Differential associations of CV risk with certain beverage types such as wine instead have been attributable to other lifestyle factors (e.g., increased physical activity) or drinking with meals (Malarcher et al. 2001). Results from another meta-analysis of 12 cohort studies found a similar dose–response relationship between alcohol consumption and HTN for males. A J-shaped relationship for females showed protective effects at or below consumption levels of 15 g/day (Taylor et al. 2009). These data highlight how gender may be an important modifier of the alcohol threshold level and can shape the alcohol benefit–risk relationship. Another trend in recent studies of alcohol and CV risk and disease is to include a measurement for binge drinking. In most investigations, this means consuming more than 5 standard drinks on a single occasion for men and more than 4 standard drinks for women.
Another curious hypothesis from Germany suspected that some ethanol additives, such as anti-foam beer products with arsenic or cobalt content, produced cardiac toxicity and development of ACM . Therefore, it is evident that ACM may develop with normal serum thiamine and electrolyte levels [38,66]. Consumption of other drugs such as cocaine or tobacco may interact with ethanol and potentiate the final ethanol-related cardiac damage [22,72]. One of the characteristics that makes ethanol harmful is its systemic toxic effect on the human body [10,11].
Pathological Aspects of ACM
In humans, endothelial function is assessed by measuring the widening (i.e., dilation) of the brachial artery under different conditions. Some research noted that endothelial function is impaired in abstinent individuals with a long-term history of alcohol abuse or alcoholism(Di Gennaro et al. 2007, 2012; Maiorano et al. 1999). Other studies have examined the effect of a single binge-drinking episode and found impairment in brachial artery endothelial-dependent and -independent vasodilation (Bau et al. 2005; Hashimoto et al. 2001; Hijmering et al. 2007). Therefore, as in animal studies, the effects of ethanol on endothelial function in humans likely depend on the dose and duration of ethanol consumption.
- These investigators also found decreases in peroxiredoxin 5, antioxidant protein 2, and glutathione transferase 5, important anti-oxidant enzymes.
- Various pathophysiological mechanisms have been postulated in the development of cardiomyopathy however one key factor undergoing active research is the role of genetic mutation and susceptibility to develop cardiomyopathy.
- At present ACM is considered a specific disease both by the European Society of Cardiology (ESC) and by the American Heart Association (AHA)[18,19].
- Therefore, complete abstinence from ethanol is the most useful measure to control the natural course of ACM [51,56,135].
Even in cases where people can undergo a heart transplant, individuals with a history of alcohol-induced cardiomyopathy are more likely to face other health problems down the road. Completely abstaining from alcohol is the key recommendation if you have alcohol-induced cardiomyopathy. Your healthcare provider will likely recommend that you also focus on improving your diet in ways that help your heart. This usually involves limiting your sodium (salt) and cholesterol intake and ensuring you are getting a diet that provides all essential nutrients. That’s because vitamin and mineral deficiencies are more common in individuals who are chronic heavy drinkers. Most common age population for ACM is males from age with significant history of alcohol use for more than 10 years.
Alcoholism—use and abuse
If you are a heavy drinker, talking to a primary care provider can help keep this condition from becoming even more severe in the future, or even prevent it from happening. Your provider is the best source of information and guidance, and they can connect you to other resources that can help and experts who can assist. Many medications can help in cases of alcohol-induced cardiomyopathy, treating the symptoms that happen because of this condition. Medications typically include beta-blockers (for heart rhythm and blood pressure issues) and diuretics (to help your body get rid of excess fluid and swelling). Alcohol has toxic effects, but your body can limit the damage and break alcohol down into non-toxic forms if you don’t drink too much too quickly.
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). The postulated mechanism includes mitochondria damage, oxidative stress injury, apoptosis, modification of actin and myosin structure, and alteration of calcium homeostasis. Studies have shown an increase in reactive oxygen species (ROS) level in myocytes following alcohol consumption and thus causes oxidation of lipids, proteins, and DNA leading to cardiac dysfunction. These changes are related to both direct alcohol toxicity on cardiac cells and the indirect toxicity of major alcohol metabolites such as acetaldehyde.
