Alcoholic Cardiomyopathy

Alcoholic cardiomyopathy is a condition resulting from long-term excessive alcohol intake. This cardiac muscle disease causes an impaired heart performance that leads to cardiac failure.

  • Processes: Poison
  • Incidence: 31 / 100.000

Overview

Alcoholic cardiomyopathy (ACM), a form of dilated cardiomyopathy, develops in individuals with chronic and heavy alcohol consumption [1]. 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. 

Management involves cessation of alcohol and treatment of heart failure with standard medications such as vasodilators, digoxin, beta blockers, and diuretics. 

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. 

Etiology

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 [2].

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 [3] resulting in structural changes such as hypertrophy to accommodate the extra blood [4]. Furthermore, the cardiac dysfunction leads to a compensatory increase in blood pressure. The resultant hypertension produces damage to the myocardium, valves and blood vessels.

Epidemiology

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% [5]. 

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 [6]. 

ACM is implicated in approximately 3.8% of all cases of cardiomyopathy [6]. In fact, chronic alcohol abuse is the second most common etiology of dilated cardiomyopathy, a condition observed more in alcoholics than the general population. 

Pathophysiology

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 [7]. 

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 [8]. 

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 [9]. 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. 

Finally, dilated cardiomyopathy is a consequence of vitamin and nutritional deficiencies such as thiamine [10]. These are attributed to alcoholism. 

Prognosis

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.   

Chronic alcohol intake can result in congestive heart failure (CHF), arrhythmias, and sudden cardiac death. 

Presentation

The clinical presentation is dependent on the stage of the heart muscle disease. In the early ACM, patients are typically asymptomatic [11]. 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. 

Sudden cardiac death may occur in individuals with dilated cardiomyopathy [12].

Other

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. 

Workup

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. 

Laboratory test

B-type natriuretic peptide (BNP) levels are sensitive for congestive heart failure. The levels of BNP can be elevated as this substance is released from the stressed ventricles.

Imaging

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 [11].

A chest radiograph may reveal evidence of heart failure [11], such as cardiomegaly, alveolar edema, pleural effusions, Kerley B lines, and other signs as well.

Cardiac catheterization evaluates systolic and diastolic performance in addition to the hemodynamic status [13]. Another technique, thallium scintigraphy, may show ischemic areas [13].

Electrocardiography (ECG)

This study identifies structural changes such as left ventricular hypertrophy [11] and any present arrhythmias. 

Other

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.

Treatment

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 [11] [13]. The vasodilators ACE inhibitors and angiotensin receptor blockers may even prevent the development of ACM [14]. 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. 

Another therapeutic aspect is the cautious use of anticoagulants in patients with left ventricular impairment and atrial fibrillation

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. 

Prevention

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.

With regards to preventing heart disease, patients should be educated about eating healthy, exercising, maintaining healthy weight, achieving glycemic control, and smoking cessation/abstinence. 

Patient Information

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:

  • Swelling of the legs
  • Waking up at night due to shortness of breath
  • A productive cough with frothy sputum
  • Shortness of breath while resting
  • Shortness of breath with physical activity
  • Decreased concentration
  • Weakness and fatigue
  • Fainting episodes
  • Feeling heart beat sensations known as palpitations
  • Rapid and abnormal pulses

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.

References

  1. McKenna CJ, Codd MB, McCann HA, et al. Alcohol consumption and idiopathic dilated cardiomyopathy: a case control study. American Heart Journal. 1998; 135(5 Pt 1):833.
  2. Mathews EC, Gradin JM, Henry WL, et al. Echocardiographic abnormalities in chronic alcoholics with and without overt congestive heart failure. American Journal of Cardiology. 1981; 47(3):570-578.
  3. Sarma JS, Ikeda S, Fischer R, et al. Biochemical and contractile properties of heart muscle after prolonged alcohol administration. Journal of Molecular and Cellular Cardiology. 1976; 8(12):951–972.
  4. Kupari M, Koskinen P, Suokas A, et al. Left ventricular filling impairment in asymptomatic chronic alcoholics. American Journal of Cardiology. 1990; 66(20):1473–1477.
  5. Fauchier L, Babuty D, Poret P, et al. Comparison of longterm outcome of alcoholic and idiopathic dilated cardiomyopathy. European Heart Journal. 2000; 21(4):306–314.
  6. Hyattsville. Vital and Health Statistics. Department of Health and Human Services. Centers for Disease Control and Prevention. 1995; 13(122).
  7. Skinner HA, Holt S, Sheu WJ, et al. Clinical versus laboratory detection of alcohol abuse: the alcohol clinical index. British Medical Journal (Clinical Research Ed). 1986; 292(6537): 1703-1708.
  8. Levi GF, Quadri A, Ratti S, Basagni M. Preclinical abnormaltiy of left ventricular function in chronic alcoholics. British Heart Journal. 1977; 39: 35-37.
  9. Conen D, Tedrow UB, Cook NR, et al. Alcohol consumption and risk of incident atrial fibrillation in women. Journal of American Medical Association.2008; 300(21): 2489-2496.
  10. Klatsky AL. Alcohol and Cardiovascular Health. Integrative and Comparative Biology. 2004 August; 44(4):324-328.
  11. Wexler RK, Elton T, Pleister A, et al. Cardiomyopathy: an overview. American Family Physician. 2009; 79(9):778-84.
  12. Binham JD, Fredlund V. A case of dilated cardiomyopathy. Rural and Remote Health. 2012; 2143.
  13. Massin EK. Current Treatment of Dilated Cardiomyopathy Texas Heart Institute Journal. 1991; 18(1):41-49.
  14. Cheng CP, Cheng HJ, Cunningham C, Shihabi ZK, Sane DC, Wannenburg T, Little WC.  Angiotensin II type 1 receptor blockade prevents alcoholic cardiomyopathy. Circulation. 2006;114(3):226-36.

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