Alcoholic Cardiomyopathy Research Articles

Patterns of alcohol consumption in Mexico and mortality from alcohol consumption related diseases: an epidemiological state-clustered study

ABSTRACT Objective The present study aims to describe the patterns of alcohol consumption in Mexico by state, emphasizing the age at onset of alcohol consumption and the epidemiologic magnitude of deaths due to the selected causes related to these medical conditions. Methods This epidemiological study has an observational, descriptive, and retrospective design. A total of 73,088 deaths occurred in Mexico due to alcoholic cardiomyopathy, alcohol-induced pancreatitis, and alcoholic liver disease between 2016 and 2020; the annual rate was 11.3 in 2016 and 12.3 in 2020, showing an increase in the studied period. Results The early onset of alcohol drinking was reported by one of every four responders. Individuals with binge drinking patterns reported an onset of < 18 years of age in 37.8%. At the state level, in Mexico, the early onset of alcohol consumption and binge drinking are directly correlated with age at death due to alcoholic cardiomyopathy, alcohol-induced pancreatitis, and alcoholic liver disease, with average age at death of 55.5 years. Discussion Multilevel, cross-national, and multidisciplinary measures are urgently needed because mortality due to alcohol consumption is a preventable problem. Still, many more issues of social and health-related nature can also be prevented by approaching the alcohol consumption patterns.

Possible involvement of Protein Tyrosine Phosphatase in Alcoholic Cardiomyopathy

Protein tyrosine phosphatases (PTPase’s) are the enzymes that dephosphorylate survival kinase PI3K/Akt pathway this may be a key mechanism in alcohol-induced cardiomyopathy. Therefore, the present study was designed to investigate the role of PTPase in alcohol-induced cardiomyopathy. Ethanol (20%) at the dose of 7.9 g/kg P.o was given regularly for 60 days that produced Alcohol-induced Cardiomyopathy (ACM). CM (cardiomyopathy) was assessed in terms of decrease in LVDP, dp/dtmax, dp/dtmin, LV protein content, CFR and increase in LVEDP, LVW/BW, MABP, LV collagen, LV cholesterol content, TNF-α, nitrite levels and iNOS expression in alcoholic cardiomyopathic rats. Sodium Orthovanadate (SOV) (PTPase inhibitor) at the dose of 2.5, 5 and 10mg/kg significantly increased LVDP, dp/dtmax, dp/dtmin, CFR, LV protein content. Moreover, significant decrease in the elevated MABP, LVEDP, LVW/BW, LV collagen, LV cholesterol content, nitrite, TNF-α and iNOS level was observed. Furthermore, administration of SMT (S-methylisothiourea), an iNOS inhibitor (5mg/kg., i.p) with SOV (10mg/kg., p.o) significantly increased the ameliorative effect of SOV (10mg/kg., p.o). The findings suggested that PTPases may have a function in regulating alcohol-induced cardiomyopathy by interfering with Akt/Pi3k and its downstream pathways, which include TNF-alpha and iNOS.

Burden of alcohol use disorder and its consequences in Iran from 1990 to 2019: Findings from the global burden of disease study

BackgroundThis study aimed to provide an up-to-date evaluation of the burden of alcohol use disorder and its consequences in Iran from 1990 to 2019. MethodsWe assessed the burden of alcohol use disorder and its three subsequent disorders, including cirrhosis and other chronic liver diseases, liver cancer, and cardiomyopathy using Global Burden of Disease (GBD) data. We retrieved data on incidence, prevalence, death, Years of Life Lost from mortality (YLL), Years of healthy life Lost due to Disability (YLD), and Disability-Adjusted Life Year (DALY), which is calculated by summing YLL and YLD values, indices, as well as sociodemographic index (SDI) values. ResultsAge-standardized DALY rate of alcohol use disorder reduced from 55.5 in 1990 to 41.8 per 100,000 in 2019 (−24.1 %). Similarly, age-standardized DALY rates of cirrhosis due to alcohol use (−28.7 %), liver cancer due to alcohol use (−20.9 %), and alcoholic cardiomyopathy (−36.3 %) decreased in Iran from 1990 to 2019. In 2019, alcohol use disorder had the highest DALY rate among individuals younger than 55 years, while cirrhosis due to alcohol use imposed the greatest burden on those older than 55. After adjusting for the year, SDI was negatively associated with the age-standardized DALY rate of liver cancer due to alcohol use (p < 0.001), positively associated with that of alcoholic cardiomyopathy (p = 0.002), and not significantly associated with the burden of other conditions (p > 0.05). ConclusionsDespite reductions in the age-standardized DALY rate of alcohol use disorders and related consequences among Iranians, they remain a serious public health concern in Iran.

