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Alcoholic cardiomyopathy

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2]; Hardik Patel, M.D.

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Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2]; Hardik Patel, M.D.

Overview

Alcoholic cardiomyopathy is a disease in which the excessive use of alcohol use damages the heart muscle causing heart failure. It is characterized by constellation of findings which includes a history of excessive alcohol intake, physical signs of alcohol abuse, heart failure, and supportive findings consistent with dilated cardiomyopathy.

Pathophysiology

Alcoholic cardiomyopathy is a type of dilated cardiomyopathy. Both acute and chronic alcohol consumption, in excessive amounts, has been associated with adverse effects on the myocardium leading to non-ischemic dilated cardiomyopathy. It accounts for 21-36% of all cases of non-ischemic dilated cardiomyopathy [1]. The maximum recommended dose of alcohol consumption in US men and women is 14 drinks and 7 drinks respectively. Consumption above these levels has been shown to be associated with the increased risk of alcoholic cardiomyopathy [2]. Pathogenesis of this condition is multi-factorial.

Differentiating Alcoholic Cardiomyopathy from Other Diseases

Alcoholic cardiomyopathy is a form of dilated cardiomyopathy (DCM). Therefore, it must be differentiated from other forms of DCM like idiopathic DCM, connective tissue disorders etc.

Epidemiology and Demographics

Alcoholic cardiomyopathy is more prevalent in middle aged males between the ages of 35-50. However, females may be more sensitive to cardiotoxic effects of alcohol, and may develop alcoholic cardiomyopathy with lesser amounts of alcohol use, than males.[3][4]

Natural History, Complications and Prognosis

In patients who continue to abuse alcohol, 4 year survival rate is 50%. On the contrary, abstinence is associated with regression of symptoms and overall improvement. Improvement in cardiac function evident from echocardiographic findings can also be noted.

Diagnosis

History and Symptoms

Symptoms presented by the occurrence of alcoholic cardiomyopathy are the result of the heart failure and usually occur after the disease has progressed to an advanced stage. Therefore the symptoms have a lot in common with other forms of cardiomyopathy. Symptoms may develop acutely or insidiously.

Physical Examination

Patients with alcoholic cardiomyopathy present with signs similar to that of heart failure. Most common findings include pedal edema, increased jugular venous pressure, pulmonary edema, and abnormal heart sounds.

Laboratory Findings

Alcoholic cardiomyopathy is majorly a clinical and echocardiographic diagnosis. There are no pathognomonic laboratory findings diagnostic of this disorder.

Electrocardiogram

Although many EKG changes are seen in patients with alcoholic cardiomyopathy, none of them are pathognomonic for this condition. However, acute alcoholic intoxication is also associated with pathological EKG changes. Common EKG abnormalities in alcoholic cardiomyopathy include non-specific ST-T changes and QT abnormalities.

Imaging

Chest X-ray

Chest X-ray findings are essentially the same as those seen in congestive heart failure.

Echocardiography

Echocardiography is the most useful initial diagnostic test in the evaluation of patients with heart failure. Because of its noninvasive nature and the ease of the test, it is the test of choice in the initial and follow-up evaluation of most forms of cardiomyopathy. It provides information not only on overall heart size and function, but also on valvular structure and function, wall motion and thickness, and pericardial disease.

Cardiac Catheterization

Cardiac catheterization or angiogram may be done to rule out coronary artery disease (CAD) as the etiology of heart failure in alcoholic cardiomyopathy. In addition to ruling out CAD, cardiac catheteriation may also be helpful to assess cardiac output, cardiac hemodynamics and filling pressures.

Treatment

Medical Therapy

Treatment for alcoholic cardiomyopathy involves lifestyle changes, including complete abstinence from alcohol use [5][6][7][8], a low sodium diet, and fluid restriction, as well as medications. If the heart failure is severe, the effectiveness of treatment will be limited.

Surgery

In severe or unresponsive patients, cardiac transplantation can be an option.

