One of the dangers of cardiomyopathy is that people may not always experience symptoms of their condition until it has advanced to a severe state. The definition of heavy drinking is drinking more than 15 drinks per week in men or drinking more than eight drinks per week for women. Untreated ACM can become severe and have life-threatening consequences, causing irregular heartbeats and congestive heart failure. Moreover, ranolazine prevents ethanol-induced atrial arrhythmias both in vitro and in vivo by blocking the late sodium current, which is activated by CaMKII.112 Its effect on preventing the decrease of LVEF in AC is currently unknown.
- Chronic liver disease, often caused by long-term alcohol abuse, is another risk factor.
- In severe cases, arrhythmias can increase the risk of stroke or sudden cardiac arrest.
- If symptoms of heart problems (including ACM) do occur, it is essential to talk to your doctor or get help right away.
- Cardiomyopathy that has developed as a result of chronic alcohol use is known as alcoholic cardiomyopathy (ACM).
Alcoholic cardiomyopathy: Cytotoxicity of alcohol on heart muscle
As the heart’s function declines, patients may also experience shortness alcoholic cardiomyopathy is especially dangerous because of breath at rest. Chronic liver disease, often caused by long-term alcohol abuse, is another risk factor. The liver plays a crucial role in metabolizing alcohol, and when damaged, the body is less able to process alcohol, leading to higher toxin levels that can affect the heart. Additionally, people with diabetes or obesity are at increased risk for heart problems, including alcoholic cardiomyopathy. Alcoholic cardiomyopathy is a type of heart disease caused by excessive alcohol consumption.
Echocardiographic and haemodynamic studies in alcoholics
- Absorption levels of Indium-111 were high in 75% of patients who continued drinking and in only 32% of those who had withdrawn from consuming alcohol.
- A persistent cough is present in about 20-30% of patients with alcoholic cardiomyopathy.
- In a subsequent study using electron microscopy, the authors found histological features that could be superimposed onto those found in hearts that had suffered hypoxia, anoxia or ischemia43.
- In patients exhibiting chronic alcohol use, other causes of dilated cardiomyopathy need workup.
This activity highlights the role of the interprofessional team in caring for patients with this condition. In ACM, it is relevant to consider the treatment of the other alcohol-induced systemic damage, such as liver cirrhosis, malnutrition, and vitamin and electrolyte disturbances 2,11,52. Notably, in patients with a history of chronic alcohol drug addiction treatment consumption complicated by significant myocardial dysfunction and chronic malnutrition, re-feeding syndrome may increase the cardiac dysfunction. Therefore, physicians should be aware of the risk of new cardiomyopathy in patients with these overlapping diagnoses 144. Control of these alcohol-related systemic diseases, as well as the strict control of the presence of other heart risk factors (tobacco, cocaine, arterial hypertension, diabetes mellitus, or anemia) contributes to ACM improvement 10,20,23,37,52.
AMOUNT OF ALCOHOL REQUIRED TO PRODUCE ACM
Myocyte cytoskeletal structure 21, connexin channel communication, and desmosomal contacts are affected by ethanol, causing structural cell instability 105. Ethanol may induce changes in nuclear regulation of transcription with a dose-dependent translocation of NFkB into the nucleus 106. The resulting effect in those multiple sites may be additive and synergistic, increasing the final damage 20,52 (Figure 1).
- Despite the key clinical importance of alcohol as a cause of DCM, relatively few studies have investigated the effects of alcohol on the heart and the clinical characteristics of DCM caused by excessive alcohol consumption (known as alcoholic cardiomyopathy).
- This was an excellent result long before ACE inhibitors or betablockers were available for heart failure treatment 57.
- 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.
1. Oxidative and Energy Disturbances in ACM
Thus, Nicolás et al73 studied the evolution of the ejection fraction in 55 patients with ACM according to their degree of withdrawal. The population was divided into 3 groups according to their intake volume during the follow-up period. At the end of the first year, no differences were found among the non-drinkers, who improved by 13.1%, and among those who reduced consumption to g/d (with an average improvement of 12.2%).
However, a possible confusion factor was identified because the group with clinical improvement also exhibited a shorter evolution of the symptoms and the disease. 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. Finally, it is worth stressing that a large majority of studies on the physiopathology and prognosis of ACM were conducted some years ago, prior to the development of our current understanding regarding the role of genetics in DCM67. According to recent data, a genetic form of DCM could be present in up to 50% of idiopathic DCM cases, and other specific forms of DCM such as peripartum cardiomyopathy have been shown to have a genetic basis in a significant number of cases68. It is therefore possible that patients with ACM could also harbour a genetic substrate that predisposes them to this form of cardiomyopathy. The suspicion that there may be an individual susceptibility to this disease is underscored by the finding that only a small group of alcoholics develop ACM, and that a proportional relationship between myocardial damage and alcohol intake has not been proven.
3. Ethanol-induced Heart Fibrosis
However, due to the absence of any symptoms, people may also simply be unaware of how their drinking could be impacting their heart. New therapeutic strategies for AC are being developed https://ecosoberhouse.com/ with the support of animal models. As the pathogenesis of AC is complex, specific treatments focus on different targets. These include damaging factors such as acetaldehyde or ROS, cardiac fibrosis, or apoptosis. Another nutritional factor classically involved in the pathophysiology of AC was cobalt excess.
Binge drinking, which involves consuming large amounts of alcohol in a short period, can also contribute to heart damage. The majority of the echocardiographic studies performed on asymptomatic alcoholics found only mild changes in their hearts with no clear impairment of the systolic function. For example, a slight increase in the pre-ejection period/left ventricular ejection time ratio (PEP/LVET) was found by some authors, suggesting a sub-clinical impairment of systolic function21,33.