Blood microcirculation under conditions of a translational model of alcohol cardiomyopathy in rats

Blood microcirculation under conditions of a translational model of alcohol cardiomyopathy in rats

Phosphoglycerate mutase 5 exacerbates alcoholic cardiomyopathy in male mice by inducing prohibitin-2 dephosphorylation and impairing mitochondrial quality control.

The induction of mitochondrial quality control (MQC) mechanisms is essential for the re-establishment of mitochondrial homeostasis and cellular bioenergetics during periods of stress. Although MQC activation has cardioprotective effects in various cardiovascular diseases, its precise role and regulatory mechanisms in alcoholic cardiomyopathy (ACM) remain incompletely understood. We explored whether two mitochondria-related proteins, phosphoglycerate mutase 5 (Pgam5) and prohibitin 2 (Phb2), influence MQC in male mice during ACM. Myocardial Pgam5 expression was upregulated in a male mouse model of ACM. Notably, following ACM induction, heart dysfunction was markedly reversed in male cardiomyocyte-specific Pgam5 knockout (Pgam5cKO) mice. Meanwhile, in alcohol-treated male mouse-derived neonatal cardiomyocytes, Pgam5 depletion preserved cell survival and restored mitochondrial dynamics, mitophagy, mitochondrial biogenesis and the mitochondrial unfolded protein response (mtUPR). We further found that in alcohol-treated cardiomyocyte, Pgam5 binds Phb2 and induces its dephosphorylation at Ser91. Alternative transduction of phospho-mimetic (Phb2S91D) and phospho-defective (Phb2S9A) Phb2 mutants attenuated and enhanced, respectively, alcohol-related mitochondrial dysfunction in cardiomyocytes. Moreover, transgenic male mice expressing Phb2S91D were resistant to alcohol-induced heart dysfunction. We conclude that ACM-induced Pgam5 upregulation results in Pgam5-dependent Phb2S91 dephosphorylation, leading to MQC destabilisation and mitochondrial dysfunction in heart. Therefore, modulating the Pgam5/Phb2 interaction could potentially offer a novel therapeutic strategy for ACM in male mice. Pgam5 knockout attenuates alcohol-induced cardiac histopathology and heart dysfunction in male mice. Pgam5 KO reduces alcohol-induced myocardial inflammation, lipid peroxidation and metabolic dysfunction in male mice. Pgam5 depletion protects mitochondrial function in alcohol-exposed male mouse cardiomyocytes. Pgam5 depletion normalises MQC in ACM. EtOH impairs MQC through inducing Phb2 dephosphorylation at Ser91. Pgam5 interacts with Phb2 and induces Phb2 dephosphorylation. Transgenic mice expressing a Ser91 phospho-mimetic Phb2 mutant are resistant to ACM.