References

  1. Skotzko CE, Vrinceanu A, Krueger L, Freudenberger R (2009). “Alcohol use and congestive heart failure: incidence, importance, and approaches to improved history taking”. Heart Failure Reviews. 14 (1): 51–5. doi:10.1007/s10741-007-9048-8. PMID 18034302. Unknown parameter |month= ignored (help)
  2. Thun MJ, Peto R, Lopez AD; et al. (1997). “Alcohol consumption and mortality among middle-aged and elderly U.S. adults”. The New England Journal of Medicine. 337 (24): 1705–14. doi:10.1056/NEJM199712113372401. PMID 9392695. Unknown parameter |month= ignored (help)
  3. Fernández-Solà J, Estruch R, Nicolás JM; et al. (1997). “Comparison of alcoholic cardiomyopathy in women versus men”. The American Journal of Cardiology. 80 (4): 481–5. PMID 9285662. Unknown parameter |month= ignored (help)
  4. Urbano-Márquez A, Estruch R, Fernández-Solá J, Nicolás JM, Paré JC, Rubin E (1995). “The greater risk of alcoholic cardiomyopathy and myopathy in women compared with men”. JAMA : the Journal of the American Medical Association. 274 (2): 149–54. PMID 7596003. Unknown parameter |month= ignored (help)
  5. Guillo P, Mansourati J, Maheu B; et al. (1997). “Long-term prognosis in patients with alcoholic cardiomyopathy and severe heart failure after total abstinence”. The American Journal of Cardiology. 79 (9): 1276–8. PMID 9164905. Unknown parameter |month= ignored (help)
  6. Masani F, Kato H, Sasagawa Y; et al. (1990). “[An echocardiographic study of alcoholic cardiomyopathy after total abstinence]”. Journal of Cardiology (in Japanese). 20 (3): 627–34. PMID 2131353.
  7. Agatston AS, Snow ME, Samet P (1986). “Regression of severe alcoholic cardiomyopathy after abstinence of 10 weeks”. Alcoholism, Clinical and Experimental Research. 10 (4): 386–7. PMID 3530014. Unknown parameter |month= ignored (help)
  8. Mansourati J, Forneiro I, Genet L, Le Pichon J, Blanc JJ (1990). “[Regression of dilated cardiomyopathy in a chronic alcoholic patient after abstinence from alcohol]”. Archives Des Maladies Du Coeur Et Des Vaisseaux (in French). 83 (12): 1849–52, discussion 1853. PMID 2125195. Unknown parameter |month= ignored (help)

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Historical Perspective

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References

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Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2]; Hardik Patel, M.D.

Overview

Alcoholic cardiomyopathy is a type of dilated cardiomyopathy. Both acute and chronic alcohol consumption, in excessive amounts, has been associated with adverse effects on the myocardium leading to non-ischemic dilated cardiomyopathy. It accounts for 21-36% of all cases of non-ischemic dilated cardiomyopathy [1]. The maximum recommended dose of alcohol consumption in US men and women is 14 drinks and 7 drinks respectively. Consumption above these levels has been shown to be associated with the increased risk of alcoholic cardiomyopathy [2]. Pathogenesis of this condition is multi-factorial.

Pathophysiology

Excessive use of alcohol has a direct toxic effect on the heart muscle cells. The heart muscle becomes weakened, subsequently dilates, and cannot pump blood efficiently. The lack of blood flow affects all parts of the body, resulting in damage to multiple tissues and organ systems. Alcohol may also simultaneously be causing direct damage to the liver. [3]

Pathogenesis of alcoholic cardiomyopathy is multi-factorial. Proposed mechanisms of myocardial injury in alcoholic cardiomyopathy include:[4]

