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Alcoholic cardiomyopathy

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From Wikipedia, the free encyclopedia

Alcoholic cardiomyopathy
Specialty	Cardiology

Alcoholic cardiomyopathy is a disease in which the chronic long-term abuse of alcohol (i.e., ethanol) leads to heart failure. Alcoholic cardiomyopathy is a type of dilated cardiomyopathy. Due to the direct toxic effects of alcohol on heart muscle, the heart is unable to pump blood efficiently, leading to heart failure. It can affect other parts of the body if the heart failure is severe. It is most common in males between the ages of 35 and 50.

Etiology[edit]

Till today, it's still heavily debated on whether alcohol use is directly correlated with inducing cardiomyopathy. Per the American Heart Association (AHA), alcohol is one of the leading causes of dilated cardiomyopathy. However, multiple longitudinal studies have shown a paradoxical lowering of dilated cardiomyopathy with modest-to-moderate alcohol consumption.

Alcoholic cardiomyopathy (ACM) is a type of heart disease that occurs due to chronic alcohol consumption. The etiology of ACM is multifactorial, with a combination of genetic, environmental, and lifestyle factors playing a role. The direct toxic effects of alcohol on the heart muscle cells (cardiomyocytes) are considered the primary cause of ACM. Chronic alcohol consumption leads to the accumulation of toxic metabolites, such as acetaldehyde and reactive oxygen species, in the heart muscle cells. These toxic substances can cause oxidative stress, inflammation, and damage to the cardiomyocytes, leading to the development of ACM.

Additionally, chronic alcohol consumption can lead to deficiencies in essential vitamins and minerals, such as thiamine, magnesium, and selenium, which are important for the proper functioning of the heart. Thiamine deficiency, in particular, is common in people with alcohol use disorder and can lead to a condition known as beriberi, which can damage the heart muscle. Furthermore, chronic alcohol consumption can also lead to other cardiovascular risk factors, such as high blood pressure, high cholesterol levels, and obesity, which can contribute to the development of ACM. Overall, the etiology of ACM is complex and involves various factors that can damage the heart muscle over time.

Signs and symptoms[edit]

Signs and symptoms presented by the occurrence of alcoholic cardiomyopathy are the result of the heart failing and usually occur after the disease has progressed to an advanced stage. Therefore, the symptoms have a lot in common with other forms of cardiomyopathy. These symptoms can include the following:

• Ankle, feet, and leg swelling (edema)
• Overall swelling
• Loss of appetite
• Shortness of breath (dyspnea), especially with activity
• Breathing difficulty while lying down
• Fatigue, weakness, faintness
• Decreased alertness or concentration
• Cough containing mucus, or pink, frothy material
• Decreased urine output (oliguria)
• Need to urinate at night (nocturia)
• Heart palpitations (irregular heart beat)
• Rapid pulse (tachycardia)

Pathophysiology

Alcohol-induced cardiac toxicity (AiCT) is characterized as either acute or chronic. With regards to acute AiCT, it's believed that consumption of large amounts of alcohol leads to cardiac inflammation, which can be detected by finding large amounts of troponin in the serum . With regards to chronic AiCT, chronic consumption of alcohol (defined as greater than 80 g per day for at least 5 years) can lead to multi-organ failure, including myocardial dysfunction . The exactly pathophysiologic mechanism by which chronic consumption of alcohol causes DCM is not well understood, however it's believed that genetic mutation, and mitochondrial damage due to oxidative stress injury may play a role.

Diagnosis[edit]

Abnormal heart sounds, murmurs, ECG abnormalities, and enlarged heart on chest x-ray may lead to the diagnosis. Echocardiogram abnormalities and cardiac catheterization or angiogram to rule out coronary artery blockages, along with a history of alcohol abuse can confirm the diagnosis.^{[citation needed]}

It's important to note that part of diagnosing Chronic ACM is noting the absence of coronary artery disease.

Prognosis[edit]

Prognosis of alcoholic cardiomyopathy is dependent on multiple factors, including the following: volume of alcohol consumption, how long the patient has been abusing alcohol, presence of atrial fibrillation, width of the QRS, and the presence/absence of certain medications all play a significant role in determining prognosis. Some indications of poor prognosis include the following: patients with QRS > 120, patients who continue to consume alcohol for prolonged periods. Consumption of alcohol is directly related to the amount of alcohol consumed and length of consumption. Indicators of good prognosis include the following: successfully quitting the consumption of alcohol (associated with decreased hospital admissions), and patient compliance with beta blockers. Mortality is between 40-80% 10 years post-diagnosis.

The prognosis of alcoholic cardiomyopathy (ACM) varies depending on the severity of the condition, the extent of heart muscle damage, and the response to treatment. Without treatment, ACM can progress to severe heart failure, arrhythmias, and sudden cardiac death. However, with proper treatment, including cessation of alcohol consumption and management of heart failure symptoms, the prognosis can improve significantly.

Research has shown that the mortality rate for people with ACM is higher than that of the general population, with a five-year survival rate of around 50%. However, studies have also shown that people who stop drinking alcohol have a significantly better prognosis than those who continue to drink. In addition, people who receive early treatment for ACM, including medication and lifestyle modifications, have a better chance of improving their heart function and overall health.

The prognosis of ACM can also depend on the presence of other comorbidities such as diabetes, hypertension, and obesity. These conditions can exacerbate the effects of ACM on the heart and increase the risk of complications. Therefore, it is important to manage these comorbidities to improve the overall prognosis of ACM.

Treatment[edit]

Treatment for alcoholic cardiomyopathy involves lifestyle changes, including complete abstinence from alcohol use, a low sodium diet, and fluid restriction, as well as medications. Medications may include ACE inhibitors, beta blockers, and diuretics which are commonly used in other forms of cardiomyopathy to reduce the strain on the heart. Persons with congestive heart failure may be considered for surgical insertion of an ICD or a pacemaker which can improve heart function. In cases where the heart failure is irreversible and worsening, heart transplant may be considered.^{[citation needed]}

Treatment will possibly prevent the heart from further deterioration, and the cardiomyopathy is largely reversible if complete abstinence from alcohol is maintained.^{[citation needed]}

Interestingly, in patients that are defined as "heavy drinkers" (defined as consuming >30g of alcohol/day) decreased alcohol consumption to moderate levels has been shown to be an effective treatment; in fact A retrospective cohort study analyzed data collected from over 3.8 million patients, and categorized patients as either abstinent drinkers, mild drinkers, moderate drinkers, and heavy drinkers. Despite having such a large sample size, the association between alcohol intake and cardiomyopathy remains unclear. The study found that patients that were either mild or moderate drinkers were the least likely to develop HF as compared to patients that were abstinent. The study also found that patients that increased there alcohol consumption from light to moderate and/or from moderate to heavy were at increased risk for heart failure (see graph for visual). Although one might think that patients that were completely abstinent from alcohol would have would be least likely of being diagnosed with heart failure, it's actually patients categorized as either light or moderate drinkers had the lowest risk for developing HF.