Alcoholic cardiomyopathy: aspects of pathogenesis and clinic

Alcoholic cardiomyopathy is the most common form of myocardial damage caused by ethanol. Ethanol and its main active metabolite acetaldehyde have a direct toxic effect on the myocardium. The mechanisms of the cardiotoxic effect of ethanol are diverse and include membranotropic action, damage to cellular organelles, activation of lipid peroxidation, and a number of others. Dissolving in the lipids of biological membranes, ethanol changes their physico-chemical properties, disrupts the activity of membrane receptors, eventually disconnecting the connection of excitation with the contraction of cardiomyocytes. Particular importance in the pathogenesis of alcoholic cardiomyopathy is attached to the ability of ethanol to cause structural and functional changes in mitochondria, which is directly related to the violation of oxidative processes and energy supply of the myocardium as a whole. Under the influence of alcohol, free-radical lipid oxidation products content increases and antioxidants activity decreases, which indicates oxidative stress development. The deterioration of myocardial contractility due to chronic alcohol intoxication triggers a cascade of compensatory mechanisms in the form of cardiomyocyte hypertrophy and progressive fibrosis, while adaptive reactions become a factor in further pathological changes. Ethanol causes myocardial damage in a dose-dependent manner.The probability of alcoholic cardiomyopathy occurrence is a derivative of the total accumulated dose of alcohol and individual predisposition. Alcoholic cardiomyopathy is considered as a variant of secondary dilated cardiomyopathy with all its clinical manifestations and consequences: dilation of the heart chambers, low left ventricular ejection fraction, progressive circulatory insufficiency, and cardiac arrhythmias. A relatively favorable prognosis in alcoholic cardiomyopathy is provided due to partial reversibility of myocardial damage under the condition of abstinence from alcohol consumption. Specific drugs for the treatment of alcoholic cardiomyopathy have not been developed. New treatment strategies include the use of myocardial growth and regulation factors synthesized by cardiomyocytes, as well as the stimulation of heart muscle regeneration and repair processes.

A Comprehensive Review on Alcohol Abuse Disorder Fatality, from Alcohol Binges to Alcoholic Cardiomyopathy.

Frequent and excessive consumption of alcohol, be it episodic or sustained misuse, ranks among the top causes of mortality globally. This comprehensive analysis seeks to elucidate how alcohol misuse precipitates death, with a particular focus on associated cardiac anomalies. Notably, the phenomenon of "Holiday Heart Syndrome", linked to binge drinking, is recognized for inducing potentially fatal cardiac arrhythmias. Moreover, persistent alcohol consumption is implicated in the development of alcoholic cardiomyopathy, a condition that underlies heart failure and arrhythmic disturbances of the heart. Additionally, individuals undergoing withdrawal from alcohol frequently exhibit disruptions in normal heart rhythm, posing a risk of death. This review further delves into additional alcohol-related mortality factors, including the heightened likelihood of hypertension, cerebrovascular accidents (strokes), and the connection between excessive alcohol use and Takotsubo syndrome.

Alcoholic Cardiomyopathy: a summary of current knowledge and possible future directions

Introduction and purpose: Ethanol is still one of the most frequently consumed drugs worldwide and is a strong risk factor for more than 60 illnesses including alcoholic cardiomyopathy which is a specific heart muscle disease caused by long-term excessive alcohol consumption. The review aims to gather available data and summarize it to give better understanding of the disease, to help select patients with the condition to implement proper treatment, and to present possible future directions as the incidence of the disease is projected to persist in the future. Brief description of the state of knowledge: Alcoholic cardiomyopathy (ACM) is characterized by dilation, increased mass of the left ventricle, and reduced ejection fraction leading to end-stage heart failure. It is caused by ethanol’s direct toxicity on myocytes disturbing many different metabolic pathways. The result is a decrease in both systolic and diastolic function of the heart. The ACM development depends on factors such as genetics, gender, dietary factors and the dosage of ethanol consumption. The goal of the treatment is total alcohol abstinence, but the reduction of ethanol intake may also be beneficial. Patients should obtain a complete pharmacological treatment for heart failure. Summary: Ethanol overconsumption remains an unresolved problem, with the incidence of ACM projected to persist in the future, especially among patients with alcohol use disorder (AUD). Efforts for prevention, early detection, and effective treatment of ACM need to be established. A primary focus should be on treating AUD because it is the most effective way to halt the progression of the disease. Further research should focus on both asymptomatic and symptomatic patients with AUD to better define clinical manifestations, diagnostic approaches, and the most effective treatments for ACM.

The burden of alcohol-related cardiovascular complications in young and middle-aged adults: rising burden of atrial fibrillation and hypertensive heart disease

