Electron microscopic studies (7,8) of biopsies from patients with alcohol-induced cardiomyopathy have shown evidence of damage to the myofibres, including separation of filaments and loss of striation. In animal studies, loss of contractile proteins and defects in myocardial protein synthesis may partly explain the altered contractility. These studies have demonstrated that acute alcohol ingestion directly reduces contractile protein synthesis in vivo by approximately 25%.
Data Availability
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. Considering all the works conducted to date, it is clear that new studies on the natural history of ACM are needed, including patients treated with contemporary heart failure therapies. In light of the available data, new studies will help to clarify the current prognosis of ACM compared to DCM and to determine prognostic factors in ACM that might differ from known prognostic factors in DCM. The latest two papers to be published, unlike previous papers, reported worse outcomes for ACM patients compared to DCM patients.
6. Cardiac Hypertrophy and Remodeling in ACM
Therefore, complete abstinence from ethanol is the most useful measure to control the natural course of ACM alcoholic cardiomyopathy symptoms 51,56,135. In fact, patients with ACM who abstain from alcohol have a better long-term prognosis than subjects with idiopathic dilated CMP 54. Out of end-stage cases, the majority of subjects affected by ACM who achieve complete ethanol abstinence functionally improve 33,82,135. The percentage of effective abstinence achievement on these patients submitted to specific programs ranges from 50% to 60% 8,9. Therefore, many ACM subjects are not able to effectively control their alcohol-consumption rates.
1. The Natural Course of ACM
- 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.
- In spite of numerous studies, the sequence of events that occur in alcohol-induced myocardial damage is still highly controversial.
- One relevant question concerning ethanol cardiac toxicity is if ethanol itself or its active metabolite acetaldehyde causes cardiac damage 73,74.
- We then proceeded with screening and selection based on the titles and abstracts of the initial search results.
- Your doctor might prescribe ACE inhibitors and beta-blockers to help lower your blood pressure.
Therefore, physicians should be aware of the risk of new cardiomyopathy in patients with these overlapping diagnoses 144. Control of these alcohol-related systemic diseases, as well as the strict control of the presence of other heart risk factors (tobacco, cocaine, arterial hypertension, diabetes mellitus, or anemia) contributes to ACM improvement 10,20,23,37,52. Atrial fibrillation should be controlled with chronotropic drugs such as digoxin or diltiazem and anticoagulant treatment to avoid arterial embolisms 60,145. Alcoholic-dilated Cardiomyopathy (ACM) is the most prevalent form of ethanol-induced heart damage. Ethanol induces ACM in a dose-dependent manner, independently of nutrition, vitamin, or electrolyte disturbances. ACM produces a progressive reduction in myocardial contractility and heart chamber dilatation, leading to heart failure episodes and arrhythmias.
- Chest radiographs usually show evidence of cardiac enlargement, pulmonary congestion, and pleural effusions.
- Alcohol-induced cardiomyopathy remains a relevant health problem, for which the mainstay of treatment is alcohol abstinence.
- Although no significant changes were found using conventional microscopy, when electron microscopy was employed he discovered intracellular swelling, glycogen and lipid accumulation, and alterations in the structure of the sarcoplasmic reticulum and of the mitochondria (Figure 2).
We were unable to do any subgroup analysis especially to look into whether there is increased mortality among certain population subsets such as those with hypertension and coronary artery disease. We were also not able to further identify the ethnic minorities included under the “other” race category. The pathologic and histologic findings of alcoholic cardiomyopathy (AC) are essentially indistinguishable from those of other forms of dilated cardiomyopathy (DC).
There are no specific targeted histological or immunological biomarkers for the diagnosis of alcohol-induced cardiomyopathy. Various pathophysiological mechanisms have been postulated in the development of cardiomyopathy however one key factor undergoing active research is the role of genetic mutation and susceptibility to develop cardiomyopathy. 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. Epidemics of heart failure in persons who had consumed beer contaminated with arsenic in the 1900s and cobalt in the 1960s also obscured the observation that alcohol could exhibit a direct toxic effect. In the 1950s, evidence began to emerge that supported the idea of a direct toxic myocardial effect of alcohol, and research during the last 35 years has been particularly productive in characterizing the disease entity of alcoholic cardiomyopathy (AC).
- Acute can be defined as large volume acute consumption of alcohol promotes myocardial inflammation leading to increased troponin concentration in serum, tachyarrhythmias including atrial fibrillation and rarely ventricular fibrillation.
- The key to diagnosis is a personal history of chronic heavy alcohol use and the absence of other etiologies.
- In the study by Gavazzi et al10, ACM patients who continued drinking exhibited worse transplant-free survival rates after 7 years than those who stopped drinking alcohol (27% vs 45%)10.
- Third and fourth heart sounds can be heard, and they signify systolic and diastolic dysfunction.
- Some cardiomyokines, such as FGF21, may regulate this process of alcohol-induced cardiac fibrosis 119.
- 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.