Alcoholic cardiomyopathy pathophysiology
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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.
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:
- ↑ HDL levels
- ↓ Plasma viscosity and fibrinogen concentration
- ↑ Fibrinolysis
- ↓ Platelet aggregation
- Improvement in endothelial function
- ↓ Inflammation
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]:
- ↓ Arterial damage
- ↓ Angiotensin II
- ↓ Platelet aggregation
- ↑ Nitric oxide
References
- ↑ 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) - ↑ 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) - ↑ 3.0 3.1 Piano MR (2002). "Alcoholic cardiomyopathy: incidence, clinical characteristics, and pathophysiology". Chest. 121 (5): 1638–50. PMID 12006456. Unknown parameter
|month=ignored (help) - ↑ 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) - ↑ 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) - ↑ 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) - ↑ 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) - ↑ 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.
- ↑ 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) - ↑ 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) - ↑ 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) - ↑ 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) - ↑ 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) - ↑ 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.