Finally, it should be noted that a large majority of studies on the long-term prognosis of ACM used the cut-off point of 80 g/d for a minimum of 5 years to consider alcohol as the cause of DCM. Since those Halfway house initial descriptions, reports on several isolated cases or in small series of patients with HF due to DCM and high alcohol intake have been published15-17. Some of these papers have also described the recovery of LVEF in many subjects after a period of alcohol withdrawal15-17.
- 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.
- Zhang et al. found significant increases in myocardial protein carbonyl and superoxide levels in mice fed an ethanol (4% v/v) diet for 6 weeks (22).
- To date, none of the ACM studies have proposed a treatment for ACM other than that recommended for DCM in current HF guidelines.
- The exact sequence for the development of ACM remains incompletely understood, data from animal models and human beings with a history of long-terms suggest oxidative stress maybe an early and initiating mechanism.
- There is also an established link between the development of ACM and apoptosis because of myocardial cell death, which contributes to heart pathology and dysfunction.
- Another curious hypothesis from Germany suspected that some ethanol additives, such as anti-foam beer products with arsenic or cobalt content, produced cardiac toxicity and development of ACM 71.
What is Alcoholic Cardiomyopathy
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. Although analytical markers of alcohol consumption, such as average erythrocyte volume and serum gamma-glutamyltranspeptidase levels, could be an aid to establish abstinence or persistence of alcohol intake in patients, the quantity of alcohol intake is dependent on the patients’ report. Furthermore, in many of these reports, comorbid conditions, especially myocarditis and other addictions such as cocaine and nicotine, were not reported. 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.
- 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 recruited10.
- More than one mechanism may be activated that lead to the multitude of ethanol-induced changes in cellular proteins and cell function.
- The myocyte mitochondria in the hearts of persons exposed to alcohol are clearly abnormal in structure, and many believe that this may be an important factor in the development of AC.
- We identified main themes and sub-themes to provide a comprehensive overview of the current state of knowledge regarding ACM.
- It has been said that ethanol is the “perfect drug” because of its pleasant effects but damaging long-term effect 1,6.
Table 1. List of literature articles reviewed in this study.
The effect of a low dose of alcohol consumption on the cardiovascular system has been also extensively evaluated with evidence of a dual effect, beneficial for coronary artery disease at low doses 44 but reversing to a damaging effect at moderate to high doses 19. Although there is beneficial potential in some patients, the coexistence of increased risk of cancer, neurological brain damage, and the high risk of ethanol addiction makes it necessary to discourage this low-dose consumption in the general population 19,41,45. Specific caution should be recommended regarding children or adolescents 4 and women 46, who are more susceptible to the damaging effects of ethanol at the same doses of consumption as men. Similarly, patients suffering from other ethanol-related diseases such as liver cirrhosis or brain atrophy should completely suppress their ethanol consumption 47,48. Excessive alcohol consumption represents one of the main causes of non-ischemic dilated cardiomyopathy.
Heart Disease Treatment: Medication, Lifestyle Changes, and More
Pharmacological restoration of autophagic reflux by inhibition of soluble epoxide hydrolase has been described to ameliorate chronic ethanol-induced cardiac fibrosis in an in vivo swine model 151. However, these new strategies have not yet demonstrated their real effectiveness in clinical trials, require further evaluation, and are not approved for clinical use 147. Since cardiac myocytes are excitable cells, and ethanol may easily damage this excitation–contraction mechanism, disruption of this coupling mechanism is involved in the ACM pathogenic process 19,58. Ethanol may produce the modification of sarcolemmal alcohol cardiomyopathy membrane L-type Ca2+ channels, leading to a decrease in transmembrane electrically induced Ca2+ transients 85,103,127.
Before recognizing that ethanol itself is the etiological factor of ACM, different theories and hypotheses emerged 1,66. It was suspected that malnutrition, frequently related to chronic alcohol misuse, was the origin of ACM 6,67. However, it has been evidenced that ACM may develop in the absence of protein or caloric malnutrition 38. Along with developing heart damage, patients with ACM may also damage other organs, such as the liver, central and peripheral nervous system, skeletal muscle, pancreas, and digestive tract, and are exposed to an increased risk of cancer 24,63,64. In fact, ACM is related to systemic damage induced by ethanol misuse and its global biological response 10,11,31.
Structurally, hypertrophy of myocytes is seen in the early stages to avoid contractile depression 52,107,125. 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. Since myocardium requires a high energy supply to maintain persistent sarcomere contractions, it was supposed that alcohol could exert its damaging effect on the mitochondrial energy supply system, with the disruption of oxidative control mechanisms 26,100.
ACM produces a progressive reduction in myocardial contractility and heart chamber dilatation, leading to heart failure episodes and arrhythmias. Pathologically, ethanol induces myocytolysis, apoptosis, and necrosis of myocytes, with repair mechanisms causing hypertrophy and interstitial fibrosis. Myocyte ethanol targets include changes in membrane composition, receptors, ion channels, intracellular Ca2+ transients, and structural proteins, and disrupt sarcomere contractility. Cardiac remodeling tries to compensate for this damage, establishing a balance between aggression and defense mechanisms. New strategies are addressed to decrease myocyte hypertrophy and interstitial fibrosis and try to improve myocyte regeneration, minimizing ethanol-related cardiac damage. Cardiac transplantation is the final measure in end-stage ACM but is limited to those subjects able to achieve abstinence.
- In long-term follow-up studies, a mortality rate of 10% of patients/year has been observed in the group of patients with persistent high-dose ethanol consumption 19,52.
- Therefore, any decrease in the previous quantity of alcohol consumption may improve, to some degree, cardiac health 51.
- 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.
- More research is required using more contemporary measures of mitochondrial function as well as determining changes in mitochondrial DNA.
Based on epidemiological evidence, ACM is recognized as a significant contributor to non-ischemic DCM in Western countries. Diagnosing ACM still relies on exclusion criteria, similar to alcoholic liver disease, as excessive alcohol consumption is observed in up to 40% of DCM patients. In a national inpatient sample study, some authors have reported ACM to be most common in white males aged between 45 and 59 2.
Alcoholic Cardiomyopathy
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. The authors highlighted the presence of an extensive intracellular accumulation of neutral lipids, principally in the form of small cytoplasmic droplets. In a subsequent study using electron microscopy, the authors found histological features that could be superimposed onto those found in hearts that had suffered hypoxia, anoxia or ischemia43.
