Alcoholic Cardiomyopathy: Overview, Cardiac Effects of Alcohol, Quantity of Alcohol Intake in Cardiac Disease

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]. Depending on the medication, these approaches can  improve heart function, and control blood pressure. You’ll be asked questions regarding your medical history and lifestyle, including how much alcohol you drink and for how long you’ve drank at those levels. In severe cases, alcoholic cardiomyopathy can negatively affect brain function because of reduced blood flow to the brain.

  • The authors highlighted the presence of an extensive intracellular accumulation of neutral lipids, principally in the form of small cytoplasmic droplets.
  • Wang et al. found evidence of ethanol-induced changes in mitochondrial structure that were more pronounced in a metallothionein knock-out mouse model compared to wild-type mouse (80).
  • ACM represents one of the leading causes of non-ischemic dilated cardiomyopathy.
  • In the second study, Gavazzi led a multicentre study in which, from 1986 to 1995, 79 patients with ACM and 259 patients with DCM were recruited[10].

There are several plasma biomarkers of oxidative stress, such as 8-isoprostane (34). Alcohol abuse has a toxic effect on many of your organs, including the heart. When it can’t pump out enough blood, the heart starts to expand to hold the extra blood. Eventually, the heart muscle and blood vessels may stop functioning properly due to the damage and strain. Alcoholic cardiomyopathy is most common in men between the ages of 35 and 50, but the condition can affect women as well. People with alcoholic cardiomyopathy often have a history of heavy, long-term drinking, usually between five and 15 years.

Histologic Findings

As the name suggests, alcoholic cardiomyopathy is caused by alcohol alone, and accounts for 10% of all cases of dilated cardiomyopathies. People who drink a dangerous amount of alcohol have a higher risk of developing alcoholic cardiomyopathy, as well as damaging other organs in the body. In all ACM studies, inclusion of patients is based on patients’ self-reported alcohol drinking habits, which may lead to an underestimation of the prevalence of ACM together with problematic identification of patients who abstain and those who continue drinking. Furthermore, in many of these reports, comorbid conditions, especially myocarditis and other addictions such as cocaine and nicotine, were not reported. Future studies with a strict classification of non-drinkers and drinkers will help clarify whether complete abstinence is mandatory for ACM patients.

Once the damage is considered irreversible, it’s difficult for the heart and rest of the body to recover. Your doctor will also ask you about your medical history and drinking habits. It’s important to be honest with your doctor about the extent of your alcohol use, including the number and amount of drinks alcoholic cardiomyopathy is especially dangerous because you have each day. This will make it easier for them to make a diagnosis and develop a treatment plan. As a net effect, negative inotropism may result and contribute to heart failure. Clinical observation confirmed that several days to weeks of drinking show higher and weeks of abstinence lower pressures.

Heart Transplant

However, researchers have pinpointed certain behaviors that make it more likely you’ll develop this condition. This review revisits our past and deals with our current thinking on the epidemiology, pathophysiology, clinical characteristics, and treatments available for alcoholic cardiomyopathy. The journey to managing ACM begins with comprehensive treatment for alcohol use disorder. In a tailored treatment program, you can safely stop drinking and learn to live without alcohol abuse. You’ll build skills that enable you to cope with triggers, and you’ll address underlying issues that led you to abuse alcohol.

  • The trace amounts of arsenic have not been comparable to the arsenic-in-beer endemic in Manchester but may still reach up to 10-times the amount admitted for arsenic in drinking water in the European Union and the US.
  • There are no specific targeted histological or immunological biomarkers for the diagnosis of alcohol-induced cardiomyopathy.
  • These oxidative stress biomarkers corresponded to myocardial fibrosis development and decreases in fractional shortening and cardiac output.
  • To diagnose this condition, healthcare providers will typically use several of the following methods.

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.

Nutritional causes of “alcoholic” cardiomyopathy

But also short- and long-term pressor effects mediated by the renin–aldosterone system and plasma vasopressin have been described [47, 48]. When compared to other types of cardiovascular disorders, alcoholic cardiomyopathy is not common. In fact, it is considered relatively rare when compared to conditions like coronary artery disease, heart failure, or arrhythmias. Some individuals have a genetic predisposition that makes them more susceptible to the toxic effects of alcohol on the heart.

alcoholic cardiomyopathy is especially dangerous because

On histological examination, various degrees of fibrosis, patchy areas of endocardial fibroelastosis, intramural blood clots and focal collections of swollen cells in both the epicardium and endocardium were found. Also, there were significant size variations in the myofibrils and they showed a relative decrease in the number of striations, in addition to swelling, vacuolisation and hyalinisation. Cell nuclei were larger than normal, morphologically difficult to define and they occasionally showed hyperpigmentation.

How should I change my diet if I have this condition?

Electrolyte abnormalities, including hypokalemia, hypomagnesemia, and hypophosphatemia, should be corrected promptly because of the risk of arrhythmia and sudden death. To date, none of the ACM studies have proposed a treatment for ACM other than that recommended for DCM in current HF guidelines. Further research is required to determine the definitive role of genetics on ACM pathophysiology. Furthermore, Fernández-Solá et al[30], when analysing a population of alcoholics, found a higher prevalence of DCM in alcoholics than among the general population. Specifically, among alcoholics they found a prevalence of DCM of 0.43% in women and 0.25% in men, whereas the described prevalence of DCM in the general population is 0.03% to 0.05%[18,19]. At present ACM is considered a specific disease both by the European Society of Cardiology (ESC) and by the American Heart Association (AHA)[18,19].

  • In susceptible individuals, chronic ethanol consumption may cause progressive myocardial damage leading to alcoholic cardiomyopathy (ACM).
  • Patel warns that «it is crucial to stop drinking alcohol completely» if your doctor advises that your dilated cardiomyopathy is caused by alcohol consumption alone.
  • In their autopsies, he described finding dilated cavities of the heart and fatty degeneration of the ventricular walls[14].
  • This can result in various symptoms, including fluid retention and episodes.