  • Ethanol induced apoptosis: Possible mechanisms by which ethanol promotes apoptosis include increased protein levels of pro-apoptotic protein Bax, increased caspase-3 enzyme activity, increased messenger RNA p21 (p21 inhibits cyclin-dependent kinases). [5]
  • Impaired contraction of myocardium due to direct toxicity
  • Inhibition of protein synthesis and decreased myocyte proliferation [6]
  • Activation of renin-angiotensin system (RAS)
  • Inhibition of oxidative phosphorylation
  • Fatty acid ester accumulation: Ethanol interferes with lipid metabolism and fatty acid composition of sarcolemma. Also, calcium content of the sarcoplasmic reticulum is affected by exposure to ethanol. Increased levels of fatty ethyl esters disrupt mitochondrial function. [7]
  • Nutritional deficiency of thiamine
  • Free radical damage [8]
  • Inflammation
  • Inhibition of calcium-myofilament interaction (negative inotropic effect)

Alcoholic cardiomyopathy occurs in two stages: asymptomatic and symptomatic. People consuming >90 grams of alcohol per day for more than 5 years are at increased risk for developing asymptomatic ACM. Those who continue to drink may become symptomatic and develop signs and symptoms of heart failure. [3]

Genetics

Genetic studies have shown that polymorphisms in angiotensin-converting enzyme gene (DD genotype) and mutations in mitochondrial DNA are associated with increased susceptibility to alcoholic cardiomyopathy. [9]

Conditions associated with Alcoholic Cardiomyopathy

Co-morbidities include:

Cardio-protective effects of Alcohol

A prospective study by Abramson JL et al showed that moderate levels of alcohol consumption are associated with decreased risk of heart failure in the older population[10]. Similar results were shown in other studies like the SAVE trial[11] and the Cardiovascular Health Study[12].

Several mechanisms have been put forward to explain these beneficial effects of alcohol on the heart. These include:

Gronbaek et al., showed in his study that wine reduced the risk of CAD more than beer or spirits[13]. This decreased risk was particularly seen in individuals who consumed less than 22 g/alcohol per day in the form of wine (approximately 2 glasses). The consumption of wine tends to reduce the homocysteine levels. Moreover, wine also contains various polyphenols, especially resveratrol, which are thought to be cardio-protective. These polyphenols are thought to prevent LDL oxidation and thrombosis. Other favorable effects of resveratrol include[14]:

