The clinical presentation is dependent on the stage of the heart muscle disease. In the early ACM, patients are typically asymptomatic . In more advanced disease, individuals manifest with congestive heart failure. Therefore, a clinical picture develops secondary to CHF and pulmonary edema. A majority will experience dyspnea on exertion. As ACM progresses, patients can develop orthopnea. Furthermore, some will have paroxysmal nocturnal dyspnea and episodic coughs that produce frothy sputum. Another common sign of CHF is peripheral edema which is enhanced in patients with cirrhosis. Patients with arrhythmias may feel palpitations.
Since alcohol affects many organs and systems, alcoholics will typically display signs of thiamine and other vitamin deficiencies. Of importance, liver cirrhosis is prevalent in this group. Therefore, these patients will likely have other sequelae in addition to cardiovascular involvement.
The workup consists of a detailed history including assessment of amount and duration of alcohol use. Also, a thorough physical exam should be performed to determine the complete clinical picture. Of importance, there are pertinent studies to help achieve the diagnosis of ACM. Early diagnosis and treatment may reverse some of the cardiac damage. Hence, it is important to recognize and address the overall health of the alcoholic patient.
Echocardiography is essential as it provides measurements of the wall thickness, which are normal or reduced. Additionally, this modality yields information about the systolic and valvular function and contractility, which are usually impaired .
Cardiac catheterization evaluates systolic and diastolic performance in addition to the hemodynamic status . Another technique, thallium scintigraphy, may show ischemic areas .
Since alcoholics are predisposed to other organ and system involvement, more tests may be warranted depending on the overall clinical picture of the patient. Additionally, testing for vitamin deficiencies and electrolyte imbalance are indicated as well. These especially include thiamine, potassium, phosphorus, and magnesium levels.
The primary therapy of ACM is the withdrawal of the source. Hence, the patient should be aided and encouraged to cease and abstain from alcohol. This includes providing the patient with education, counseling, and resources to guide the challenging process. Alcohol cessation in the early stages of ACM may reverse the damage. In fact, it is also beneficial to abstain in later stages as well.
Medical treatment involves the same approach as in heart failure secondary to other causes. The main cardiovascular drugs are vasodilators, digoxin, and diuretics  . The vasodilators ACE inhibitors and angiotensin receptor blockers may even prevent the development of ACM . Digoxin is useful for those with symptomatic left ventricular dysfunction while diuretics are helpful for symptomatic relief. Beta blockers could be beneficial for stable cases while intravenous inotropic drugs may be indicated for certain patients. Heart transplantation may be necessary for those with advanced disease.
Since patients with prolonged abuse of alcohol are prone to vitamin insufficiencies, treatment with thiamine, vitamin B-12, folate, and mineral supplementation is advised. Any electrolyte imbalance should be treated early to help prevent the occurrence of an arrhythmia and sudden death.
The prognosis for recovery depends on the length and amount of alcohol use. If the heart is damaged, then full recovery is highly unlikely. However, if patients with early disease cease consumption of alcohol. Then the damage is reversible to a certain degree.
As the name suggests, this type of cardiomyopathy is caused by alcohol. While there is no set amount of alcohol intake or duration of use correlated with the severity of the disease, asymptomatic alcoholics may exhibit cardiac changes if they use more than 90 grams of alcohol daily for a duration greater than 5 years. Furthermore, symptomatic patients have likely consumed excessive alcohol for a decade or more .
The heart is one of many organs affected by alcohol abuse as this substance is toxic to the myocardial cells. Specifically, alcoholic cardiomyopathy causes an impaired contractility  resulting in structural changes such as hypertrophy to accommodate the extra blood . Furthermore, the cardiac dysfunction leads to a compensatory increase in blood pressure. The resultant hypertension produces damage to the myocardium, valves and blood vessels.
ACM occurs in correlation with prolonged and high levels of alcohol intake. However, not all alcoholics develop this condition. The prevalence ranges from 23% to 40% .
The patient demographic demonstrates a gender preference with men accounting for 86% of all cases. Additionally, mortality is higher in men than women. With regards to race, death rates are greater in African Americans than white people .