Background and Aims The burden of alcohol-related complications is high and rising. However, there are notable deficiencies in comprehensive epidemiological study focusing on cardiovascular complications from alcohol, especially among young and middle-aged adults. We thus aimed to determine the burden of these conditions in young and middle-aged adults globally. Methods and Results We used data from the Global Burden of Disease Study 2019 and analysed the mortality and disability-adjusted life years of alcohol-associated cardiovascular complications in young and middle-aged adults. The findings were classified by sex, region, country, and Sociodemographic Index (SDI). The highest age-standardized death rates (ASDR) were observed in stroke 0.84 (95% UI 0.60–1.09), followed by alcoholic cardiomyopathy 0.57 (95% UI 0.47–0.66) per 100,000 population. The overall burden of alcohol-associated cardiovascular complications decreased globally but increased in atrial fibrillation and hypertensive heart disease. Regionally, most regions underwent a decrease in ASDR, but an increase was observed in Southeast Asia (+2.82%), Western Pacific (+1.48%), low-middle (+1.81%), and middle SDI (+0.75%) countries. Nevertheless, the ASDR and ASDALYs were highest in Europe. Conclusions The impact of alcohol-associated atrial fibrillation and hypertensive heart disease has increased over the last decades. Regarding region, the burden in Europe and the rising burden in Asia, require immediate public health policy to lessen these cardiovascular complications from alcohol in young and middle-aged adults.

Biventricular Impairment and Ventricular Interdependence in Patients With Alcoholic Cardiomyopathy: Insights Through Cardiac Magnetic Resonance Imaging.

Alcoholic cardiomyopathy (ACM) can lead to progressive cardiac dysfunction and heart failure, but little is known about biventricular impairment and ventricular interdependence (VI) in ACM patients. To use cardiac MRI to investigate biventricular impairment and VI in ACM patients. Retrospective. Forty-one male patients with ACM and 45 sex- and age-matched controls. 3.0 T/balanced steady-state free precession sequence, inversion recovery prepared echo-planar imaging sequence and phase-sensitive inversion recovery sequence. Biventricular structure, function, and global strain (encompassing peak strain [PS], peak systolic, and diastolic strain rate), PS of interventricular septal (IVS), microvascular perfusion (including upslope and time to maximum signal intensity [TTM]), late gadolinium enhancement (LGE), and baseline characteristics were compared between the controls and ACM patients. Student's t-test, Mann-Whitney U test, Pearson's correlation, and multivariable linear regression models with a stepwise selection procedure. A two-tailed P value <0.05 was deemed as statistically significant. Compared to control subjects, ACM patients showed significantly biventricular adverse remodeling, reduced left ventricle (LV) global upslope and prolonged global TTM, and the presence of LGE. ACM patients were characterized by a significant decline in all global strain within the LV, right ventricle (RV), and IVS compared with the controls. RV global PS was significantly associated with LV global PS and IVS PS in radial, circumferential, and longitudinal directions. Multivariable analyses demonstrated the longitudinal PS of IVS was significantly correlated with RV global radial PS (β = 0.614) and circumferential PS (β = 0.545). Additionally, RV global longitudinal PS (GLPS) was significantly associated with radial PS of IVS (β = -0.631) and LV GLPS (β = 1.096). ACM patients exhibited biventricular adverse structural alterations and impaired systolic and diastolic function. This cohort also showed reduced LV microvascular perfusion, the presence of LGE, and unfavorable VI. 3 TECHNICAL EFFICACY: Stage 3.

Socioeconomic position indicators and risk of alcohol-related medical conditions: A national cohort study from Sweden.