References

  1. Skotzko CE, Vrinceanu A, Krueger L, Freudenberger R (2009). “Alcohol use and congestive heart failure: incidence, importance, and approaches to improved history taking”. Heart Failure Reviews. 14 (1): 51–5. doi:10.1007/s10741-007-9048-8. PMID 18034302. Unknown parameter |month= ignored (help)
  2. Thun MJ, Peto R, Lopez AD; et al. (1997). “Alcohol consumption and mortality among middle-aged and elderly U.S. adults”. The New England Journal of Medicine. 337 (24): 1705–14. doi:10.1056/NEJM199712113372401. PMID 9392695. Unknown parameter |month= ignored (help)
  3. 3.0 3.1 Piano MR (2002). “Alcoholic cardiomyopathy: incidence, clinical characteristics, and pathophysiology”. Chest. 121 (5): 1638–50. PMID 12006456. Unknown parameter |month= ignored (help)
  4. Iacovoni A, De Maria R, Gavazzi A (2010). “Alcoholic cardiomyopathy”. Journal of Cardiovascular Medicine (Hagerstown, Md.). 11 (12): 884–92. doi:10.2459/JCM.0b013e32833833a3. PMID 20308914. Unknown parameter |month= ignored (help)
  5. Jänkälä H, Eklund KK, Kokkonen JO; et al. (2001). “Ethanol infusion increases ANP and p21 gene expression in isolated perfused rat heart”. Biochemical and Biophysical Research Communications. 281 (2): 328–33. doi:10.1006/bbrc.2001.4343. PMID 11181050. Unknown parameter |month= ignored (help)
  6. Fernández-Solà J, Lluis M, Sacanella E, Estruch R, Antúnez E, Urbano-Márquez A (2011). “Increased myostatin activity and decreased myocyte proliferation in chronic alcoholic cardiomyopathy”. Alcoholism, Clinical and Experimental Research. 35 (7): 1220–9. doi:10.1111/j.1530-0277.2011.01456.x. PMID 21463333. Unknown parameter |month= ignored (help)
  7. Waldenström A (1998). “Alcohol and congestive heart failure”. Alcoholism, Clinical and Experimental Research. 22 (7 Suppl): 315S–317S. PMID 9799954. Unknown parameter |month= ignored (help)
  8. Popovici I, Rezuş C, Cosovanu A (2001). “[Enzymatic markers in the alcoholic cardiomyopathy]”. Revista Medico-chirurgicală̆ a Societă̆ţ̜ii De Medici Ş̧i Naturaliş̧ti Din Iaş̧i (in Romanian). 105 (3): 504–8. PMID 12092182.
  9. Fernández-Solà J, Nicolás JM, Oriola J; et al. (2002). “Angiotensin-converting enzyme gene polymorphism is associated with vulnerability to alcoholic cardiomyopathy”. Annals of Internal Medicine. 137 (5 Part 1): 321–6. PMID 12204015. Unknown parameter |month= ignored (help)
  10. Abramson JL, Williams SA, Krumholz HM, Vaccarino V (2001). “Moderate alcohol consumption and risk of heart failure among older persons”. JAMA : the Journal of the American Medical Association. 285 (15): 1971–7. PMID 11308433. Unknown parameter |month= ignored (help)
  11. Aguilar D, Skali H, Moyé LA; et al. (2004). “Alcohol consumption and prognosis in patients with left ventricular systolic dysfunction after a myocardial infarction”. Journal of the American College of Cardiology. 43 (11): 2015–21. doi:10.1016/j.jacc.2004.01.042. PMID 15172406. Unknown parameter |month= ignored (help)
  12. Bryson CL, Mukamal KJ, Mittleman MA; et al. (2006). “The association of alcohol consumption and incident heart failure: the Cardiovascular Health Study”. Journal of the American College of Cardiology. 48 (2): 305–11. doi:10.1016/j.jacc.2006.02.066. PMID 16843180. Unknown parameter |month= ignored (help)
  13. Grønbaek M, Deis A, Sørensen TI, Becker U, Schnohr P, Jensen G (1995). “Mortality associated with moderate intakes of wine, beer, or spirits”. BMJ (Clinical Research Ed.). 310 (6988): 1165–9. PMC 2549555. PMID 7767150. Unknown parameter |month= ignored (help)
  14. Saremi A, Arora R (2008). “The cardiovascular implications of alcohol and red wine”. American Journal of Therapeutics. 15 (3): 265–77. doi:10.1097/MJT.0b013e3180a5e61a. PMID 18496264.

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Differentiating Alcoholic cardiomyopathy from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2]; Hardik Patel, M.D.

Overview

Alcoholic cardiomyopathy is a form of dilated cardiomyopathy (DCM). Therefore, it must be differentiated from other forms of DCM like idiopathic DCM, connective tissue disorders etc.

Differentiating Alcoholic Cardiomyopathy from other Diseases

Alcoholic cardiomyopathy must be differentiated from other causes of dilated cardiomyopathy like:

References

Template:WH Template:WS CME Category::Cardiology

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2]; Hardik Patel, M.D.

Please help WikiDoc by adding more content here. It’s easy! Click here to learn about editing.

Overview

Alcoholic cardiomyopathy is more prevalent in middle aged males between the ages of 35-50. However, females may be more sensitive to cardiotoxic effects of alcohol, and may develop alcoholic cardiomyopathy with lesser amounts of alcohol use, than males.[1][2]

References

  1. Fernández-Solà J, Estruch R, Nicolás JM; et al. (1997). “Comparison of alcoholic cardiomyopathy in women versus men”. The American Journal of Cardiology. 80 (4): 481–5. PMID 9285662. Unknown parameter |month= ignored (help)
  2. Urbano-Márquez A, Estruch R, Fernández-Solá J, Nicolás JM, Paré JC, Rubin E (1995). “The greater risk of alcoholic cardiomyopathy and myopathy in women compared with men”. JAMA : the Journal of the American Medical Association. 274 (2): 149–54. PMID 7596003. Unknown parameter |month= ignored (help)

Template:WH Template:WS CME Category::Cardiology

Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2]; Hardik Patel, M.D.

