Alcoholic Cardiomyopathy an overview

Ethanol may produce the modification of sarcolemmal membrane L-type Ca2+ channels, leading to a decrease in transmembrane electrically induced Ca2+ transients [85,103,127]. One of the most relevant targets of ethanol in the membrane alcoholic cardiomyopathy is the disruption of membrane receptor composition and activities [86]. The ryanodine L-type Ca2+ receptor at the sarcoplasmic reticulum (SR) is also significantly affected by ethanol in a dose-dependent manner [86,102].

In these studies, haemodynamic and echocardiographic parameters were measured in individuals starting an alcohol withdrawal program. The findings were analysed taking into account the amount and chronicity of intake and they were compared with the same parameters measured in a control group of non-drinkers. The first study, which specifically focused on the amount of alcohol necessary to cause ACM, was conducted by Koide et al[20] in 1975. 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. They found that 2 of the 6 individuals (33%) whose alcohol consumption exceeded 125 mL/d had cardiomegaly. In contrast, an enlarged heart was found in only 1 of 25 subjects with moderate consumption (4%), in 6 of 105 very mild consumers (5.7%), and in 4.5% of non-drinking individuals.

1 Study limitations

In long-term follow-up studies, a mortality rate of 10% of patients/year has been observed in the group of patients with persistent high-dose ethanol consumption [19,52]. It is equally important for the doctor to rule out other potential causes for cardiology issues, such as coronary artery disease, high levels of angiotensin,
Untreated cardiomyopathy can lead to a number of additional health issues, including congestive heart failure. Other types of cardiomyopathy, such as dilated cardiomyopathy (DCM), may not be caused by alcohol abuse, but by genetics or other factors. While dilated cardiomyopathy is not preventable, alcoholic cardiomyopathy is a preventable condition.

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 [112]. They try to control myocardial remodeling to avoid the progression of myocyte hypertrophy [39,148] or fibrosis [149] and ventricle dysfunction and dilatation, as well as to increase the degree of myocyte regeneration [150].

Hypertrophic cardiomyopathy

The major risk factor for developing ACM is chronic alcohol use; however, there is no cutoff value for the amount of alcohol consumption that would lead to the development of ACM. 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). This activity examines when this condition should be considered on differential diagnosis. This activity highlights the role of the interprofessional team in caring for patients with this condition.

In particular, mitochondrial DNA is highly susceptible to oxidative stress because of the close proximity to ROS generation and lack of protective histones and DNA repair mechanisms compared to nuclear DNA (55). The baseline clinical, ECG, and echocardiographic characteristics of the ACM patients are shown in Table 1. Among the ACM patients, no differences between the patients in the death and survival groups were observed at baseline with respect to age, disease duration, smoking status, presence of syncope, heart rate, gender, and blood test results. The frequencies of a high New York Heart Association (NYHA; class III/IV) classification, atrial fibrillation (AF) and atrioventricular block were higher in the death group than those in the survival group.

Arrhythmias and Sudden Cardiac Death

Among the many ethanol and heart studies, mitochondrial dysfunction or evidence of impaired bioenergetics has been a common finding. This is exemplified by either a change in mitochondrial ultrastructure and/or depressed indices of bioenergetics and oxidative phosphorylation. This is not surprising because mitochondria are a major target for free-radical injury; however, dysfunctional mitochondria are not only less bioenenergetically efficient, they can also generate increased amounts of ROS and are more likely to initiated apoptosis (55). As reviewed below, it is possible that mitochondria serve as a site for ethanol-induced ROS generation, but also may be a target of ethanol-induced ROS injury.

• Ballester specifically analysed the effects of alcohol withdrawal on the myocardium using antimyosin antibodies labelled with Indium-111[72].
• Echocardiography may reveal a mild or severe depression of cardiac function and ejection fraction or even show hypertrophy in the beginning [109].
• Transplant-free survival after 7 years was worse among patients with ACM than among those with DCM (41% vs 53%).
• We review the current thinking on the pathophysiology, clinical characteristics, and treatments available for alcoholic cardiomyopathy.
• Alcohol can also worsen hyperlipidemia, primarily by elevating the triglyceride levels, although it can also increase both the total cholesterol and low-density lipoprotein concentration [35].