NATURAL HISTORY OF ALCOHOLIC CARDIOMYOPATHY
In addition, people who receive early treatment for ACM, including medication and lifestyle modifications, have a better chance of improving their heart function and overall health. Abnormal heart sounds, murmurs, ECG abnormalities, and enlarged heart on chest x-ray may lead to the diagnosis. Alcoholic cardiomyopathy (ACM) is a disease in which the long-term consumption of alcohol leads to heart failure. ACM is a type of dilated cardiomyopathy. Some of the potential cellular changes related to ethanol consumption reviewed above are illustrated in figure 5.
However, consistent heavy drinking strains those protective processes — especially in your liver — making them less effective. Ultimately, your body can’t keep up with the damage to multiple organ systems, including your heart. Even if cardiomyopathy isn’t part of your family history, it’s still important to take steps to make https://ecosoberhouse.com/article/alcoholics-heart-problems-cardiomyopathy/ sure you don’t develop a heart condition or disease that could put you at an increased risk of cardiomyopathy. There are many different types of cardiomyopathy, caused by a range of factors, from coronary heart disease to certain drugs. Cardiomyopathy can lead to an irregular heartbeat, heart failure, or other complications.
Quantity of Alcohol Intake in Cardiac Disease
Data derived from systematic reviews and meta-analyses suggest that alcohol-dose and CV-health relationships differ for various CV conditions. For example, certain levels of alcohol consumption that lower risk for CHD may increase it for other CV conditions, such as stroke. In addition, data from studies using new research methods, including Mendelian randomization, suggest that the relationship between low-to-moderate alcohol consumption and cardioprotection merits more critical appraisal (Holmes et al. 2014). In fact, Rehm has argued that methodological issues render the utility of cohort studies assessing the relationship between alcohol use and all‐cause mortality as ‘almost meaningless’ 10. New strategies to improve the natural course of ACM have been proposed as promising agents in this field [112,147]. Since ethanol has multiple cell targets with different pathological mechanisms implicated, those different strategies to directly target alcohol-induced heart damage are only partially effective and can only be used as support medication in a multidisciplinary approach .
- These data suggest that antioxidant defense mechanisms that attempt to protect the heart against oxidative damage appear to be initiated soon after drinking alcohol.
- Pharmacological restoration of autophagic reflux by inhibition of soluble epoxide hydrolase has been described to ameliorate chronic ethanol-induced cardiac fibrosis in an in vivo swine model .
- In the 1950s, evidence began to emerge that supported the idea of a direct toxic myocardial effect of alcohol, and research during the last 35 years has been particularly productive in characterizing the disease entity of alcoholic cardiomyopathy (AC).
- Polyphenols of red barrique wines and flavonoids have been shown to inhibit endothelin-1 synthase  and PDGF-induced vasoproliferation thus also contributing to cardiovascular protection .
The relationship of alcohol with heart disease or dementia is complicated by the fact that moderate alcohol consumption was shown not only to be detrimental but to a certain degree also protective against cardiovascular disease  or to cognitive function in predementia. Diastolic dysfunction is the earliest sign of ACM and is usually seen in approximately 30% of patients with a history of chronic alcohol abuse with no evidence of systolic dysfunction nor left ventricle hypertrophy. Alcoholic cardiomyopathy can present with signs and symptoms of congestive heart failure. Symptoms include gradual onset worsening shortness of breath, orthopnea/paroxysmal nocturnal dyspnea. Palpitations and syncopal episodes can occur due to tachyarrhythmias seen in alcoholic cardiomyopathy. Doctors have known for a long time that abusing alcohol for a long period of time can weaken and thin the heart muscles, which can impact the heart’s ability to pump blood.
The sooner you can get treatment for this condition, the lower your risk of heart damage and loss of function. In the course of ethanol-induced cardiac damage, one of the more relevant findings is that ethanol exerts its deleterious effects on cardiac myocytes at multiples sites (membrane, receptors, mitochondria, ribosomes, sarcolemma, DNA, or cytoskeleton) [18,19,98] (Table 1). Investigating the mechanisms, consequences, and potential treatment options for ACM remains a very important https://ecosoberhouse.com/ area of research. In this section, we briefly discuss the patterns of drinking, specifically binge, as well as genetic variants in certain proteins/enzymes and variability in nutrition or dietary nutrients that may influence the occurrence of ACM. For tens of years, the literature has documented many clinical cases or small series of patients who have undergone a full recovery of ejection fraction and a good clinical evolution after a period of complete alcoholic abstinence.