Alcohol consumption contributes to excess morbidity and mortality in part through the development of alcohol-related medical conditions (AMCs, including alcoholic cardiomyopathy, hepatitis, cirrhosis, etc.). The current study aimed to clarify the extent to which risk for these outcomes differs as a function of socioeconomic position (SEP), as discrepancies could lead to exacerbated health disparities. We used longitudinal Swedish national registries to estimate the individual and joint associations between 2 SEP indicators, educational attainment and income level, and risk of AMC based on International Classification of Diseases codes, while controlling for other sociodemographic covariates and psychiatric illness. We conducted Cox proportional hazards models in sex-stratified analyses (N = 1,162,679 females and N = 1,196,659 males), beginning observation at age 40 with follow-up through December 2018, death, or emigration. By the end of follow-up, 4,253 (0.37%) females and 11,183 (0.93%) males had received an AMC registration, corresponding to overall AMC incidence rates among females and males of 2.01 and 5.20, respectively. In sex-stratified models adjusted for birth year, marital status, region of origin, internalizing and externalizing disorder registrations, and alcohol use disorder (AUD) registration, lower educational attainment was associated with higher risk of AMC in both females (hazard ratios [HRs] = 1.40 to 2.46 for low- and mid-level educational attainment across 0 to 15 years of observation) and males (HRs = 1.13 to 1.48). Likewise, risk of AMC was increased for those with lower income levels (females: HRs = 1.10 to 5.86; males: HRs = 1.07 to 6.41). In secondary analyses, we further adjusted for aggregate familial risk of AUD by including family genetic risk scores for AUD (FGRSAUD), estimated using medical, pharmacy, and criminal registries in extended families, as covariates. While FGRSAUD were associated with risk of AMC in adjusted models (HR = 1.17 for females and HR = 1.21 for males), estimates for education and income level remained largely unchanged. Furthermore, FGRSAUD interacted with income level, but not education level, such that those at higher familial liability to AUD were more susceptible to the adverse effect of low income. Limitations of these analyses include the possibility of false negatives for psychiatric illness registrations, changes in income after age 40 that were not accounted for due to modeling restrictions, restriction to residents of a high-income country, and the inability to account for individual-level alcohol consumption using registry data. Using comprehensive national registry data, these analyses demonstrate that individuals with lower levels of education and/or income are at higher risk of developing AMC. These associations persist even when accounting for a range of sociodemographic, psychiatric, and familial risk factors. Differences in risk could contribute to further health disparities, potentially warranting increased screening and prevention efforts in clinical and public health settings.

Clinical and cardiac MRI characteristics: prognosis in patients with alcoholic cardiomyopathy

Alcoholic cardiomyopathy (ACM) is recognized as a type of non-ischemic dilated cardiomyopathy (DCM). To date, the clinical prognosis of ACM remains a topic of debate in previous studies and there are limited studies on its cardiac MRI characteristics. The aim of this study was to summarize the clinical and MRI features of ACM patients and to identify the predictors of adverse prognosis based on clinical characteristics and MRI imaging findings. Adult patients who were clinically diagnosed with ACM and underwent enhanced CMR between September 2015 and August 2022 were retrospectively enrolled. The primary endpoints were major adverse cardiovascular events, including cardiac-related death, heart transplantation, hospitalization for heart failure and life-threatening ventricular arrhythmias (sustained ventricular tachycardia, ventricular fibrillation, or ICD shock). The risk factors associated with these primary end points were identified using multivariable Cox analysis. A total of 62 ACM patients (50±9 years, 62 men) were included. The majority of patients presented with symptoms of heart failure. Over a median follow-up period of 30.3 months (IQR 12.2-57.7 months), 24 patients reached the primary endpoints. For clinical variables, multivariable analysis showed that drinking duration (HR=1.05; 95%CI:1.01, 1.11; p=0.03) and persistent drinking (HR=3.71; 95%CI:1.46, 9.44; p=0.01) were associated with MACE. For CMR variables, late gadolinium enhancement (LGE) percent (HR = 1.09; 95% CI: 1.03, 1.14; p<0.001) stood out as an independent predictor for MACE. In ACM patients, persistent drinking and cardiac MRI-defined myocardial scar were associated with adverse outcomes such as cardiac death, heart transplantation, hospitalization for heart failure or life-threatening ventricular arrhythmias.

Elevated levels of alcohol dehydrogenase aggravate ethanol-evoked cardiac remodeling and contractile anomalies through FKBP5-yap-mediated regulation of ferroptosis and ER stress

