Some of these papers have also described the recovery of LVEF in many subjects after a period of alcohol withdrawal15-17. Some of the potential cellular changes related to ethanol consumption reviewed above are illustrated in figure 5. More than one cellular event may be happening at the same time, and, as with other chronic health conditions, the relevant mechanisms may be synergistic symptoms of alcoholic cardiomyopathy and interrelated. New therapeutic strategies for AC are being developed with the support of animal models. As the pathogenesis of AC is complex, specific treatments focus on different targets.

Alcoholic cardiomyopathy: Cytotoxicity of alcohol on heart muscle

• We reviewed the effects of ethanol on the cardiovascular system in 1996 15, including aspects of inflammation 16, rhythm disturbances 17, and hypertension 18.
• Other researchers have used genetic approaches (i.e., transgenic animals) to prevent ethanol-induced oxidative stress.
• To date, none of the ACM studies have proposed a treatment for ACM other than that recommended for DCM in current HF guidelines.
• NIAAA defines binge drinking as a pattern of drinking alcohol that brings the blood alcohol concentration to 0.08 percent or above.
• In addition, ethanol induces mitochondrial-dependent apoptosis pathways with Bax and caspase activation 101.
• 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.
• One relevant question concerning ethanol cardiac toxicity is if ethanol itself or its active metabolite acetaldehyde causes cardiac damage 73,74.

Experts do not know what quantity of alcohol a person needs to consume to develop ACM. They also have not identified the minimum length of time someone needs to drink alcohol before developing the condition. Alcoholic cardiomyopathy (ACM) is a heart disease that occurs due to chronic alcohol consumption. It is a type of dilated cardiomyopathy since it involves dilation or enlargement of one of the heart’s chambers.

• The prevalance of alcoholic cardiomyopathy in addiction units is estimated around %.
• Ethyl alcohol, also known as “ethanol” or usually just as “alcohol”, is the most consumed drug in human history 1.
• List of the 15 articles reviewed in this study, indicating the study authors, objectives, design, sample size, patient characteristics, experimental procedures, outcome measures, and main findings.
• More contemporary studies have not found evidence of mitochondrial injury in biopsy samples from long-term alcohol drinkers (Miró et al. 2000).
• Alternatively, studies have analysed its effect by combining ethanol with cyanamide.

Broken heart syndrome

• For instance, a single drink of beer is typically considered as a 12-ounce (355 ml) serving of regular beer, usually containing around 5% alcohol by volume (ABV).
• Alcohol in excessive quantities has a directly toxic effect on heart muscle cells.
• Alcohol-induced cardiomyopathy remains a relevant health problem, for which the mainstay of treatment is alcohol abstinence.
• In 1893, Graham Steell, well known for the Graham Steell murmur due to pulmonary regurgitation in pulmonary hypertension or in mitral stenosis, reported 25 cases in whom he recognized alcoholism as one of the causes of muscle failure of the heart.

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. The diagnosis of ACM is usually one of exclusion in a patient with DCM with no identified cause and a long history of heavy alcohol abuse. 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. Greenfield and colleagues (2005) studied the effects of alcohol at meal time in a group of nonsmoking, healthy postmenopausal women.

Cardiac Effects of Alcohol

Third and fourth heart sounds can be heard, and they signify systolic and diastolic dysfunction. Pulmonary rales signify pulmonary congestion secondary to elevated left atrial and left ventricular end-diastolic pressures. Jugular venous distention, peripheral edema, and hepatomegaly are evidence of elevated right heart pressures and right ventricular dysfunction.

Accelerated Protein Degradation

Data from animal models and human beings with a history of long-term drinking suggest that oxidative stress may be an early and initiating mechanism. Many cellular events, such as intrinsic myocyte dysfunction, characterized by changes in calcium homeostasis and regulation and decreased myofilament sensitivity, can come about due to oxidative stress. Despite the progress in standardizing measurement of alcohol, studies still vary in how they define the different levels of drinking, such as low-risk or moderate and heavy drinking.