Overview

In patients who continue to abuse alcohol, 4 year survival rate is 50%. On the contrary, abstinence is associated with regression of symptoms and overall improvement. Improvement in cardiac function evident from echocardiographic findings can also be noted.

Natural History, Complications and Prognosis

Natural History

Natural course of alcoholic cardiomyopathy depends on the ability of the patient to abstain from alcohol after being diagnosed. Many case reports and small studies have shown that abstinence from alcohol lead to marked improvement in the clinical condition of the patient. Similarly, conditions of a few patients worsened with continued alcohol intake.[1][2][3][4] Estruch et al found that a positive correlation exists between alcoholic cardiomyopathy and cirrhosis. The study stated that alcoholics who were hospitalized solely for cardiomyopathy had a higher prevalence of cirrhosis than those without heart disease.[5]

Complications

Common cardiovascular complications of chronic alcohol abuse include:

Prognosis

The prognosis of alcoholic cardiomyopathy is better compared with that of idiopathic dilated cardiomyopathy; approximately 2/3 of the patients are stable. Poor prognostic factors include atrial fibrillation, wide QRS, and lack of beta blocker therapy.[6]

Studies have shown conflicting results regarding the effect of abstinence or reduction in alcohol intake on clinical outcomes in alcoholic cardiomyopathy.[6][7] The four-year survival rate in patients who continue to consume alcohol was reported to be 50%.[7]

References

  1. Guillo P, Mansourati J, Maheu B; et al. (1997). “Long-term prognosis in patients with alcoholic cardiomyopathy and severe heart failure after total abstinence”. The American Journal of Cardiology. 79 (9): 1276–8. PMID 9164905. Unknown parameter |month= ignored (help)
  2. Masani F, Kato H, Sasagawa Y; et al. (1990). “[An echocardiographic study of alcoholic cardiomyopathy after total abstinence]”. Journal of Cardiology (in Japanese). 20 (3): 627–34. PMID 2131353.
  3. Agatston AS, Snow ME, Samet P (1986). “Regression of severe alcoholic cardiomyopathy after abstinence of 10 weeks”. Alcoholism, Clinical and Experimental Research. 10 (4): 386–7. PMID 3530014. Unknown parameter |month= ignored (help)
  4. Mansourati J, Forneiro I, Genet L, Le Pichon J, Blanc JJ (1990). “[Regression of dilated cardiomyopathy in a chronic alcoholic patient after abstinence from alcohol]”. Archives Des Maladies Du Coeur Et Des Vaisseaux (in French). 83 (12): 1849–52, discussion 1853. PMID 2125195. Unknown parameter |month= ignored (help)
  5. Estruch R, Fernández-Solá J, Sacanella E, Paré C, Rubin E, Urbano-Márquez A (1995). “Relationship between cardiomyopathy and liver disease in chronic alcoholism”. Hepatology (Baltimore, Md.). 22 (2): 532–8. PMID 7635421. Unknown parameter |month= ignored (help)
  6. 6.0 6.1 Guzzo-Merello G, Segovia J, Dominguez F, Cobo-Marcos M, Gomez-Bueno M, Avellana P; et al. (2015). “Natural history and prognostic factors in alcoholic cardiomyopathy”. JACC Heart Fail. 3 (1): 78–86. doi:10.1016/j.jchf.2014.07.014. PMID 25458176.
  7. 7.0 7.1 Skotzko CE, Vrinceanu A, Krueger L, Freudenberger R (2009). “Alcohol use and congestive heart failure: incidence, importance, and approaches to improved history taking”. Heart Failure Reviews. 14 (1): 51–5. doi:10.1007/s10741-007-9048-8. PMID 18034302. Unknown parameter |month= ignored (help)

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Diagnosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | Chest X Ray | Echocardiography | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Surgery | Primary Prevention |Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

Case #1

Related Chapters

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