Alcoholic cardiomyopathy pathophysiology: Difference between revisions
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* Fatty acid ester accumulation | * Fatty acid ester accumulation | ||
* Nutritional deficiency of [[thiamine]] | * Nutritional deficiency of [[thiamine]] | ||
* Free radical damage | * Free radical damage <ref name="pmid12092182">{{cite journal |author=Popovici I, Rezuş C, Cosovanu A |title=[Enzymatic markers in the alcoholic cardiomyopathy] |language=Romanian |journal=[[Revista Medico-chirurgicală̆ a Societă̆ţ̜ii De Medici Ş̧i Naturaliş̧ti Din Iaş̧i]] |volume=105 |issue=3 |pages=504–8 |year=2001 |pmid=12092182 |doi= |url=}}</ref> | ||
* [[Inflammation]] | * [[Inflammation]] | ||
* Inhibition of calcium-myofilament interaction | * Inhibition of calcium-myofilament interaction | ||
Revision as of 21:00, 21 June 2013
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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.
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. 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. [1]
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.[2].
Proposed mechanisms of myocardial injury in alcoholic cardiomyopathy include:[3]
- Ethanol induced apoptosis
- Impaired contraction of myocardium due to direct toxicity
- Inhibition of protein synthesis and decreased myocyte proliferation [4]
- Activation of renin-angiotensin system (RAS)
- Inhibition of oxidative phosphorylation
- Fatty acid ester accumulation
- Nutritional deficiency of thiamine
- Free radical damage [5]
- Inflammation
- Inhibition of calcium-myofilament interaction
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. [2]
References
- ↑ 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) - ↑ 2.0 2.1 Piano MR (2002). "Alcoholic cardiomyopathy: incidence, clinical characteristics, and pathophysiology". Chest. 121 (5): 1638–50. PMID 12006456. Unknown parameter
|month=ignored (help) - ↑ 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) - ↑ 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) - ↑ 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.