Alcoholic cardiomyopathy: Treatments, outlook, and more

To make a diagnosis, your doctor will perform a physical examination and ask you about your medical history.

Risk factors

On ECG, unspecific abnormalities like complete or incomplete left bundle branch block, atrioventricular conduction disturbances, alterations in the ST segment, and P wave changes can be found comparable to those in idiopathic DCM 113. In ACM, it is relevant to consider the treatment of the other alcohol-induced systemic damage, such as liver cirrhosis, malnutrition, and vitamin and electrolyte disturbances 2,11,52. Notably, in patients with a history of chronic alcohol consumption complicated by significant myocardial dysfunction and chronic malnutrition, re-feeding syndrome may increase the cardiac dysfunction. Therefore, physicians should be aware of the risk of new cardiomyopathy in patients with these overlapping diagnoses 144. Control of these alcohol-related systemic diseases, as well as the strict control of the presence of other heart risk factors (tobacco, cocaine, arterial hypertension, diabetes mellitus, or anemia) contributes to ACM improvement 10,20,23,37,52. Atrial fibrillation should be controlled with chronotropic drugs such as digoxin or diltiazem and anticoagulant treatment to avoid arterial embolisms 60,145.

• Kino et al22 found increased ventricular thickness when consumption exceeded 75 mL/d (60 g) of ethanol, and the increase was higher among those subjects who consumed over 125 mL/d (100 g), without specifying the duration of consumption.
• This review will provide an updated view of this condition, including its epidemiology, pathogenesis, diagnosis, and treatment (Graphical Abstract).
• According to recent data, a genetic form of DCM could be present in up to 50% of idiopathic DCM cases, and other specific forms of DCM such as peripartum cardiomyopathy have been shown to have a genetic basis in a significant number of cases68.
• Cardiac remodeling is a global process that myocardium establishes as a result of different aggressions 31,132.

Organ-Specific Toxicologic Pathology

The only factor to predict a poor outcome was the duration of symptoms before admission. In this review, we evaluate the available evidence linking alcohol consumption with HF and DCM. The mainstay of management is providing support, resources including but not limited to alcoholic anonymous and encouragement for alcohol abstinence and address underlying stressors if any which requires assistance from nursing staff and pharmacy. Some studies have suggested that even moderation of alcohol consumption similar outcomes as compared to abstinence.

• Finally, it should be noted that a large majority of studies on the long-term prognosis of ACM used the cut-off point of 80 g/d for a minimum of 5 years to consider alcohol as the cause of DCM.
• Myocyte ethanol targets include changes in membrane composition, receptors, ion channels, intracellular Ca2+ transients, and structural proteins, and disrupt sarcomere contractility.
• Unfortunately Lazarević et al23, as in most of these studies, systematically excluded patients with a history of heart disease or with HF symptoms.
• The effect of a low dose of alcohol consumption on the cardiovascular system has been also extensively evaluated with evidence of a dual effect, beneficial for coronary artery disease at low doses 44 but reversing to a damaging effect at moderate to high doses 19.
• One liter of wine was cooked for 4 min with 10 fresh parsley stems, 1 spoon of vinegar, and 300 g honey and then filtered 11.

International Patients

Indeed, there are case reports of reversibility of cardiac function after cessation of drug use. In patients who develop cardiomyopathy, the traditional therapy for LV dysfunction is appropriate. Two decades ago, the treatment of cocaine-induced cardiovascular effects favored the use of β-blockers, especially propranolol. As the clinical use of propranolol increased, reports of accentuation of cocaine-induced hypertension and myocardial ischemia began to surface, blaming the unopposed alpha effects of the β-blockers. Although these reports were isolated, the routine use of propranolol and subsequently all β-blockers were considered relatively contraindicated in treating cocaine-induced cardiovascular emergencies.

What Are the Risk Factors for Alcoholic Cardiomyopathy?

Out of end-stage cases, the majority of subjects affected by ACM who achieve complete ethanol abstinence functionally improve 33,82,135. The percentage of effective abstinence achievement on these patients submitted to specific programs ranges from 50% to 60% 8,9. Therefore, many ACM subjects are not able to effectively control their alcohol-consumption rates. Therefore, any decrease in the previous quantity of alcohol consumption may improve, to some degree, cardiac health 51. Since ACM is related to frequent perioperative events and high postoperative morbidity 139, detection and treatment of ACM is compulsory to avoid anesthetic and surgical complications 140.

In fact, there is an increasing consumption in particular groups, such as adolescents and young people 3,4. According to the National Institute on Alcohol Abuse and Alcoholism (NIAAA), AUD is a brain disorder that doctors characterize by the inability to stop or control alcohol consumption. This inability occurs despite adverse effects on the person’s health, occupation, or relationships.

However, cardiac apoptosis may also develop independently of the mitochondrial pathway 115 through the extrinsic pathway, which involves cell surface death receptors 116. In addition to inducing apoptosis, ethanol inhibits the effect of anti-apoptotic molecules such as BCL-2 101. Ethanol-induced myocyte apoptosis may be regulated by growth factors 117,118 and cardiomyokines 119. The percentage of alcoholic cardiomyopathy symptoms 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.

Echocardiographic and haemodynamic studies in alcoholics

According to recent data, a genetic form of DCM could be present in up to 50% of idiopathic DCM cases, and other specific forms of DCM such as peripartum cardiomyopathy have been shown to have a genetic basis in a significant number of cases68. It is therefore possible that patients with ACM could also harbour a genetic substrate that predisposes them to this form of cardiomyopathy. In this respect, a higher prevalence of excessive alcohol consumption has been reported among individuals diagnosed with DCM than in the general population8.

History and Physical

In fact, ethanol itself decreases the myocyte regeneration capacity and increases the fibrogenic process 52,126. Subendocardial and interstitial fibrosis progressively appear in the course of ACM, usually in advanced stages 52,56. More than 30% of the myocyte ventricular fraction can be replaced by fibrotic tissue, thus decreasing the heart elasticity and contractile capacity 64 (Figure 2).

Links to NCBI Databases

In another study on this topic, Lazarević et al23 divided a cohort of 89 asymptomatic individuals whose consumption exceeded 80 g/d (8 standard units) into 3 groups according to the duration of their alcohol abuse. Subjects with a shorter period of alcohol abuse, from 5 to 10 years, had a significant increase in left ventricular diameter and volume compared to the control group. However, a systolic impairment was not found as the years of alcoholic abuse continued. The signs and symptoms of alcoholic cardiomyopathy (ACM) can vary depending on the severity of the condition.6 In the early stages, people with ACM may not experience any symptoms. However, as the condition progresses, they may experience symptoms such as fatigue, shortness of breath, palpitations, and swelling of the legs and ankles.6 They may also experience chest pain, dizziness, and fainting.