National trends in hospitalizations and outcomes in patients with alcoholic cardiomyopathy

Analogous to the sarcoplasmic reticulum, the mitochondria were swollen or oedema was present, with crest alterations and intra-mitochondrial inclusions suggesting degenerative processes (Figure 2). Moreover, myofibrils showed a progressively distorted structure, resulting in a homogeneous mass. Myocardial impairment following chronic excessive alcohol intake has been evaluated using echocardiographic and haemodynamic measurements in a significant number of reports.

Periprocedural Myocardial Infarction: Is the Debate Over?

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. Abstinence is the preferred goal, although controlled drinking may still improve cardiac function. New strategies are addressed to decrease myocyte hypertrophy and interstitial fibrosis and try to improve myocyte regeneration, minimizing ethanol-related cardiac damage.

The Effects of Ethanol on the Heart: Alcoholic Cardiomyopathy

• In this review, we evaluate the available evidence linking alcohol consumption with HF and DCM.
• This may be explained by the fact that the increased catalase activity in those who have a long history of alcohol abuse may represent a protective and adoptive reaction to the persistent high ethanol levels 11.
• According to several articles, even moderate alcohol use has comparable effects to abstinence.
• Diastolic dysfunction, characterized by impaired left ventricular relaxation and reduced diastolic filling capacity, serves as an early indicator of ACM.
• Recent data favored a role for micro RNA, such as the involvement of miR-378a-5p in cardiomyocyte apoptosis and ACM development through ALDH2 gene suppression 120.

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. The outlook for people with alcoholic cardiomyopathy varies depending on how long alcohol was abused and how much alcohol was consumed during that time. In cases where the damage to the heart is severe, the chances of complete recovery are low.

National trends in hospitalizations and outcomes in patients with alcoholic cardiomyopathy

In fact, mitochondrial structural changes have been described in chronic alcohol consumers, with swollen megamitochondria and the distortion of inner cristae 107,108. Functionally high ethanol produces disruptions in the myocyte oxidative pattern and decreases in Complex I, II, and IV of the mitochondrial respiratory chain 100,109,110. As a reflection of this metabolic derangement, cytoplasmic lipid droplets and glycogen deposits appear. Occidental Berberi is the term used for the clinical scenario caused by thiamine deficit, a situation commonly present in chronic alcohol misuse, and was attributed as the cause of ACM 68,69. Similarly, electrolyte (Na, K, Ca, Mg, P) deficiencies or disturbances may play a major role in cardiac function, and ethanol misuse may be related to them 52.

• Enzymatic activity changes which are seen in the idiopathic cardiomyopathy including decreased activity of oxygen reduction mitochondrial enzymes, increased fatty acid uptake and increased lysosomal/microsomal enzyme activity can be seen.
• In addition, there is a relevant role on each organ, particularly on defense and adaptive mechanisms, with a clear induction of anti-oxidant, metabolic, and anti-inflammatory protective responses as a result of ethanol aggression 18,25,26.
• Daily consumption of low to moderate amounts of alcohol has beneficial effects on cardiovascular health among both ischemic and non-ischemic patients1-3.
• Alcoholic cardiomyopathy can present with signs and symptoms of congestive heart failure.

Inclusion criteria encompassed articles that focused on ACM or the relationship between alcohol abuse and cardiac dysfunction, involved human subjects or relevant animal models, were written in the English language, and were published within the last 10 years. Meanwhile, we excluded duplicates, case reports, letters, editorials, and reviews not alcoholic cardiomyopathy symptoms specifically addressing ACM. We then proceeded with screening and selection based on the titles and abstracts of the initial search results. Two independent reviewers assessed each article for relevance and eligibility for full-text review. Once the 15 articles were selected (see Appendix Table 1 for the list of included articles), we extracted and organized relevant information from them.

Patient education

Auscultation can help to reveal the apical murmur of mitral regurgitation and the lower parasternal murmur of tricuspid regurgitation secondary to papillary muscle displacement and dysfunction. Third and fourth heart sounds can be heard, and they signify systolic and diastolic dysfunction. Pulmonary rales signify pulmonary congestion secondary to elevated left atrial and left ventricular end-diastolic pressures. Jugular venous distention, peripheral edema, and hepatomegaly are evidence of elevated right heart pressures and right ventricular dysfunction.

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. Transplant-free survival after 7 years was worse among patients with ACM than among those with DCM (41% vs 53%). Among patients who continued drinking heavily, transplant-free survival was significantly worse than in non-drinkers (27% vs 45%). It has been said that ethanol is the “perfect drug” because of its pleasant effects but damaging long-term effect 1,6. It is distributed worldwide, with easy social access, and is pleasant when consumed, with positive sensations of welfare, but its negative effects, which include depressive and damaging noxious health effects, are reserved for later. Ethanol is one of the most addictive drugs for humans, with high physical and psychological addiction potential 7.

Alcohol consumption and risk of cardiovascular disease among hypertensive women

• However, if alcoholic cardiomyopathy is caught early and the damage isn’t severe, the condition can be treated.
• In these studies, the authors estimated the amount and chronicity of alcohol intake and subsequently related the figures to a number of echocardiographic measurements and parameters.
• More specifically, atrial fibrillation with rapid ventricular response is a cause of arrhythmia-induced cardiomyopathy,61 which can potentially worsen LVEF in AC patients, on top of the direct toxic effect of ethanol, acetaldehyde damage, or the aforementioned genetic factors.
• This substance is a potent inhibitor of the enzyme acetaldehyde dehydrogenase, so it increases the presence of acetaldehyde, and it promotes its effects.48,50 The harmful effects of this substance have been found to be exerted at various levels, in both animal and human models.

Surprisingly, the damaged mitochondria not only become less efficient but also increases the generation of ROS that aid the apoptosis process. Furthermore, in contrast to nuclear DNA, mitochondrial DNA is susceptible to oxidative stress due to its close proximity to the formation of ROS and the limited protective mechanisms in place to safeguard DNA integrity. Post-mortem biopsies from the hearts of human alcoholics revealed that the myocardial mitochondria is enlarged and damaged 1-9.