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Alcoholic cardiomyopathy: What is known and what is not known

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. 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]. The patient continued to experience tachycardia and blood pressure fluctuations, leading to hemodynamic instability due to fluid overload and ultimately resulting in cardiac shock. The medical team administered intravenous injections of norepinephrine and dobutamine for treatment.

  • Myocardial impairment following chronic excessive alcohol intake has been evaluated using echocardiographic and haemodynamic measurements in a significant number of reports.
  • Additionally, the accepted ACM definition does not take into account a patient’s sex or body mass index (BMI).
  • During the first half of the 20th century, the concept of beriberi heart disease (ie, thiamine deficiency) was present throughout the medical literature, and the idea that alcohol had any direct effect on the myocardium was doubted.
  • 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.

Animal studies have suggested a benefit from vitamins B-1 and B-12, speculated to be due to protective effects against apoptosis and protein damage. A 12-month observational study of 20 patients with AC noted smaller cavity diameters, better clinical evaluation findings, and fewer hospitalizations in the 10 patients who abstained from alcohol use. Alcoholic cardiomyopathy affects the heart’s ability to pump oxygen-rich blood around the body. This can cause various symptoms, including shortness of breath, fluid retention, and fainting.

Clinical Presentations Relating to the Heart

Excessive consumption of alcohol is one of a number of modifiable causes of health problems in the developed world. As medical care moves towards a chronic disease model there have been calls to incorporate effective behaviour change strategies into medical practice, and a number have been identified for changing alcohol use 53. The acute effects of alcohol on the myocardium include a weakening of the heart’s ability to contract (negative inotropic effect). Data from isolated papillary and heart muscle cell (myocyte) experiments demonstrate that acute physiologic intoxicating doses of alcohol (80 mg% to 250 mg%) can have a negative inotropic effect (Danziger et al. 1991; Guarnieri and Lakatta 1990). These effects also may involve an irregular and often very fast heart rate (arrhythmia) during which the heart’s upper chambers (atria) contract chaotically out of coordination with its lower chambers (ventricles), known as atrial fibrillation, or (rarely) sudden cardiac death.

  • For example, alcohol consumption typically has been measured through self-report.
  • However, a possible confusion factor was identified because the group with clinical improvement also exhibited a shorter evolution of the symptoms and the disease.
  • 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.
  • Data on the amount of alcohol consumption required to cause ACM are limited and controversial.

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 alcoholic cardiomyopathy conditions, especially myocarditis and other addictions such as cocaine and nicotine, were not reported. Also, low to moderate daily alcohol intake was proved to be a predictor of better prognosis for both ischemic cardiomyopathy and heart failure regardless of the presence of coronary disease[1,2].

How common is this condition?

Guillo et al[17] in 1997 described the evolution of 9 ACM patients who had been admitted. He divided this cohort into two groups according to the evolution of the ejection fraction during 36 mo in which no deaths were recorded. The 6 subjects who experienced a clear improvement in their https://ecosoberhouse.com/ 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 of his ejection fraction.

alcoholic cardiomyopathy

Studies using different methodologies have shown that low-to-moderate alcohol consumption decreases platelet activation and aggregation in certain cases—for example, in response to certain physiologic stimuli such as adenosine 5′-diphosphate (Salem and Laposata 2005). On the other hand, significant daily alcohol consumption increases platelet aggregation and reactivity. Infection or other stressful events also can lead to immune-triggered platelet production, a condition called rebound thrombocytosis, which may occur immediately after withdrawal from both heavy and one-time heavy (binge) drinking (Numminen et al. 1996). Although highly individualized and dose dependent, alcohol use also can increase bleeding time (i.e., taking longer to develop a clot)(Salem and Laposata 2005). Excessive intake of alcohol may result in increased systemic blood pressure in a dose-response relationship, and this may contribute to chronic myocardial dysfunction. Patients who consume more than two drinks per day have a 1.5- to 2-fold increase in hypertension compared with persons who do not drink alcohol, and this effect is most prominent when the daily intake of alcohol exceeds five drinks.

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In a two step process, ethanol is metabolized to acetate, via an acetaldehyde intermediate [14]. Although this process predominantly occurs in the liver, the alcohol metabolizing enzymes, alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), are also present in the heart and other tissues [13,15,16]. Acetaldehyde is ten times more toxic than ethanol, and has been shown to concentrate in cardiac tissue [13,16]. The consequence is a rise of intracellular free oxygen radicals (ROS) which is viewed as a major damage inducing pathway within the cell [17,18]. Experimental studies that used 4-methylpyrazole (an alcohol dehydrogenase inhibitor) or cyanamide (an aldehyde dehydrogenase inhibitor) found that ROS generation was blocked [19]. In addition to the two-step process of ethanol degradation to acetate, the enzyme fatty acid ethyl ester (FAEE) synthase performs an esterification reaction coupling ethanol to free fatty acids as a non-oxidative means of alcohol metabolism [20].

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