Alcohol-Induced Cardiomyopathy: Causes, Symptoms and Treatment

alcoholic cardiomyopathy is especially dangerous because

The only way to completely prevent alcohol-induced cardiomyopathy is not to drink alcohol at all. Many changes can be observed including premature atrial or ventricular contractions, supraventricular tachycardias, atrioventricular blocks,  bundle branch blocks, QT prolongation, non-specific ST and T wave changes and abnormal Q waves. Alcoholic cardiomyopathy is a leading cause of non-ischemic dilated cardiomyopathy in United States. Myocardial depression secondary to alcohol is initially reversible however prolonged sustained alcohol use leads to irreversible dysfunction. Illustrations of a typical heart, as shown on the left, and a heart with hypertrophic cardiomyopathy.

alcoholic cardiomyopathy is especially dangerous because

Acute vs. chronic

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. Abnormal heart sounds, murmurs, ECG abnormalities, and enlarged heart on chest x-ray may lead to the diagnosis. Caution for anticoagulation is warranted due to the problems of noncompliance, trauma, and overdosage especially in hepatic dysfunction. In Munich, the annual consumption of beer reached 245 l per capita and year in the last quarter of the 19th century. In 1884, the pathologist and veterinarian Otto von Bollinger (Fig. 2a) described the “Munich beer heart” with fibrosis, hypertrophy, and fatty degeneration in postmortem cardiac tissue of alcoholics who consumed an estimated average of 432 liters of beer per year (Fig. 2b; [23]). 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.

  • Your healthcare provider is the best person to explain the risks and possible complications that you might face from this condition itself, related health concerns or any of the treatments that you will receive.
  • In general, you should talk to your healthcare provider if you notice changes in your symptoms over time, especially if they are starting to affect your normal life and routine.
  • 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.

History and Physical

The 6 subjects who experienced a clear improvement in their ejection fraction had fully refrained from drinking. Conversely, the 3 subjects recording a less satisfactory evolution had persisted in their consumption of alcohol. It should be noted that a moderate drinker included in this latter group showed an improvement alcoholic cardiomyopathy is especially dangerous because of his ejection fraction. One of the few papers analysing genetic susceptibility in ACM was published by Fernández-Solà et al[64] in 2002. He compared the prevalence of different polymorphisms of the angiotensin-converting enzyme gene in 30 ACM patients and in 27 alcoholics with normal ventricular function.

1. The Natural Course of ACM

Myocytolysis progressively develops, disturbing the sarcomere contractile system. The heart output is progressively lower in a dose-dependent relationship with the lifetime accumulated total dose of alcohol consumed [38]. Several growth factors and cardiomyokines exert an autocrine or paracrine effect that tries to compensate for this heart damage [119,133]. Antioxidant, anti-inflammatory, anti-apoptotic, and antifibrogenic mechanisms try to avoid myocyte necrosis and heart fibrosis [14,30,58]. The final result is that achieved from the equilibrium between the degree of damage and the capacity of heart repair mechanisms in each specific individual [31,56]. In fact, the particular effects that ethanol produces in a specific organ depend on several factors [18,19].

alcoholic cardiomyopathy is especially dangerous because

  • What you should expect with this condition depends strongly on several factors.
  • New strategies are addressed to decrease myocyte hypertrophy and interstitial fibrosis and try to improve myocyte regeneration, minimizing ethanol-related cardiac damage.
  • Ethanol abstinence allows for recovery in the majority of cases, including in those with previous severe depression of LV EF [81,88,135].
  • The key to diagnosis is a personal history of chronic heavy alcohol use and the absence of other etiologies.

Furthermore, 89% of the alcoholics with a DD genotype developed ACM, whereas only 13% of those with an II or ID genotype developed this condition. However, this individual susceptibility mediated by polymorphisms of the angiotensin-converting enzyme gene does not appear to be specific to ACM insofar as several diseases, including some that are not of a cardiologic origin, have been related to this genetic finding[65]. The first study, which specifically focused on the amount of alcohol necessary to cause ACM, was conducted by Koide et al[20] in 1975.

Treatment of ACM

More than 1.8 million individuals in Germany with a total population of 81 million inhabitants are alcohol dependant. In a world-wide setting, alcohol use disorders show similarities in developed countries, where alcohol is cheap and readily available [8]. The many complications of alcohol use and abuse are both mental and physical—in particular, gastrointestinal [9], neurological [10, 11], and cardiological [12, 13]. The relationship of alcohol with heart disease or dementia is complicated by the fact that moderate alcohol consumption was shown not only to be detrimental but to a certain degree also protective against cardiovascular disease [14] or to cognitive function in predementia. Studies in experimental animals have demonstrated that both acute and chronic ethanol administration impairs cardiac contractility. Additionally, echocardiographic data suggest that subjects who do not fully withdraw from alcohol consumption, but who reduce it to moderate amounts recover LVEF in a similar manner to strict non-drinkers.

Is this condition only a chronic (long-term) problem?

alcoholic cardiomyopathy is especially dangerous because

People with alcoholic cardiomyopathy often have a history of heavy, long-term drinking, usually between five and 15 years. Heavy drinking is alcohol consumption that exceeds the recommended daily limits. For many decades, ACM has been considered one of the main causes of left ventricular dysfunction in developed countries. Specifically in the United States, ACM was declared the leading cause of non-ischemic DCM[7]; a fact related to the high consumption of alcoholic beverages worldwide, which is particularly elevated in Western countries[26] . 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.

Enhancing Healthcare Team Outcomes

  • Alcoholic cardiomyopathy affects the heart’s ability to pump oxygen-rich blood around the body.
  • Changes in your heart’s shape can also disrupt that organ’s electrical system.
  • New strategies to improve the natural course of ACM have been proposed as promising agents in this field [112,147].
  • Biomarkers of heart failure such as NT-proBNP and of myocardial necrosis such as the troponins and CKMB indicate heart failure or myocytolysis.
  • For tens of years, the literature has documented many clinical cases or small series of patients who have undergone a full recovery of ejection fraction and a good clinical evolution after a period of complete alcoholic abstinence.

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