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 countries. However, very few studies have investigated the relationship between clinical characteristics and prognosis in ACM. If you suspect you at risk of or are suffering from the early stages of alcoholic cardiomyopathy, your doctor will run tests to make an accurate diagnosis. Your doctor will also ask you about your medical history and alcohol use behaviors. It is important to be honest with your doctor about your alcohol use, including the number and amount of drinks you have each day.
- Irregular heartbeats, or arrhythmias, are present in about 40-50% of patients with alcoholic cardiomyopathy.
- Amy Scanlon, MD, FACC, is a practicing private practice cardiologist at Consultants in Cardiology and the current team cardiologist for Seton Hall University.
- Doctors may ask about your alcohol history and perform blood tests, including liver function tests, to detect alcohol-related damage.
What Is Alcoholic Cardiomyopathy?
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 is a form of dilated cardiomyopathy (heart disease) alcoholic cardiomyopathy is especially dangerous because caused by chronic alcohol consumption or long-term alcohol abuse. This condition is characterized by an enlarged and weakened heart muscle, which significantly impairs the heart’s ability to pump blood efficiently.
How to treat alcoholic cardiomyopathy
- Post-mortem biopsies from the hearts of human alcoholics revealed that the myocardial mitochondria is enlarged and damaged 1-9.
- It should be noted that a moderate drinker included in this latter group showed an improvement of his ejection fraction.
- Continued heavy alcohol use, on the other hand, will continue to make alcoholic cardiomyopathy worse.
- Previous studies were conducted on rats that are fed alcohol for about eight months.
- The damaged heart muscles (myocardium) allow blood to remain in the right and left ventricles of the heart, and the heart thins out and expands to hold the accumulating blood.
- Among them, ethanol-induced activation of the renin-angiotensin system is important for the pathology observed in ACM 100.
Social, psychological, and economic factors further shape risk profiles, especially in underserved populations with limited access to healthcare or addiction treatment. The process by which alcohol leads to an enlarged heart involves multiple mechanisms, each contributing to the deterioration of cardiac structure and function. This means that it has a toxic effect on heart muscle cells, damaging them at a cellular level. https://ecosoberhouse.com/ Over time, this damage accumulates and impairs the ability of the heart to contract and relax properly.
According to the National Institute on Alcohol Abuse and Alcoholism (NIAAA), AUD is a brain disorder that doctors characterize by the inability to stop or control alcohol consumption. This inability occurs despite adverse effects on the person’s health, occupation, or relationships. If left untreated, alcoholic cardiomyopathy can lead to long-term health complications and death. If you see any signs of alcoholic cardiomyopathy, contact emergency medical services immediately. By being more susceptible to the damaging effects of alcohol, you’re more likely to develop alcoholic cardiomyopathy.
NATURAL HISTORY OF ALCOHOLIC CARDIOMYOPATHY
Early diagnosis and intervention are key to improving outcomes and preventing irreversible heart damage. With commitment and comprehensive care, many patients can achieve significant recovery and lead healthier, longer lives. Ethanol-induced changes may be related to oxidative or non-oxidative pathways of ethanol metabolism.
Individuals with certain mitochondrial DNA mutations and angiotensin-converting enzyme (ACE) genotypes (DD genotype) may be particularly susceptible to the damaging effects of alcohol. 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. Pharmacologic therapy should include goal-directed heart failure therapy as used in idiopathic dilated cardiomyopathy with reduced ejection fraction. This includes a combination of beta-blockers, an angiotensin-converting enzyme inhibitor, diuretics, aldosterone receptor antagonist and angiotensin blocker-neprilysin inhibitor (if LVEF is less than or equal to 40%).
Heavy drinkers had larger left ventricles and a higher volume of blood when the heart was relaxed and dilated after 20 years. However, alcohol consumption didn’t appear to have any significant effect on the ability of the heart to pump blood. Alcohol abuse can cause cardiomyopathy indistinguishable from other types of dilated nonischemic cardiomyopathy. Most heavy drinkers remain asymptomatic in the earlier stages of disease progression, and many never develop the familiar clinical manifestations that typify heart failure. We review the current thinking on the pathophysiology, clinical characteristics, and treatments available for alcoholic cardiomyopathy.
In Munich, the annual consumption of beer reached 245 l per capita and year in the last quarter of the 19th century. At that time every 10th necropsy in men at the Munich pathology institute named cardiac dilatation and fatty degeneration as “Bierherz” being its underlying cause. For comparison, the mean annual beer consumption in Bavaria is nowadays estimated to be 145 l and in the rest of Germany around 100 l beer per person and year 24. This review revisits our marijuana addiction past and deals with our current thinking on the epidemiology, pathophysiology, clinical characteristics, and treatments available for alcoholic cardiomyopathy.
- Surprisingly, the damaged mitochondria not only become less efficient but also increases the generation of ROS that aid the apoptosis process.
- The preponderance of data suggests that drinking one to two drinks in men and one drink in women will benefit the cardiovascular system over time.
- Subendocardial and interstitial fibrosis progressively appear in the course of ACM, usually in advanced stages 52,56.
In some cases, alcoholic cardiomyopathy is caused by a genetic mutation that makes your body process alcohol much slower than others.5 You can become intoxicated or damage your body with fewer drinks. Dependence is characterized by uncontrollable drinking patterns and a strong urge to drink alcohol. This stage of alcohol misuse is when tolerance develops, and serious withdrawal symptoms can occur. Enzymatic activity changes which are seen in the idiopathic cardiomyopathy including decreased activity of oxygen reduction mitochondrial enzymes, increased fatty acid uptake and increased lysosomal/microsomal enzyme activity can be seen.
Treatment / Management
Your lifestyle choices can also worsen your condition, especially when you use substances that affect your heart, lungs, and circulatory system. Alcohol can have a toxic effect on many of your organs, such as the liver and heart. Alcoholic cardiomyopathy is diagnosed when the heart muscle and surrounding blood vessels stop functioning correctly.
Alcoholic cardiomyopathy: Cytotoxicity of alcohol on heart muscle
When alcohol is consumed in large amounts, over time, it damages the heart muscle. When the heart can’t pump enough blood, it starts to expand to hold the extra blood. At some point, the heart muscle and blood vessels could stop working due to this type of strain. The major risk factor for developing ACM is chronic alcohol abuse; however, there is no specific cutoff value for the amount of alcohol consumption that would lead to the development of ACM. As early as in 1915, Lian 45 reported in middle-aged French servicemen during the first world war that heavy drinking could lead to hypertension. It took almost 60 years before further attention was paid to the complex interaction between the heart and the peripheral vasculature in various cross-sectional and prospective epidemiologic studies, which have empirically confirmed this early report.