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Alcohol Pharmacology and Pharmacotherapy of Alcoholism
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Aman Upaganlawar, Sindhu Ramesh, Ellery Jones, Vishnu Suppiramaniam, Timothy Moore, Muralikrishnan Dhanasekaran
Left ventricular dysfunction and decreased cardiac contractility, subsequently leading to cardiomyopathy is noted in chronic alcoholics. Alcohol-dependent patients who discontinue drinking are seen to have improved prognosis associated with alcoholic cardiomyopathy. Men have decreased risk alcoholic cardiomyopathy when compared to women (UrbanoMárquez et al., 1995). Abstinence remains the principal treatment as most of alcoholic cardiomyopathy patients who prolong drinking habits die within 3–5 years.
Barbiturates, Alcohol, And Tranquilizers
Published in S.J. Mulé, Henry Brill, Chemical and Biological Aspects of Drug Dependence, 2019
Alcoholic cardiomyopathy occurs in patients with a long history of excessive alcohol ingestion. These individuals most commonly notice dyspnea upon exertion, palpitations, night cough, weakness, and edema. In the early stages tachycardia or atrial fibrillation is seen. In later stages cardi-omegaly with frank signs of heart failure develop. Among the electrocardiographic changes considered by some authorities to be distinctive in this form of heart failure are an early “spinous” T wave (needle-like spike), and a T wave which has either a shallow notch or deeper cleft at its summit. These effects may be due to progressive myocardial fibrosis which may eventually lead to inversion of the T wave. Electrocardiographic evidence of atrioventricular block is also common.
Heart failure
Published in Clive Handler, Gerry Coghlan, Nick Brown, Management of Cardiac Problems in Primary Care, 2018
Clive Handler, Gerry Coghlan, Nick Brown
Alcohol should be consumed only in moderation, because it increases weight and can be arrhythmogenic in patients with more advanced stages of heart failure and structural heart disease. It should be avoided in patients with alcoholic cardiomyopathy.
Atorvastatin reduces alcohol-induced endoplasmic reticulum stress in AC16 cardiomyocytes
Published in Scandinavian Cardiovascular Journal, 2019
Ning Li, Chengyan Wen, Pinghe Huang, Yang Tao, Feng Jin, Xin Liu
Alcoholic cardiomyopathy (ACM) is a non-ischemic dilated heart muscle condition caused by heavy, chronic ethanol consumption. Its major clinical manifestations are cardiac enlargement, cardiac insufficiency, and arrhythmia [1]. Studies have shown that ACM pathogenesis involves several mechanisms at different layers and levels. These include the ethanol metabolic pathway, nutritional imbalance, oxidative stress, cell necrosis and apoptosis, and calcium dyshomeostasis [2,3]. Some studies have also shown that in ACM patients, dyslipidemia is very common, and statins are the most commonly used therapeutic agents for dyslipidemia. In recent years, increased attention has been given to the role of endoplasmic reticulum stress (ERS) in ACM pathogenesis. Previous studies mainly focused on the effects of ERS on the liver, kidney, nervous system, pancreas, and certain types of tumors [4,5]. In contrast, relatively few studies have examined the effects of ERS on cardiomyocytes or ACM cell models.
Mechanisms of toxic cardiomyopathy
Published in Clinical Toxicology, 2019
The existence of a direct causal link between excessive alcohol intake and the development of dilated cardiomyopathy is still controversial, but alcoholic cardiomyopathy is now considered as a distinct entity [38,39]. Basic research is still ongoing to identify the mechanisms of alcohol-induced damage to the cardiomyocyte. It is now well accepted that the mechanisms are multifactorial and would include at least the following: apoptosis, alterations of the excitation–contraction coupling in cardiac myocytes, structural and functional alterations of the mitochondria and sarcoplasmic reticulum, changes in cytosolic calcium flows, changes in calcium sensitivity of myofilaments, alterations of mitochondrial oxidation, deregulation of protein synthesis, decrease of contractile proteins and disproportion between the different types of myofibrils, changes in the regulation of myosin ATPase, up-regulation of the L-type calcium channels, increase of oxidative stress, induction of ANP and p21 mRNA expression in ventricular myocardium, and activation of the renin–angiotensin system and of the sympathetic nervous system [38–43]
Aldehyde dehydrogenase-2 as a therapeutic target
Published in Expert Opinion on Therapeutic Targets, 2019
Mitsuru Kimura, Akira Yokoyama, Susumu Higuchi
Acetaldehyde is also considered to regulate cardiac toxicity. Excessive ethanol consumption causes alcoholic cardiomyopathy characterized by structural and functional changes of the myocardium [57,58]. Even light to moderate ethanol consumption is reported to be associated with structural and functional cardiac changes including greater mass of the left ventricle and worsening of the diastolic function, particularly among carriers of inactive ALDH2 [59]. Ueta et al. reported that the effect of acetaldehyde was bimodal; low levels of acetaldehyde demonstrated a cardio-protective effect but high levels caused cardiac damage in an ex vivo model of ischemia/reperfusion injury [60].