Alcoholic cardiomyopathy (ACM) is a cardiac disease caused by chronic alcohol consumption. It is characterized by ventricular dilation and impairment in cardiac function. ACM represents one of the leading causes of non-ischemic dilated cardiomyopathy in developed countries. The major risk factor for developing ACM is chronic alcohol abuse; however, there is no specific cutoff value for the amount of alcohol consumption that would lead to the development of ACM. ACM is characterized by increased left ventricular mass, dilatation of the left ventricle, and heart failure (both systolic and diastolic).
ACM is generally attributed to heavy alcohol use over a prolonged period. There is neither a certain amount of alcohol known to be toxic to myocardial cells nor is there a specified period of exposure time to develop ACM. Alcohol consumption of 80 g per day for at least 5 years significantly increases the risk of developing ACM but, not all chronic alcohol abusers develop ACM.
ACM is a leading cause of non-ischemic dilated cardiomyopathy in the western world. The exact prevalence of ACM cannot be determined because of insufficient and inconclusive data. Among patients in alcohol addiction units, it is estimated that around 21% and 31% have ACM and this number could be higher. ACM is more common in middle age African American men and women than in the white population. Prevalence of ACM is equal between males and females, with males being higher alcohol consumers and having a higher mortality rate than females. In contrast to males, females are much more susceptible to alcohol-induced cardiac damage after consumption of less amount of alcohol and for a shorter period of time compared to males. This may be explained by the lower total female body free water.
Chronic alcohol consumption can cause multi-organ damage including myocardial dysfunction. Other adverse effects include mitochondria damage, oxidative stress injury, apoptosis, modification of actin and myosin structure, and alteration of calcium homeostasis. Alcohol consumption causes a decrease in mitochondria number and increases in its fragmentation. Studies have shown an increase in reactive oxygen species (ROS) level in myocytes following alcohol consumption and thus causes oxidation of lipids, proteins, and DNA leading to cardiac dysfunction. These changes are related to both direct alcohol toxicity on cardiac cells and indirect toxicity of major alcohol metabolites such as acetaldehyde. The pathogenesis of ACM also involves interaction between genetically related factors, such as HLA subtypes or the alcohol dehydrogenase enzyme allele as well as non-genetic factors including thiamine deficiency and exposure of various substances that are directly toxic to cardiac cells. These structural and intracellular alterations cause activation in compensatory mechanisms in response to cardiac dysfunction such as renin-angiotensin-aldosterone system, increase in sympathetic signaling firing, an increase in brain natriuretic peptide release. These mechanisms are responsible for an increase in preload, left ventricular dilation, and decreased cardiac output which all contribute to the clinical manifestation of ACM.
Alcohol induces many changes in cardiomyocytes. These changes include necrosis and fibrosis of cardiac cells. It also causes a reduction in myofibrils and mitochondria as well as enlargement or fragmentation of these cells. All of these changes occurring at the cellular level contribute to ACM; however, they lack specificity.
Patients with ACM present with signs and symptoms of congestive heart failure. Patients may present with dilated cardiomyopathy with systolic dysfunction. Diastolic dysfunction is the earliest sign of ACM and is usually seen in approximately 30% of patients with a history of chronic alcohol abuse with no evidence of systolic dysfunction nor left ventricle hypertrophy.
On physical examination, patients present with non-specific signs and symptoms of congestive heart failure such as dyspnea, fatigue, peripheral edema, third spacing, and jugular venous distention. ACM can also cause tachyarrhythmia (most common is atrial fibrillation), third and/or fourth heart sounds and a systolic murmur can also be heard.
ACM patients may also show signs of liver disease, folate deficiency, increase the risk for bleeding, malnutrition, peripheral neuropathy, and neurological disorders such as Wernicke-Korsakoff syndrome.
Diagnosis of ACM is a diagnosis of exclusion as there are no specific features for classifying ACM. In patients exhibiting chronic alcohol use, other causes of dilated cardiomyopathy must be excluded first. Blood tests such as mean corpuscular volume (MCV), gamma-glutamyl-transpeptidase (GGT), elevated transaminases (AST, ALT) and elevated INR usually are seen in liver injury and likely confirm alcohol abuse.
Chest x-ray in a patient with ACM would show pulmonary congestion, cardiomegaly, and pleural effusions.
ECG is usually not specific but may show left ventricular hypertrophy and widened QRS in end-stage ACM.
Echocardiography would show ventricular dilation and diastolic and systolic dysfunction.
Coronary angiography shows normal and patent coronary flow.
To confirm the diagnosis of ACM, the healthcare provider should rely on the improvement in cardiac function after the abstinence from alcohol.
As for alcohol-induced organ damage, ACM is mainly treated by total abstinence from alcohol or a significant reduction in alcohol consumption.
Pharmacological treatment, therefore, should be directed toward the management of alcohol abuse in combination with psychotherapy and follow up.
Patients are also required to receive the standard of care for the management of heart failure such as beta blockers, diuretics, ACE inhibitors, angiotensin receptor antagonists, among others.
Patients on maximum medical treatment with a persistent severe left ventricular dysfunction may benefit from ICD implant and heart transplantation. The use of ICD implant in non-ischemic cardiomyopathies is still a subject to debate.
Some promising new treatments are targeting the pathways that are involved in the pathogenesis of ACM such as myocyte hypertrophy, cell necrosis and fibrosis, and oxidative stress; however, these are still under investigation.
Generally, ACM is associated with a good prognosis in comparison with other causes of dilated cardiomyopathy. Long-term survival is affected directly by both the amount of alcohol use and the duration of this usage. Studies have shown that one-third of the patients either die or receive heart transplantation; one-third have a stable course, and one-third have a complete recovery.
The presence of certain factors such as an absence of treatment with beta-blockers, atrial fibrillation, QRS greater than or equal to 120 ms, and digoxin use in patients with ACM are all associated with a worse cardiac outcome.
Alcoholic cardiomyopathy is best managed by a team of healthcare professionals. The key is to prevent the condition in the first place. The nurse and pharmacist should encourage alcohol abstinence. These patients may also benefit from a dietary consult. In addition, the patient should be encouraged to enter a cardiac rehabilitation program to improve exercise endurance. For those who continue to drink alcohol, a referral to alcoholic anonymous may be beneficial. Finally, the pharmacist should educate the patient on medication compliance because, without proper treatment, heart failure is a potential complication.  (Level V)
For patients with ACM who continue to drink, the prognosis is poor. For those who discontinue alcohol, the prognosis is improved with a marked improvement in symptoms. Patients who abstain from alcohol have fewer hospital admissions and echo usually reveals a small diameter of the left ventricle. For those who continue to drink, complications may include heart failure, arrhythmias and cardioembolic phenomenon. Data reveal that depending on the alcohol consumed, mortality rates of 40-80% are seen within 10 years. (Level V)