Alcoholic Cardiomyopathy Kaiser Permanente
Some studies have suggested that a genetic vulnerability exists to the myocardial effects of alcohol consumption. Individuals with certain mitochondrial deoxyribonucleic acid (DNA) mutations and angiotensin-converting enzyme (ACE) genotypes (DD genotype) may be particularly susceptible to the damaging effects of alcohol. Exactly how these genetic variables create this higher risk is not known. Guillo et al in 1997 described the evolution of 9 ACM patients who had been admitted. He divided this cohort into two groups according to the evolution of the ejection fraction during 36 mo in which no deaths were recorded.
Khanna et al. demonstrated that inducible nitric oxide synthase (iNOS) is increased in cardiomyocytes isolated from rats exposed to 1 month of ethanol (13 g/day, Lieber-DeCarli diet) (42). Increased cardiac tissue iNOS levels can lead to the formation of superoxide and peroxynitrite (16). Ethanol-fed animals had reduced systolic contractility and responses to adrenergic stimuli (isoproterenol) compared to control animals (42). Pharmacological inhibition of iNOS with NG –monomethyl-L-arginine reversed this depression in systolic function and adrenergic signaling. Zhang et al. found significant increases in myocardial protein carbonyl and superoxide levels in mice fed an ethanol (4% v/v) diet for 6 weeks (22). These oxidative stress biomarkers corresponded to myocardial fibrosis development and decreases in fractional shortening and cardiac output.
Alcoholic cardiomyopathy: Pathophysiologic insights
Experts do not know what quantity of alcohol a person needs to consume to develop ACM. They also have not identified the minimum length of time someone needs to drink alcohol before developing the condition. The postulated mechanism includes mitochondria damage, oxidative stress injury, apoptosis, modification of actin and myosin structure, and alteration of calcium homeostasis.
- Acute AIC can occur following the consumption of a large volume of alcohol.
- They found that 2 of the 6 individuals (33%) whose alcohol consumption exceeded 125 mL/d had cardiomegaly.
- The diagnosis of ACM is usually one of exclusion in a patient with DCM with no identified cause and a long history of heavy alcohol abuse.
- Kino et al found increased ventricular thickness when consumption exceeded 75 mL/d (60 g) of ethanol, and the increase was higher among those subjects who consumed over 125 mL/d (100 g), without specifying the duration of consumption.
- Recently, Hu et al. found decreased myocardial ATP content levels along with decreased myocardial contractility (e.g., decreased ejection fraction and factional shortening) in mice receiving ethanol (18% v/v ethanol in drinking water) for 4 weeks (33).
At that time every 10th necropsy in men at the Munich pathology institute named cardiac dilatation and fatty degeneration as “Bierherz” being its underlying cause. For comparison, the mean annual beer consumption in Bavaria is nowadays estimated to be 145 l and in the rest of Germany around 100 l beer per person and year . The most common inherited cardiomyopathy, alcoholic cardiomyopathy hypertrophic, affects about 1 in 500 people in the world. Anyone with concerns about alcohol consumption or heart health needs to consult a doctor for further advice and guidance. Alcoholic cardiomyopathy affects the heart’s ability to pump oxygen-rich blood around the body. This can cause various symptoms, including shortness of breath, fluid retention, and fainting.
Daily consumption of low to moderate amounts of alcohol has beneficial effects on cardiovascular health among both ischemic and non-ischemic patients[1-3]. In contrast, chronic and excessive alcohol consumption could lead to progressive cardiac dysfunction and heart failure (HF). Also, low to moderate daily alcohol intake was proved to be a predictor of better prognosis for both ischemic cardiomyopathy and heart failure regardless of the presence of coronary disease[1,2]. Experimental studies analysing the depressive properties of alcohol on the cardiac muscle invariably use similar approaches[31-39]. Accordingly, a given amount of alcohol is administered to volunteers or alcoholics, followed by the measurement of a number of haemodynamic parameters and, in some cases, echocardiographic parameters. Generally, following alcohol intake, healthy, non-drinking individuals showed an increase in cardiac output due to a decline in peripheral arterial resistance and an increase in cardiac frequency.
Although all of the studies reported an increase in left ventricular mass and volume, it cannot generally be stated that they provided the alcohol consumption dosage required to cause ACM. In 1887, Maguire reported on 2 patients with severe alcohol consumption who benefitted from abstinence. In 1890, Strümpell listed alcoholism as a cause of cardiac dilatation and hypertrophy, as did Sir William Osler in 1892 in his textbook Principles and Practices of Medicine. In 1893, Graham Steell, well known for the Graham Steell murmur due to pulmonary regurgitation in pulmonary hypertension or in mitral stenosis, reported 25 cases in whom he recognized alcoholism as one of the causes of muscle failure of the heart. In his 1906 textbook The Study of the Pulse, William MacKenzie described cases of heart failure attributed to alcohol and first used the term “alcoholic heart disease” . Alcoholic cardiomyopathy (ACM) is a type of heart disease that can result from chronic alcohol consumption.