Alcoholic Cardiomyopathy: Causes, Symptoms, and Treatment Options

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.

• The percentage of apoptotic myocytes in ACM is relatively low but, in combination with a persistent decrease in myocyte proliferation, they may contribute to an absolute cell loss and decreased cardiac contractility 52,115.
• If you or someone you know consumes large amounts of alcohol regularly, you should encourage them to try moderation or seek professional help to cut back or quit drinking.
• New strategies are addressed to decrease myocyte hypertrophy and interstitial fibrosis and try to improve myocyte regeneration, minimizing ethanol-related cardiac damage.
• Most people who develop alcohol-induced cardiomyopathy have a history of heavy drinking—especially those who have been drinking heavily for 5 to 15 years.
• Understanding these risk factors can help individuals make informed decisions about their health and seek early intervention if they are at risk.

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This influences the maintenance of cardiac geometry and contractile function, increasing the development of ACM 121. In ACM, protein degradation with sarcomere disarray and contractile protein loss has been suggested to be a key point of autophagy induction 18. Different pathogenic hypotheses have been suggested, such as the pivotal role of acetaldehyde 122, the role of oxidative stress and stress signaling cascades 109, and the translocation of NFkB into the nucleus 106. Alcoholic cardiomyopathy is a form of dilated cardiomyopathy (heart disease) caused by chronic alcohol consumption or long-term alcohol abuse. New strategies to improve the natural course of ACM have been proposed as promising agents in this field 112,147.

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Furthermore, the inclusion criteria for ACM were very strict and required a minimum consumption of 8 oz of alcohol (200 g or 20 standard units) each day for over 6 mo. In contrast, European studies focusing on the prevalence of ACM included only subjects diagnosed with DCM and applied the consumption threshold of 80 g/d for ≥ 5 years, finding an ACM prevalence of 23%-47% among idiopathic DCM patients9-12 (Figure 1). Both conditions involve weakened heart muscles, causing similar symptoms like shortness of breath, fatigue, and leg swelling.

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This is especially true if your genetic condition affects how your body metabolizes alcohol. However, the best way to completely prevent alcoholic cardiomyopathy is not to drink at all. Some studies have suggested that even moderation of alcohol alcoholic cardiomyopathy is especially dangerous because consumption similar outcomes as compared to abstinence. Patients can expect relief from chest pain within minutes of taking nitrates, with long-term use helping improve heart function and reduce angina attacks. Patients may experience improved heart function and reduced fatigue and shortness of breath within a few weeks, though careful monitoring is needed to avoid toxicity. Chronic alcohol use tends to have far-reaching effects on all aspects of a person’s life, and not just their health.

Basic studies on molecular mechanisms of myocardial damage

• This influences the maintenance of cardiac geometry and contractile function, increasing the development of ACM 121.
• There are no specific targeted histological or immunological biomarkers for the diagnosis of alcohol-induced cardiomyopathy.
• Abstinence is the preferred goal, although controlled drinking may still improve cardiac function.
• While palpitations are not always dangerous, they should be evaluated by a healthcare provider to determine their underlying cause.
• In the first of these studies, Fauchier et al11 studied 50 patients with ACM and 84 patients with DCM between 1986 and 1997.
• Alcoholic cardiomyopathy is a specific cause of heart failure, so the two share many symptoms, such as shortness of breath, fatigue, and leg swelling.
• One such potential risk of alcohol use disorder is alcoholic cardiomyopathy, a condition that can lead to heart failure.

In his 1972 review article, Bridgen was the first to introduce the term alcoholic cardiomyopathy 27. Furthermore, there are conflicting data among studies regarding the prognosis of the condition, with some showing overall mortality near 60% and others showing a mortality rate of only 19% (Table 1). Additionally, the accepted ACM definition does not take into account a patient’s sex or body mass index (BMI). As women typically have a lower BMI than men, a similar amount of alcohol would reach a woman’s heart after consuming smaller quantities of alcohol.

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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. It can occur when the heart is unable to pump enough blood to the brain, leading to lightheadedness or a sensation of spinning. Dizziness may also be related to arrhythmias or low blood pressure, both common in patients with weakened heart function. In some cases, dizziness can lead to fainting, particularly during episodes of irregular heartbeat. Irregular heartbeats, or arrhythmias, are present in about 40-50% of patients with alcoholic cardiomyopathy. Alcohol can directly affect the heart’s electrical system, leading to abnormal rhythms like atrial fibrillation or ventricular tachycardia.

Prognosis

Similarly, people with pre-existing heart conditions, such as coronary artery disease, are more vulnerable to alcohol’s effects on the heart muscle. The most significant lifestyle risk factor for developing alcoholic cardiomyopathy is chronic, excessive alcohol consumption. Drinking large amounts of alcohol over many years can directly damage the heart muscle. According to the Centers for Disease Control https://ecosoberhouse.com/ and Prevention (CDC), heavy drinking is defined as more than 8 drinks per week for women and more than 15 drinks per week for men.

In long-term follow-up studies, a mortality rate of 10% of patients/year has been observed in the group marijuana addiction of patients with persistent high-dose ethanol consumption 19,52. Along with developing heart damage, patients with ACM may also damage other organs, such as the liver, central and peripheral nervous system, skeletal muscle, pancreas, and digestive tract, and are exposed to an increased risk of cancer 24,63,64. In fact, ACM is related to systemic damage induced by ethanol misuse and its global biological response 10,11,31. Pharmacologic therapy should include goal-directed heart failure therapy as used in idiopathic dilated cardiomyopathy with reduced ejection fraction.

Beriberi heart disease

Heart remodeling is an adaptive mechanism, susceptible to being modified in ACM by the use of cardiomyokines (FGF21, Metrnl) and growth factors (IGF-1, Myostatin) 112,119. Alcoholic cardiomyopathy (ACM) is a cardiac disease caused by chronic alcohol consumption. The major risk factor for developing ACM is chronic alcohol use; however, there is no cutoff value for the amount of alcohol consumption that would lead to the development of ACM. This activity describes the pathophysiology of ACM, its causes, presentation and the role of the interprofessional team in its management.ACM is characterized by increased left ventricular mass, dilatation of the left ventricle, and heart failure (both systolic and diastolic). This activity examines when this condition should be considered on differential diagnosis.

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In addition, acetaldehyde is able to interact with proteins and produce protein-adduct compounds that are highly reactive and may induce additional inflammatory and immunologic heart damage 78. Therefore, because of its multiple actions, acetaldehyde may influence ACM pathogenesis in addition to ethanol effect itself 20,76,77. Occidental Berberi is the term used for the clinical scenario caused by thiamine deficit, a situation commonly present in chronic alcohol misuse, and was attributed as the cause of ACM 68,69.