Alcohol intake provokes severe organ injuries including alcoholic cardiomyopathy with hallmarks of cardiac remodeling and contractile defects. This study examined the toxicity of facilitated ethanol metabolism in alcoholism-evoked changes in myocardial morphology and contractile function, insulin signaling and various cell death domains using cardiac-selective overexpression of alcohol dehydrogenase (ADH). WT and ADH mice were offered an alcohol liquid diet for 12 weeks prior to assessment of cardiac geometry, function, ER stress, apoptosis and ferroptosis. Alcohol intake provoked pronounced glucose intolerance, cardiac remodeling and contractile anomalies with apoptosis, ER stress, and ferroptosis, the effects were accentuated by ADH with the exception of global glucose intolerance. Hearts from alcohol ingesting mice displayed dampened insulin-stimulated phosphorylation of insulin receptor (tyr1146) and IRS-1 (tyrosine) along with elevated IRS-1 serine phosphorylation, the effect was augmented by ADH. Alcohol challenge dampened phosphorylation of Akt and GSK-3β, and increased phosphorylation of c-Jun and JNK, the effects were accentuated by ADH. Alcohol challenge promoted ER stress, FK506 binding protein 5 (FKBP5), YAP, apoptosis and ferroptosis, the effects were exaggerated by ADH. Using a short-term ethanol challenge model (3 g/kg, i.p., twice in three days), we found that inhibition of FKBP5-YAP signaling or facilitated ethanol detoxification by Alda-1 alleviated ethanol cardiotoxicity. In vitro study revealed that the ethanol metabolite acetaldehyde evoked cardiac contractile anomalies, lipid peroxidation, and apoptosis, the effects of which were mitigated by Alda-1, inhibition of ER stress, FKBP5 and YAP. These data suggest that facilitated ethanol metabolism via ADH exacerbates alcohol-evoked myocardial remodeling, functional defects, and insulin insensitivity possibly through a FKBP5-YAP-associated regulation of ER stress and ferroptosis.

Clinical Trajectories and Long-Term Outcomes of Alcoholic Versus Other Forms of Dilated Cardiomyopathy

Alcoholic cardiomyopathy (ACM) is a form of dilated cardiomyopathy (DCM) occurring secondary to long-standing heavy alcohol use and is associated with poor outcomes, but the cause-specific risks are insufficiently understood. Between 1997 and 2018, we identified all patients with a first diagnosis of ACM or DCM. The cumulative incidence of different causes of hospitalisation and mortality in the two groups was calculated using the Fine-Gray and Kaplan-Meier methods. A Total of 1,237 patients with ACM (mean age 56.3±10.1 years, 89% men) and 17,211 individuals with DCM (mean age 63.6±13.8 years, 71% men) were identified. Diabetes (10% vs 15%), hypertension (22% vs 31%), and stroke (8% vs 10%) were less common in ACM than DCM, whereas obstructive lung disease (15% vs 12%) and liver disease (17% vs 2%) were more prevalent (p<0.05). Cumulative 5-year mortality was 49% in ACM vs 33% in DCM, p<0.0001, multivariable adjusted hazards ratio 2.11 (95% confidence interval 1.97-2.26). The distribution of causes of death was similar in ACM and DCM, with the predominance of cardiovascular causes in both groups (42% in ACM vs 44% in DCM). 5-year cumulative incidence of heart failure hospitalisations (48% vs 54%) and any somatic cause (59% vs 65%) were also similar in ACM vs DCM. At 1 year, the use of beta blockers (55% vs 80%) and implantable cardioverter defibrillators (3% vs 14%) were significantly less often used in ACM vs DCM. Patients with ACM had similar cardiovascular risks and hospitalisation patterns as other forms of DCM, but lower use of guideline-directed cardiovascular therapies and greater mortality.

Alcoholic Cardiomyopathy: Drinking to Excess

Alcoholic Cardiomyopathy: Drinking to Excess

Кросс-секционное исследование потребления алкоголя с вредными последствиями у пациентов кардиологического профиля, госпитализированных по неотложным показаниям в многопрофильный стационар

