Alcoholic cardiomyopathy pathophysiology: Difference between revisions
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Proposed mechanisms of myocardial injury in alcoholic cardiomyopathy include:<ref name="pmid20308914">{{cite journal |author=Iacovoni A, De Maria R, Gavazzi A |title=Alcoholic cardiomyopathy |journal=[[Journal of Cardiovascular Medicine (Hagerstown, Md.)]] |volume=11 |issue=12 |pages=884–92 |year=2010 |month=December |pmid=20308914 |doi=10.2459/JCM.0b013e32833833a3 |url=}}</ref> | Proposed mechanisms of myocardial injury in alcoholic cardiomyopathy include:<ref name="pmid20308914">{{cite journal |author=Iacovoni A, De Maria R, Gavazzi A |title=Alcoholic cardiomyopathy |journal=[[Journal of Cardiovascular Medicine (Hagerstown, Md.)]] |volume=11 |issue=12 |pages=884–92 |year=2010 |month=December |pmid=20308914 |doi=10.2459/JCM.0b013e32833833a3 |url=}}</ref> | ||
* Ethanol induced [[apoptosis]]: Possible mechanisms include increased protein levels of pro-apoptotic protein Bax, increased caspase-3 enzymae activity, increased messenger RNA p21 (p21 inhibits cyclin-dependent kinases). | * Ethanol induced [[apoptosis]]: Possible mechanisms by which ethanol promotes apoptosis include increased protein levels of pro-apoptotic protein Bax, increased caspase-3 enzymae activity, increased messenger RNA p21 (p21 inhibits cyclin-dependent kinases). | ||
* Impaired contraction of [[myocardium]] due to direct toxicity | * Impaired contraction of [[myocardium]] due to direct toxicity | ||
* Inhibition of protein synthesis and decreased myocyte proliferation <ref name="pmid21463333">{{cite journal |author=Fernández-Solà J, Lluis M, Sacanella E, Estruch R, Antúnez E, Urbano-Márquez A |title=Increased myostatin activity and decreased myocyte proliferation in chronic alcoholic cardiomyopathy |journal=[[Alcoholism, Clinical and Experimental Research]] |volume=35 |issue=7 |pages=1220–9 |year=2011 |month=July |pmid=21463333 |doi=10.1111/j.1530-0277.2011.01456.x |url=}}</ref> | * Inhibition of protein synthesis and decreased myocyte proliferation <ref name="pmid21463333">{{cite journal |author=Fernández-Solà J, Lluis M, Sacanella E, Estruch R, Antúnez E, Urbano-Márquez A |title=Increased myostatin activity and decreased myocyte proliferation in chronic alcoholic cardiomyopathy |journal=[[Alcoholism, Clinical and Experimental Research]] |volume=35 |issue=7 |pages=1220–9 |year=2011 |month=July |pmid=21463333 |doi=10.1111/j.1530-0277.2011.01456.x |url=}}</ref> | ||
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Alcoholic cardiomyopathy Microchapters |
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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: Possible mechanisms by which ethanol promotes apoptosis include increased protein levels of pro-apoptotic protein Bax, increased caspase-3 enzymae activity, increased messenger RNA p21 (p21 inhibits cyclin-dependent kinases).
- 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: 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.
- 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.