The Effects of Ethanol on the Heart: Alcoholic Cardiomyopathy PMC

The QRS duration, LVEDD, and diameter of the right ventricle (RV) and left atrium (LA) were higher in the death group than those in the survival group, but the LVEF and blood pressure (systolic [SBP] or diastolic [DBP]) were lower in the death group than those in the survival group. Ballester specifically analysed the effects of alcohol withdrawal on the myocardium using antimyosin antibodies labelled with Indium-111[72]. This radiotracer has been acknowledged as an indicator of irreversible myocardial damage. Of the 56 patients included in the study, 28 were former drinkers and 28 continued consuming alcohol during the study. Absorption levels of Indium-111 were high in 75% of patients who continued drinking and in only 32% of those who had withdrawn from consuming alcohol. The good news is that making these lifestyle changes could improve your condition, although this will depend on how much damage has already been done to the heart muscle.

alcoholic cardiomyopathy stages

Data on the amount of alcohol consumption required to cause ACM are limited and controversial. Biomarkers of heart failure such as NT-proBNP and of myocardial necrosis such as the troponins and CKMB indicate heart failure or myocytolysis. In his 1972 review article, Bridgen was the first to introduce the term alcoholic cardiomyopathy [27].

Quebec‘s beer drinker disease

Further, we allowed for nonlinear associations by including polynomials of the independent variable. In this contribution, we performed similar regression models using proportion of ACM deaths among all CVD deaths as target disease and proportion of heart failure deaths among all CVD deaths as garbage codes. We selected heart failure deaths as they were cited as source for redistributing deaths to ACM in the GBD 2017 study [12].

The population was divided into 3 groups according to their intake volume during the follow-up period. At the end of the first year, no differences were found among the non-drinkers, who improved by 13.1%, and among those who reduced consumption to g/d (with an average improvement of 12.2%). Conversely, those whose consumption remained in excess of 80 g/d showed an average decline of 3.8% in their ejection fraction. Although some studies have detailed structural and functional damage in proportion to the amount of alcohol consumed during a patient’s lifetime[24], a large majority of authors have discarded this theory[21-23,25].

Alcoholic cardiomyopathy

In the mid-1960s, another unexpected heart failure epidemic among chronic, heavy beer drinkers occurred in two cities in the USA, in Quebec, Canada, and in Belgium. It was characterized by congestive heart failure, pericardial effusion, and an elevated hemoglobin concentration. As the syndrome could be attributed to the toxicity of this trace element, the additive was prohibited thereafter. After myocyte apoptosis or necrosis, the heart tries to repair alcoholic cardiomyopathy and regenerate this tissue damage [39,123], but the heart regenerative capacity is low as a result of the ethanol aggressive damage and develops ineffective repair mechanisms such as progressive fibrosis [124,125]. In fact, ethanol itself decreases the myocyte regeneration capacity and increases the fibrogenic process [52,126]. Subendocardial and interstitial fibrosis progressively appear in the course of ACM, usually in advanced stages [52,56].

  • Caution for anticoagulation is warranted due to the problems of noncompliance, trauma, and overdosage especially in hepatic dysfunction.
  • In spite of the high prevalence of excessive alcohol consumption and of its consideration as one of the main causes of DCM, only a small number of studies have analysed the long-term natural history of ACM.
  • These investigators also found decreases in peroxiredoxin 5, antioxidant protein 2, and glutathione transferase 5, important anti-oxidant enzymes.
  • Myocyte cytoskeletal structure [21], connexin channel communication, and desmosomal contacts are affected by ethanol, causing structural cell instability [105].
  • Similarly, when the right ventricle is dilated, the tricuspid valve may leak, a condition known as tricuspid regurgitation.
  • However, as the condition progresses, they may experience symptoms such as fatigue, shortness of breath, palpitations, and swelling of the legs and ankles.[6] They may also experience chest pain, dizziness, and fainting.

At a pathological level, sarcomere Z-line distortion and disruption of the sarcomere pattern leads to myocytolysis [107,129]. Myocytolysis is evident through focal myofiber dissolution, cell vacuolization, and fiber disarray [19] (Figure 2). The sarcomere complex is early affected by ethanol, decreasing the titin content, a protein that is responsible for sarcomere relaxation and LV distensibility [130]. This damage first induces diastolic dysfunction, which is initially subclinical and later clinically apparent [57]. In addition, contractile sarcomere proteins such as Myosin, Actin, and Troponin are also affected by ethanol, causing the functional progressive depression of myocyte contractility, inducing progression to heart failure [56,104,131]. Mortality in ACM is related to the progression of heart failure and malignant arrhythmias [58,65].

3. Relationship between independent predictors and all-cause mortality

The first paper to assess the natural history and long-term prognosis of ACM was published by McDonald et al[69] in 1971. He recruited 48 patients admitted to hospital with cardiomegaly without a clear aetiology and severe alcoholism. The only factor to predict a poor outcome was the duration of symptoms before admission. Hypertrophic cardiomyopathy is a condition where the heart muscle walls are thickened.

There is a large gap between registered and estimated deaths due to ACM but also due to all other cardiomyopathies. Primarily, a large number of deaths assigned with garbage codes may be the result of inaccurate cause of death coding. However, this gap could also be an indicator for suboptimal clinical care (detection, treatment) during a lifetime. To diagnose ACM, clinicians need to identify a dilated heart muscle, rule out other potential causes, and conduct an extensive assessment of the patients’ alcohol use [3,22].

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 the ESC consensus document on the classification of cardiomyopathies, ACM is classified among the acquired forms of DCM[19]. Our patients tell us that the quality of their interactions, our attention to detail and the efficiency of their visits mean health care like they’ve never experienced. Alcoholic cardiomyopathy is best managed with an interprofessional approach with the involvement of primary care physician and cardiology. To find a treatment program, browse the top-rated addiction treatment facilities in each state by visiting our homepage, or by viewing the SAMHSA Treatment Services Locator.

  • Studies of alcohol and stroke are complicated by the various contributing factors to stroke.
  • This refers to the finding in the last century that moderate alcohol consumption could be the reason for the relatively low cardiovascular disease incidence in wine-drinking regions [92].
  • To find a treatment program, browse the top-rated addiction treatment facilities in each state by visiting our homepage, or by viewing the SAMHSA Treatment Services Locator.
  • 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].
  • Hypertrophic cardiomyopathy is a condition where the heart muscle walls are thickened.

More than 30% of the myocyte ventricular fraction can be replaced by fibrotic tissue, thus decreasing the heart elasticity and contractile capacity [64] (Figure 2). Some cardiomyokines, such as FGF21, may regulate this process of alcohol-induced cardiac fibrosis [119]. 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%). The use of carvedilol, trimetazidine with other conventional heart failure drugs have been proven to be beneficial in some studies.

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