Background. Alcohol use affects many aspects of the functioning of the cardiovascular system. It causes an increased risk of: hypertension; pathological conditions caused by disorders of generation and conduction of electrical signals in the myocardium; cardiovascular diseases such as ischaemic and haemorrhagic strokes. Aim of the study. To study the prevalence of alcohol consumption among acutely ill cardiac patients, not requiring intensive care, hospitalized in a multidisciplinary urban clinical hospital, using screening self-questionnaires (AUDIT-4) and a highly sensitive and specific marker of chronic alcohol intoxication phosphatidylethanol (PEth). Materials and Methods. Using AUDIT-4 and PEth, we studied the prevalence of alcohol use in cardiac patients with regard to their socio-demographic characteristics. Statistical analysis was performed using IBM SPSS Statistics 25.0 software. We applied descriptive statistics and logistic regression model to estimate adjusted odds ratio for socio-demographic and diagnostic cofactors associated with alcohol abuse. Study results. PEth values in peripheral blood of 0.3 µmol/l or more, indicating excessive alcohol consumption during 2-4 weeks prior to hospitalization, were noted in 8.9% of patients. At the same time, 3.0% of patients admitted the fact of alcohol consumption during the day preceding hospitalization. The presence of only one patient with a diagnosis of alcoholic cardiomyopathy is noteworthy. Negatively associated with PEth level ≥0.3 μmol/L were patients in age group ≥71 compared with patients aged 18-40 as the reference group, (AOR 0.058; CI 95% 0.009-0.379; p&lt;0.003) and women compared with men (AOR 0.227, CI 95% 0,113-0,445; р&lt;0,001). There was a positive association with PEth level ≥0.3 μmol/L for patients who defined their marital status as divorced/separated compared to the reference group married/married/civil partnership (AOR 2.535; CI 95% 1.218-5.276; p=0.013). A significant positive association with a PEth level ≥0.3 μmol/L (AOR 6.668; CI 95% 2.592-17.155; p&lt;0.001) was observed in those who admitted drinking alcoholic beverages within 24 hours before hospitalization compared with the reference group who denied it. Diagnostic groups had no statistically significant associations with the outcome variable. Conclusions. Our findings support the need for brief anti-alcohol interventions by primary care physicians, especially when diagnosing alcohol-associated conditions in cardiac patients. It seems necessary to aim internists to work more carefully with diagnoses of alcohol-associated and alcohol-attributable conditions.

Protective Effect of Deer Heart Peptide on Cardiac Injury in Mice.

Peptides are widely used as natural bio-small molecules because of their various pharmacological activities such as enhancing immunity, promoting wound healing, and improving inflammation. Alcoholic heart injury has become one of the major health problems worldwide, and alcohol consumption is now the main cause of alcoholic cardiomyopathy. In this study, deer heart peptides were extracted from deer hearts by enzymatic digestion and the antioxidant activity of deer heart peptides extracted at different times was evaluated by three in vitro antioxidant methods, and the active peptide with the best enzymatic effect has been selected for in vivo animal experiments. The anti-inflammatory and antioxidant properties of deer heart enzymatic extracts were evaluated in in vivo experiments in mice. In this study, mice were orally gavaged with white wine (12 mL/kg body weight) to induce a mouse model of cardiac injury, while mice were orally administered a single dose of 100 mg/kg/bw and 200 mg/kg/bw of deer heart enzyme digest and were examined for body weight, dietary intake, water intake, and coat gloss, as well as for general behaviors, adverse effects, and mortality. Histology, serum, anti-inflammatory factors, and oxidative stress parameters were subsequently assessed. In all modeled mice, no four-way or any significant behavioral changes were observed in all groups, but in the modeled group, mice showed weight loss, decreased diet and water intake, and decreased cardiac index. For in vivo tests, the extract inhibited the anti-inflammatory activity with a significant decrease in inflammatory factors of TNF-α, IL-6, and IL-1β in cardiac tissues, a significant increase in serum levels of both CAT and SOD, an increase in MDA content, and a remarkable increase in the level of the marker CK in the cardiac myocardial enzyme profile. Significant improvement in myocardial disorders by deer heart peptide could be observed from heart tissue sections. The present study emphasizes the anti-inflammatory and antioxidant activity of deer heart peptide, an enzymatic digest of deer heart, which provides empirical as well as supportive role for the anti-inflammatory properties of traditional medicine.

Factors influencing in-hospital mortality for salvage percutaneous transjugular intrahepatic portosystemic shunting in cirrhotic patients with recalcitrant variceal bleeding after failed endoscopic intervention

