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 drug addiction treatment various levels, in both animal and human models. The pathophysiology of AC involves a combination of direct toxic effects of alcohol on the myocardium, oxidative stress, mitochondrial dysfunction, and genetic susceptibility. Among non-tribal population, no differences in the death and survival groups were observed at the baseline in terms of age, sex, chest pain, basal crepts, orthopnoea, PND, JVP and oedema.
3. Statistical analysis
- 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.
- The suspicion that there may be an individual susceptibility to this disease is underscored by the finding that only a small group of alcoholics develop ACM, and that a proportional relationship between myocardial damage and alcohol intake has not been proven.
- Also, current common cardiac therapies such as ICD and CRT devices were not used because of the period when the study was conducted.
And there is no significant correlation between dataset pairs in the analysis of DKD, DCM and NAFLD (Fig. 2, Table S2). Additionally, it should be noted that there are results with rg greater than 1 in HDL analysis. Here’s both the LDSC and HDL developers explain that when the real rg is close to the boundary (− 1 or 1) (Table S2), it’s possible that the estimate (true rg + error) will be greater than 1 (Bulik-Sullivan et al. 2015; Ning et al. 2020). We perform Bayesian colocalization analysis to assess whether FRGs and T2D were consistent with a shared causal variant based on the “coloc” package with default parameters.
Genetic correlation analysis
The diagnosis of ACM is usually one of exclusion in a patient with DCM with no identified cause and a long history of heavy alcohol abuse. According to most studies, the alcohol consumption required to establish a diagnosis of ACM is over 80 g per day during at least 5 years9-12. Unfortunately, it is well known that abstinence is difficult to achieve, and it is important to stress that alternative treatments are needed, including therapies to help with alcohol withdrawal, heart failure drugs, and other promising therapeutic approaches that focus on pathogenesis. Our study indicated that the QRS duration, systolic blood pressure, and New York Heart Association classification at admission provided independent prognostic information in patients with ACM.
Data Availability
In contrast, European studies focusing on the prevalence of ACM included only subjects diagnosed with DCM and applied the consumption threshold of 80 g/d what is alcoholic cardiomyopathy for ≥ 5 years, finding an ACM prevalence of 23%-47% among idiopathic DCM patients9-12 (Figure 1). Despite the key clinical importance of alcohol as a cause of DCM, relatively few studies have investigated the effects of alcohol on the heart and the clinical characteristics of DCM caused by excessive alcohol consumption (known as alcoholic cardiomyopathy). Askanas et al21 found a significant increase in the myocardial mass and of the pre-ejection periods in drinkers of over 12 oz of whisky (approximately 120 g of alcohol) compared to a control group of non-drinkers. However, no differences were found in these parameters between the sub-group of individuals who had been drinking for 5 to 14 years and the sub-group of individuals who had a drinking history of over 15 years. Kino et al22 found increased ventricular thickness when consumption exceeded 75 mL/d (60 g) of ethanol, and the increase was higher among those subjects who consumed over 125 mL/d (100 g), without specifying the duration of consumption. In another study on this topic, Lazarević et al23 divided a cohort of 89 asymptomatic individuals whose consumption exceeded 80 g/d (8 standard units) into 3 groups according to the duration of their alcohol abuse.
The frequencies of CTP (Grade B, C), NYHA (class III/IV) classification, AF and AVB were higher in the death group and sinus rhythm was observed to be more in the patients of survival group. The QRS duration, LVESD and LVEDD were higher in the https://ecosoberhouse.com/ death group and LVEF was observed to be lower in the patients of death group than those in the survival group. In this respect, a higher prevalence of excessive alcohol consumption has been reported among individuals diagnosed with DCM than in the general population8. Since those 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.
- Another nutritional factor classically involved in the pathophysiology of AC was cobalt excess.
- Timely visit to the medical facility and with proper management, morbidity and mortality of patients with ACM in tribal population would be reduced.
- Despite these features, the structural changes do not seem to be specific, furthermore, they are not qualitatively different from those found in idiopathic DCM and they do not allow us to differentiate between the two conditions44.
- 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.
Subjects with a shorter period of alcohol abuse, from 5 to 10 years, had a significant increase in left ventricular diameter and volume compared to the control group. DCM, dilated cardiomyopathy; HF, heart failure; HFrEF, heart failure with reduced ejection fraction; HTx, heart transplant; LVEDD, left ventricular end-diastolic diameter; LVEF, left ventricular ejection fraction; SD, standard deviation. We performed genetic correlation analyses via the Linkage Disequilibrium Score and High-Definition Likelihood approaches for type 2 diabetes (T2D) and its complications. The data concerning the expression of ferroptosis-related genes (FRGs) were obtained from the meta-analysis of studies on gene expression and protein abundance.
- (B) Kaplan-Meier plots displaying the estimated survival probability in groups categorised according to LVEF.
- Normally distributed variables were presented as the means and SD, whereas non-normally distributed variables were expressed as the medians and IQRs.
- All 299 patients underwent a routine evaluation including a physical examination, 12-lead electrocardiography, 2-dimensional echocardiography, and a complete biochemical evaluation.