Alcohol-induced cardiomyopathy remains a relevant health problem, for which the mainstay of treatment is alcohol abstinence. In recent years, basic and clinical research has shed light on its pathogenesis, which includes direct toxic effects of alcohol on the myocardium, oxidative stress, mitochondrial dysfunction, and genetic susceptibility. Alcoholic cardiomyopathy (ACM) is considered one of the main causes of left ventricular dysfunction and is the leading cause of nonischemic dilated cardiomyopathy (DCM) in developed Halfway house countries. However, very few studies have investigated the relationship between clinical characteristics and prognosis in ACM.

Incidence & prevalence

A second set of studies that are quoted when addressing this topic are those conducted in individuals who started an alcohol withdrawal program21-24. In these studies, the authors estimated the amount and chronicity of alcohol intake and subsequently related the figures to a number of echocardiographic measurements and parameters. 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. Improvement in left ventricular function has been observed as early as six months after abstinence from alcohol, and complete recovery can be achieved in 18 months (5,6). In an echocardiographic study of 13 patients with alcohol-induced cardiomyopathy, five demonstrated the normalization of left ventricular function after total abstinence for six months (6). Some patients have shown improvement in left ventricular function within six months of stopping alcohol, with full recovery within 18 months.

History and Physical

In one six-patient study (12) focusing on alcoholic cardiomyopathy, the surprising histological findings on endomyocardial biopsy of two patients was found to be myocarditis with lymphocytic infiltration in association with myocyte degeneration or focal necrosis. However, no other biopsy study of patients with presumed alcohol-induced cardiomyopathy has found this. It is likely that those two patients were incorrectly labelled with alcohol-induced cardiomyopathy. Her baseline laboratory evaluation showed pancytopenia, abnormal liver function tests (Table 1) and elevated cardiac enzyme levels (Table 2). The initial chest x-ray revealed a normal cardiothoracic ratio and no evidence of heart failure. Her electrocardiogram showed sinus tachycardia, a nonspecific T-wave abnormality and right axis deviation.

Direct toxic effect of ethanol

Additionally, Standardized disease definitions and classification systems may not align with local disease patterns and healthcare practices. This misalignment can affect the comparability and generalizability of the results. Because it might be difficult to ascertain the actual cause of death, death certificates—despite being essential for public health information—can be incorrectly labeled. Furthermore, what is alcoholic cardiomyopathy the estimates are location- and time-specific, so they might not account for variations among regions or nations or changes over time. Consequently, it’s critical to take these restrictions into account and proceed cautiously when interpreting the study’s findings.

• In the case of patients with any form of cardiomyopathy, this can ultimately lead to heart failure.
• S3 gallop sound along with apical pansystolic murmur due to mitral regurgitation is often heard.
• Acute cases of alcohol-induced cardiomyopathy may be reversible under total abstinence from alcohol, with first signs of improvement within the first month.
• The authors examined the prevalence of cardiomegaly by means of chest x-rays and related it to alcohol consumption among a consecutive series of Japanese males of working age.
• This study included 321 patients with ACM admitted to our hospital between 2003 and 2013.

Alcoholic Cardiomyopathy and Your Health

The sub-group of patients in whom symptoms improved was made up of a larger proportion of non-drinkers (73%), compared to 25% in the group who did not improve, or 17% in the group whose condition worsened. However, a possible confusion factor was identified because the group with clinical improvement also exhibited a shorter evolution of the symptoms and the disease. The first paper to assess the natural history and long-term prognosis of ACM was published by McDonald et al69 in 1971.

Imaging Studies

It also appears that the changes emerging in ACM patients only differ from idiopathic DCM in quantitative terms, with histological changes being more striking in idiopathic DCM than in ACM44. Furthermore, Fernández-Solá et https://ecosoberhouse.com/ al30, when analysing a population of alcoholics, found a higher prevalence of DCM in alcoholics than among the general population. Specifically, among alcoholics they found a prevalence of DCM of 0.43% in women and 0.25% in men, whereas the described prevalence of DCM in the general population is 0.03% to 0.05%18,19. Data on the amount of alcohol consumption required to cause ACM are limited and controversial. In one common form of cardiomyopathy, known as dilated cardiomyopathy, the heart’s chambers are enlarged. These symptoms occur due to fluid overload (swelling, weight gain), a backup of blood in the lungs (shortness of breath) or the body (leg, testicular, or abdominal swelling), or poor output of blood to the rest of the body (fatigue, light-headedness).

Data availability

• 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.
• Lee is an Ohio-based board-certified physician specializing in cardiovascular diseases and internal medicine.
• In the U.S., heart disease is the primary cause of mortality across most genders, races and ethnicities, claiming lives every 33 seconds in the country.
• This eventually limits the heart’s ability to pump oxygen-rich blood around the body.
• Ischemic heart disease (IHD) dominated the burden in almost all countries, consistently ranked as the first or second most significant cardiovascular condition, in line with previous global and regional studies 1, 15, 33.
• Also, there were significant size variations in the myofibrils and they showed a relative decrease in the number of striations, in addition to swelling, vacuolisation and hyalinisation.

The status of all patients was followed up by telephone interview, outpatient clinic attendance, or hospitalization during the follow-up period. This study protocol was approved by the Ethics Commission of Fuwai Hospital. The patient came to the emergency room with a decreased level of consciousness, hallucinations and convulsions after 24 h to 48 h of abstinence from alcohol. Her clinical assessment was consistent with the symptoms of delirium tremens. The primary treatment for ACM is complete abstinence from alcohol, which may require a combination of behavioral therapy and medication.

In some cases, ACM can cause arrhythmias or irregular heartbeats, which can be life-threatening. The age-standardized rate of prevalence, incidence, deaths, DALYs, YLLs, and YLDs were all higher in men compared to women in overall CVD burden which is mostly attributable to the protective effects of sex hormones 28. Men, particularly in countries like Lebanon, Algeria, and Yemen exhibit higher rates of smoking, a top-five risk factor, which might contribute to higher incidences of IHD and stroke in these populations which is consistent with current literature 30, 31.

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. The baseline clinical, ECG, and echocardiographic characteristics of the ACM patients are shown in Table 1.