Background. Endoscopic therapy is the first-line treatment of choice for control of acute variceal bleeding (AVB). In high-risk patients with persistent AVB despite pharmacological treatment and endoscopic intervention, percutaneous transjugular intrahepatic portosystemic shunting (TIPS) provides a minimally invasive salvage method to reduce portal pressure and control bleeding. Objectives. To evaluate factors influencing in-hospital mortality after salvage TIPS (sTIPS) in patients with exsanguinating variceal bleeding despite medical treatment and endoscopic intervention. Methods. Clinical and laboratory data were analysed in all patients treated with sTIPS following failed endoscopic therapy for AVB between August 1991 and November 2020. Factors associated with and predictors of death were determined using bivariate analysis and univariate logistic regression analysis. Results. Thirty-four patients (29 men, 5 women), mean age 52 years (range 31 - 80), received sTIPS for uncontrolled (n=11) or refractory (n=23) AVB. The causes of portal hypertension were alcohol-related (n=24) and non-alcohol-related cirrhosis. Salvage TIPS controlled bleeding in 32 patients, with recurrence in 1. Ten patients died in hospital (mean 4.8 days, range 1 - 10) of liver failure (n=4), multiorgan failure (n=3), alcoholic cardiomyopathy (n=2) and uncontrolled gastric variceal bleeding (n=1). On bivariate analysis, factors associated with death were Child-Pugh (C-P) score ≥10 (p=0.006), sodium Model for End-stage Liver Disease (MELD-Na) score ≥22 (p&lt;0.001), ≥8 units of blood transfused (p&lt;0.001), Sengstaken-Blakemore balloon tube placement (p&lt;0.001), endotracheal intubation (p&lt;0.001), inotropic support (p&lt;0.001) and endoscopically uncontrolled bleeding (p&lt;0.001). Univariate logistic regression analysis showed that the most significant predictors of mortality were inotrope dependency (odds ratio (OR) 134; p&lt;0.001), endotracheal intubation (OR 99; p&lt;0.001), endoscopically uncontrolled bleeding (OR 28; p=0.001), grade 3 ascites (OR 20.9; p=0.012) and C-P grade C (OR 8.8; p=0.011). Conclusion. Salvage TIPS controlled variceal bleeding in 94% of patients after failed endoscopic therapy with 29% in-hospital mortality. The most significant predictors of mortality were C-P grade C, grade 3 ascites, inotrope requirement, endotracheal intubation and endoscopically uncontrolled bleeding.

Alcohol and Heart Failure

Alcohol is the most frequently consumed toxic substance in the world and remains a major global public health issue, with one in three adults consuming it worldwide. Alcohol use is a leading risk factor for disease, contributing to over 60 acute and chronic health conditions, with a particularly complex association with cardiovascular disease. Chronic excessive alcohol consumption is associated with a range of cardiac complications, including decreased myocardial contractility, hypertension, arrhythmias, MI and heart failure. However, low-level alcohol consumption is believed to have a protective effect against ischaemic heart disease and diabetes. In most cohort studies, small to moderate amounts of alcohol consumption have not been linked to heart failure, indicating a threshold effect of alcohol with individual (possibly genetic) predisposition rather than a continuous effect of exposure. This review article explores the potential benefits of alcohol on the heart, the association between alcohol use and alcoholic cardiomyopathy and the epidemiology, clinical correlates and management of alcoholic cardiomyopathy.

ABHD5 protects cardiac function in alcoholic cardiomyopathy via HDAC4-NT to inhibit CAMKII/MEF2 axis.

Excessive intake of Alcohol is associated with a high incidence of alcoholic cardiomyopathy (ACM), which may impair cardiac function. In our study, we explored the Abhydrolase Domain Containing 5 (ABHD5) mechanism in ACM about histone deacetylase 4 (HDAC4) and CaM-CaMKII/MEF2 signaling pathway. Rat models of ACM were established in Wistar rats, and in vitro cell models were constructed in rat cardiomyocytes H9C2 utilizing 12-h of treatment of Alcohol (200 mM) to study the regulatory role of ABHD5 in ACM with the involvement of HDAC4 and CaM-CaMKII/MEF2 signaling pathway, as evidenced by determination of cardiac function, myocardial fibrosis, apoptosis of cardiomyocytes and oxidative stress condition. We found that both ABHD5 mRNA and protein expression was significantly lower in the ACM rats and rat cardiomyocytes H9C2. ACM rats with oe-ABHD5 injection showed repressed myocardial hypertrophy and myocardial fibrosis. Also, overexpression of ABHD5 reduced apoptosis and oxidative stress in H9C2 cells. Mechanistic studies demonstrated that ABHD5 via HDAC4-NT inhibits CAMKII/MEF2 axis. This study highlighted that ABHD5 decreased cardiac hypertrophy and myocardial fibrosis and limited cardiomyocyte apoptosis and oxidative stress injury in ACM.