(iii) A meta-analysis of large datasets of eQTLs and pQTLs was conducted to enhance statistical power and evade bias. https://ecosoberhouse.com/ Among tribal population, no differences between the survival and death groups were observed at the baseline in terms of age, sex, chest pain, basal crepts, orthopnoea, PND (paroxysmal nocturnal dyspnoea), JVP (jugular venous pressure), oedema and New York Heart Association (NYHA) classification. The frequencies of atrial fibrillation (AF), atrioventricular block (AVB) and CTP (Score B, C) were higher in the death group and sinus rhythm was observed to be more in the survival group. The QRS duration, LVESD (left ventricular end-systolic dimension) and LVEDD were higher in the death group but the LVEF was lower in the patients of death group than those patients in the in the survival group. In spite of the fact that alcohol plays a major role in the causation of DCM, very few studies have been published on the long-term outcome of patients with ACM in India and there is a major paucity of data comparing ACM in tribal and non-tribal population. This study was undertaken to find out the long-term outcome and prognostic markers of ACM and to compare the different characteristics of the patients between the death and survival groups in tribal and non-tribal population, simultaneously.
1. Clinical features
Although some authors contend that the initial event is the appearance of hypertrophy, the majority accept that the core event is the loss of cardiomyocytes. Basic research studies have described an abundance of mechanisms that could underscore the functional and structural alterations found in ACM. Because of this, their origin could be multifactorial and linked both to the alcohol molecule and to its main metabolite, acetaldehyde.
Study design:
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 amphetamine addiction treatment similar manner to strict non-drinkers. Thus, Nicolás et al73 studied the evolution of the ejection fraction in 55 patients with ACM according to their degree of withdrawal. 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%).
- By inhibiting NOX2 (the most important superoxide-producing enzyme) with apocynin, they observed a decrease in ethanol- and acetaldehyde-induced superoxide levels.
- The synchronization of the physiological circadian rhythm is extremely crucial for metabolic health and is also an important strategy for the treatment of obesity and NAFLD (Ray et al. 2020).
- Experimental studies analysing the depressive properties of alcohol on the cardiac muscle invariably use similar approaches31-39.
Study design and population
The renal, cardiac and hepatic complications were included in the secondary analysis in this study as they are the main causes of disease progression and mortality in diabetic patients (Liu et al. 2024). Approximately 30–40% of patients with T2D concurrently experience DKD, which leading to manifestations such as frailty, diminished quality of life, end-stage renal disease. Diabetic cardiomyopathy (DCM) constitutes a notable complication for patients with T2D and stands as the primary cause of heart failure in individuals afflicted with T2D (Tan et al. 2020). Non-alcoholic fatty liver disease (NAFLD) which may progress to cirrhosis and hepatocellular carcinoma, affecting approximately 25% of the global population. Statistics show that the prevalence of NAFLD in patients with T2D (76%) is significantly higher (Younossi et al. 2016).
Renal tubules are also the site where ferroptosis and other forms of cell death often occur in DKD. Ctsb was mainly enriched in endocardial cells and fibroblasts, where most cell death and fibrosis occur. what is alcoholic cardiomyopathy At the same time, the level of enrichment in macrophages was also higher than that of other cell types (Fig. 6C and Figure S2). While ferroptosis induced by hepatic steatosis and lipid peroxidation may lead to the development of the simple NAFLD to non-alcoholic steatohepatitis (NASH). A second set of studies that are quoted when addressing this topic are those conducted in individuals who started an alcohol withdrawal program21-24. 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.
Myocardial impairment following chronic excessive alcohol intake has been evaluated using echocardiographic and haemodynamic measurements in a significant number of reports. In these studies, haemodynamic and echocardiographic parameters were measured in individuals starting an alcohol withdrawal program. The findings were analysed taking into account the amount and chronicity of intake and they were compared with the same parameters measured in a control group of non-drinkers. Although our hospital is the largest cardiovascular disease hospital that admits patients from all areas of China, the data described herein cannot be extrapolated to the entire ACM population. In addition, because the present study was a retrospective analysis, we did not collect precise information on medication use and alcohol abstinence in the patients with ACM.
Studies that have assessed the prevalence of ACM among IDCM patients have found high alcohol consumption in 3.8% to 47% of DCM patients. The lowest prevalence of ACM among DCM (3.8%) was obtained from a series of 673 patients admitted to hospital consecutively due to HF in the state of Maryland27. This study included not only DCM, but also all causes of left ventricular dysfunction, including hypertensive heart disease, ischemic cardiomyopathy and heart valve disease. Furthermore, the inclusion criteria for ACM were very strict and required a minimum consumption of 8 oz of alcohol (200 g or 20 standard units) each day for over 6 mo.
- Mathews and Kino found a small, but significant increase in left ventricular mass in individuals consuming at least 12 oz of whisky during 6 years and 60 g of ethanol per day, respectively22,40.
- This study identified FRGs in relation to T2D and its complications, which may enhance the understanding of the pathogenic mechanisms of their development.
- This section collects any data citations, data availability statements, or supplementary materials included in this article.
- This study was a retrospective, observational study and a diagnosis of ACM was made in accordance to the definition provided in the European Society of Cardiology consensus document on the classification of cardiomyopathies.
- In accordance with the protocol of each original GWAS datasets, all participants provided informed consent, and all ethical approvals for the GWAS were acquired by the original authors of the GWAS.
- Alcohol-induced cardiomyopathy treatment includes a combination of lifestyle modifications, pharmacological treatment, management of arrhythmia, and supportive care.
Indeed, the first account of the possible harmful effects of alcohol specifically on heart muscle was reported in the latter half of the 19th century. Expressions referring to “the heart of a wine drinker in Tubingen” and particularly a “Munich beer heart” were used and known in Germany during this time13. From January 2013 to December 2016, we collected data of 290 patients with ACM referred for evaluation to the Department of Internal Medicine and Department of Cardiology in our institute RIMS, Ranchi. This study was a retrospective, observational study and a diagnosis of ACM was made in accordance to the definition provided in the European Society of Cardiology consensus document on the classification of cardiomyopathies. 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. In spite of numerous studies, the sequence of events that occur in alcohol-induced myocardial damage is still highly controversial.