitoring and cardiac magnetic resonance imaging.
• The toxic effects of alcohol abuse can be heart failure, organ failure, or a multitude of other health issues, some more dangerous than others.
• The cardiovascular system is, after the liver and gastrointestinal system, the second most affected system by global ethanol toxicity 1,33,34.

Because hypertension may directly contribute to LV dysfunction, this may be a confounding comorbidity in persons who abuse alcohol, and it should be differentiated from pure forms of alcoholic cardiomyopathy. Long-term alcohol abuse weakens and thins the heart muscle, affecting its ability to pump blood. When your heart can’t pump blood efficiently, the lack of blood flow disrupts all your body’s major functions. Alcoholic cardiomyopathy can present with signs and symptoms of congestive heart failure.

• The authors highlighted the presence of an extensive intracellular accumulation of neutral lipids, principally in the form of small cytoplasmic droplets.
• Heart myocytes are relatively resistant to the toxic effect of ethanol, developing a functional and structural compensatory mechanism able to minimize or repair the ethanol-induced myocyte damage 20,31,39.
• Pulmonary rales signify pulmonary congestion secondary to elevated left atrial and LV end-diastolic pressures.

Before delving into how alcohol damages the heart, it’s important to understand what the heart is supposed to do. The heart is a muscular organ responsible for pumping oxygen-rich blood throughout the body. It consists of four chambers—the left and right atria and ventricles—which work together in a synchronized rhythm to ensure effective blood circulation. The strength and structure of the heart muscle are critical for maintaining this function. The more severe the alcoholic cardiomyopathy, additional treatment options may be necessary.

Heart transplant

As the heart’s function deteriorates, the kidneys may become less efficient at removing excess fluid drug addiction treatment from the body, leading to weight gain. Patients may notice swelling in the legs, abdomen, or other areas as fluid accumulates. Regional wall motion abnormalities are not uncommon, but they are usually less prominent than those observed in persons with ischemic heart disease.