Natural history and prognostic factors in alcoholic cardiomyopathy

It is therefore possible that most of these studies may have also consistently omitted most alcohol abusers in whom alcohol had already caused significant ventricular dysfunction. 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. Myocardial impairment following chronic excessive alcohol intake has been evaluated using echocardiographic and haemodynamic measurements in a significant number of reports. In these studies, haemodynamic and echocardiographic parameters were measured in individuals starting an alcohol withdrawal program.

How might this impact on clinical practice?

Kino et al22 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. In another study on this topic, Lazarević et al23 divided a cohort of 89 asymptomatic individuals whose consumption exceeded 80 g/d (8 standard units) into 3 groups according to the duration of their alcohol abuse. Subjects with a shorter period of alcohol abuse, from 5 to 10 years, had a significant increase in left ventricular diameter and volume compared to the control group. 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).

Natural history and prognostic factors in alcoholic cardiomyopathy

• Myocardial impairment following chronic excessive alcohol intake has been evaluated using echocardiographic and haemodynamic measurements in a significant number of reports.
• 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.
• This activity describes the pathophysiology of ACM, its causes, presentation and the role of the interprofessional team in its management.ACM is characterized by increased left ventricular mass, dilatation of the left ventricle, and heart failure (both systolic and diastolic).
• Since those initial descriptions, reports on several isolated cases or in small series of patients with HF due to DCM and high alcohol intake have been published15-17.
• In this review, we evaluate the available evidence linking alcohol consumption with HF and DCM.

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. The postulated mechanism includes mitochondria https://ecosoberhouse.com/ 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.

Associated Data

These changes are related to both direct alcohol toxicity on cardiac cells and the indirect toxicity of major alcohol metabolites such as acetaldehyde. Regarding ICD and CRT implantation, the same criteria as in DCM are used in ACM, although it is known that excessive alcohol intake is specifically linked to ventricular arrhythmia and sudden cardiac death71. As it is not uncommon in ACM for patients to experience a significant recovery of systolic function, it is particularly challenging in this disease to decide the most appropriate time to implant an ICD and whether it is necessary to replace a previously implanted device. Future studies in ACM should also address this topic, which has important economic consequences. Pharmacologic therapy should include goal-directed heart failure therapy as used in idiopathic dilated cardiomyopathy with reduced ejection fraction.

Statistical analysis

Another nutritional factor classically involved in the pathophysiology of AC was cobalt excess. The ‘Quebec beer drinkers’ cardiomyopathy’ was related to cobalt supplementation to beer that was made in the past. It was described as a form of DCM with severe pericardial effusion, low cardiac output, and purplish skin coloration. On comparing tribal with non-tribal population, no differences were observed at baseline in terms of age and sex. The frequencies of chest pain, basal crepts, orthopnoea, PND, JVP, oedema, NYHA (class III/IV) classification, CTP (Score B, C), AF and AVB were higher in tribal population but sinus rhythm was more in non-tribal population.

• Moreover, myofibrils showed a progressively distorted structure, resulting in a homogeneous mass.
• A comprehensive upbringing of tribals in the social, economic and educational aspects would show direct implications in the primary prevention of problems related to alcohol.
• In the interim it seems appropriate to continue discouraging any alcohol consumption in these patients, as it would be difficult for them to maintain a limited alcohol intake considering their history of alcohol dependence and abuse.
• Although analytical markers of alcohol consumption, such as average erythrocyte volume and serum gamma-glutamyltranspeptidase levels, could be an aid to establish abstinence or persistence of alcohol intake in patients, the quantity of alcohol intake is dependent on the patients’ report.
• Another nutritional factor classically involved in the pathophysiology of AC was cobalt excess.
• 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.

Thus, Nicolás et al73 studied the evolution of the ejection fraction in 55 patients with ACM alcoholic cardiomyopathy is especially dangerous because 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%).

• The population was divided into 3 groups according to their intake volume during the follow-up period.
• To date, none of the ACM studies have proposed a treatment for ACM other than that recommended for DCM in current HF guidelines.
• The postulated mechanism includes mitochondria damage, oxidative stress injury, apoptosis, modification of actin and myosin structure, and alteration of calcium homeostasis.
• Alcoholic cardiomyopathy is a leading cause of non-ischemic dilated cardiomyopathy in United States.
• They found that 2 of the 6 individuals (33%) whose alcohol consumption exceeded 125 mL/d had cardiomegaly.
• According to most studies, the alcohol consumption required to establish a diagnosis of ACM is over 80 g per day during at least 5 years9-12.

Although some authors contend that the initial event is the appearance of hypertrophy, the majority accept that the core event is the loss of cardiomyocytes. Indeed, the first account of the possible harmful effects of alcohol specifically on heart muscle was reported in the latter half of the 19th century. Expressions referring to “the heart of a wine drinker in Tubingen” and particularly a “Munich beer heart” were used and known in Germany during this time13. In Substance abuse this review, we evaluate the available evidence linking alcohol consumption with HF and DCM. These include damaging factors such as acetaldehyde or ROS, cardiac fibrosis, or apoptosis.