Cardiotoxicity refers to heart damage that occurs in response to certain drugs, such as alcohol. Still, medical professionals have not identified a specific alcohol level toxic to heart cells. They also have not established how long a person would need to consume alcohol before developing ACM. According to the National Institute on Alcohol Abuse and Alcoholism (NIAAA), AUD is a brain disorder that doctors characterize https://ecosoberhouse.com/article/dealing-with-internal-and-external-relapse-triggers/ by the inability to stop or control alcohol consumption. This inability occurs despite adverse effects on the person’s health, occupation, or relationships. Since myocardium requires a high energy supply to maintain persistent sarcomere contractions, it was supposed that alcohol could exert its damaging effect on the mitochondrial energy supply system, with the disruption of oxidative control mechanisms [26,100].
Signs and symptoms
In some cases, especially those that are more severe, heart failure symptoms and related conditions may develop or get worse. Your healthcare provider is the best person to explain the risks and possible complications alcoholic cardiomyopathy is especially dangerous because that you might face from this condition itself, related health concerns or any of the treatments that you will receive. As you reduce your alcohol intake, your provider will also treat your symptoms.
How should I change my diet if I have this condition?
Markers for chronic alcohol consumption rely on liver enzymes such as gamma-glutamyltransferase (GGT) [119], glutamic oxalacetic transaminase (GOT), and glutamic pyruvic transaminase (GPT). Elevations of the transaminases (GOT, GPT), especially a ratio of GOT/GPT higher than 2 might be indicative of alcoholic liver disease instead of liver disease from other etiologies [120, 121]. An excellent marker is carbohydrate deficient transferrin (CDT), which best detects chronic alcohol consumption alone [122, 123] or in combination with the other markers such as GGT [8, 124]. Markers such as ethyl sulphate, phosphatidyl ethanol, and fatty acid ethyl esters are not routinely done.
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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).
- Future studies in ACM should also address this topic, which has important economic consequences.
- Other treatments aim to treat the symptoms of ACM and prevent any disease complications.
- This study included not only DCM, but also all causes of left ventricular dysfunction, including hypertensive heart disease, ischemic cardiomyopathy and heart valve disease.
- Apoptosis may be induced by ethanol through mitochondrial membrane permeabilization and the release of pro-apoptotic factors (cytochrome c) from the mitochondrial inter-membrane space to the cytosol.
Acute vs. chronic
Weakening in the muscles around the ventricles means they can’t pump as hard, which negatively affects your entire body. Alcohol-induced cardiomyopathy can affect anyone who consumes too much alcohol, even those who don’t have alcohol use disorder. However, it’s more likely to happen in people with alcohol use disorders or who have genetic mutations that cause them to process alcohol more slowly. Data suggests patients with successful quitting of alcohol have improved overall outcomes with a reduced number of inpatient admissions and improvement in diameter size on echocardiogram.
These changes are related to both direct alcohol toxicity on cardiac cells and the indirect toxicity of major alcohol metabolites such as acetaldehyde. 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.
Patient History
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. Based on these data, acute ethanol-induced injury appears to be mediated by ethanol and acetaldehyde; the latter may play a more important role. Some studies have suggested that a genetic vulnerability exists to the myocardial effects of alcohol consumption. Individuals with certain mitochondrial deoxyribonucleic acid (DNA) mutations and angiotensin-converting enzyme (ACE) genotypes (DD genotype) may be particularly susceptible to the damaging effects of alcohol.
- Alcohol abuse can cause cardiomyopathy indistinguishable from other types of dilated nonischemic cardiomyopathy.
- Illustrations of a typical heart, as shown on the left, and a heart with hypertrophic cardiomyopathy.
- Epidemics of heart failure in persons who had consumed beer contaminated with arsenic in the 1900s and cobalt in the 1960s also obscured the observation that alcohol could exhibit a direct toxic effect.