ACM is implicated in approximately 3.8% of all cases of cardiomyopathy . In fact, chronic alcohol abuse is the second most common etiology of dilated cardiomyopathy, a condition observed more in alcoholics than the general population.
The deterioration of the cardiac function in alcoholics is related to a complex pathophysiology. In asymptomatic cases, there is cardiac dysfunction, but clinical manifestations such as dyspnea do not emerge until advanced disease. Structural changes have been noted in autopsies of chronic alcoholics without congestive heart failure .
In a study assessing chronic alcoholics without cardiac symptoms, echocardiography revealed abnormal left ventricular diastolic function with altered early and late diastolic filling velocity. These observations in the early stages of alcohol abuse have been corroborated in other investigations as well. Further findings demonstrate systolic dysfunction as indicated by a prolonged pre-ejection period (PEP) and a diminished left ventricular ejection time (LVET). Specifically, the elevated PEP/LVET ratio reflects reduced myocardial function .
Gender variability has been demonstrated in a study evaluating carotid pulse measurements in asymptomatic ACM patients. Men exhibited changes in PEP and LVET while women did not.
Long-term and heavy alcohol use in men makes them susceptible to arrhythmias and sudden cardiac death. The most frequent sequel in acute and chronic alcoholics is atrial fibrillation . The pathogenesis of atrial fibrillation has not been fully established. It is believed that the weakened cardiac performance and rhythmicity resulting from alcoholism are likely secondary to multiple changes in cellular processes.
The primary method of preventing ACM is by avoiding excessive consumption of alcohol. Patients should be educated on what constitutes moderate intake. They should also be counseled on signs of addiction and be made aware of all available resources.
Alcoholic cardiomyopathy (ACM), a form of dilated cardiomyopathy, develops in individuals with chronic and heavy alcohol consumption . The heart muscle becomes weak and this results in limited contractility and eventually cardiac failure. Other risk factors such as hypertension, smoking, and diabetes mellitus are typically present in these patients.
There are two stages of this disease which are asymptomatic and symptomatic. The pathophysiology involves a process of cardiovascular changes in which the heart pump function becomes diminished causing the compensatory heart enlargement to accommodate for the extra blood. Consequently, diastolic dysfunction is exhibited followed by systolic dysfunction and eventually congestive heart failure. The latter produces symptoms. In men, sudden cardiac death is a risk especially in the setting of fatal arrhythmias.
Diagnosis is achieved through obtaining the medical and social history, physical exam, laboratory studies, and cardiac imaging. The echocardiogram is very important as it provides information on the heart size and overall function. Other imaging techniques are also useful.
Early diagnosis and treatment may reverse the cardiac damage. Additionally, any patient exhibiting signs of alcoholism should prompt studies regarding vitamin deficiencies and electrolyte abnormalities. Also, other risk factors should be addressed and controlled.
Alcoholic cardiomyopathy is a condition that results from drinking too much alcohol over years. The excessive alcohol causes toxic effects on the heart cells and, therefore, the muscle of the heart becomes too weak to pump blood efficiently. This means that the body receives less blood supply and hence experiences damage to organs and tissues. Over years of heavy abuse, the heart fails and the patients experience symptoms.
In the early stages of the disease, the patients do not have symptoms even though the heart undergoes structural changes. Once it becomes advanced, heart failure symptoms being to manifest. These include:
The diagnosis is determined when the clinician obtains the patient's history and performs a physical exam. Laboratory tests are also helpful. Additionally, imaging techniques such as an echocardiogram will provide beneficial information on the size of the heart, the function of the valves and the pumping function. An EKG will show abnormal heart rhythms (if present) and findings suggestive of an enlarged heart. A chest x-ray can show evidence of heart failure such as fluid buildup in the lungs.
The main therapy is quitting alcohol and remaining abstinent. This is a challenging task but the patient should be provided with education, counseling, and resources to help. The treatment of heart failure includes medications such as ACE inhibitors, beta blockers, digoxin, diuretics, and others as needed.
In cases with advanced cardiomyopathy, heart transplantation may be needed.
Since alcoholics tend to have vitamin and electrolyte deficiencies, these should be treated promptly to help prevent further complications.