The Prognostic Factors of Alcoholic Cardiomyopathy: A single-center cohort study PMC

Also, acute alcohol administration in a rat model significantly raised plasma cardiac troponin T level after 2.5 h (11). In our patient, the elevated troponin T is suggestive of acute myocardial damage. However, the falling level of troponin T in hospital suggested that the myocardial damage had occurred before admission. Her baseline laboratory evaluation showed pancytopenia, abnormal liver function tests (Table 1) and elevated cardiac enzyme levels (Table 2). The initial chest x-ray revealed a normal cardiothoracic ratio and no evidence of heart failure. Her electrocardiogram showed sinus tachycardia, a nonspecific T-wave abnormality and http://kgpi.ru/katalog/priemniki-kupyur/132921.html right axis deviation.

Clinical manifestations and diagnosis of alcohol-induced cardiomyopathy

• In the interim it seems appropriate to continue discouraging any alcohol consumption in these patients, as it would be difficult for them to maintain a limited alcohol intake considering their history of alcohol dependence and abuse.
• As early as in 1915, Lian 45 reported in middle-aged French servicemen during the first world war that heavy drinking could lead to hypertension.
• To our knowledge, our study determined prognostic factors for ACM outcome in the largest cohort of ACM patients described to date.
• This induces a variety of effects, since more than 14 different sites in the myocyte can be affected by ethanol 19,98.
• It took almost 60 years before further attention was paid to the complex interaction between the heart and the peripheral vasculature in various cross-sectional and prospective epidemiologic studies, which have empirically confirmed this early report.

Recently, new cardiomyokines (FGF21, Metrnl) and several growth factors (myostatin, IGF-1, leptin, ghrelin, miRNA, and ROCKs inhibitors) have been described as being able to regulate cardiac plasticity and decrease cardiac damage, improving cardiac repair mechanisms 112,119. They aim to control oxidative damage, myocyte hypertrophy, interstitial fibrosis, and persistent apoptosis. Pharmacological https://acousticlyrics.ru/1996-music/ restoration of autophagic reflux by inhibition of soluble epoxide hydrolase has been described to ameliorate chronic ethanol-induced cardiac fibrosis in an in vivo swine model 151. In addition to these, stem-cell therapy tries to improve myocyte regeneration 112,152. However, these new strategies have not yet demonstrated their real effectiveness in clinical trials, require further evaluation, and are not approved for clinical use 147. Alcohol-induced cardiomyopathy remains a relevant health problem, for which the mainstay of treatment is alcohol abstinence.

Treatment of ACM

In our patient, myocardial biopsy was contemplated, but given the rapid recovery of ventricular function, its diagnostic limitations and the absence of its clinical implications, the risk of this procedure outweighed its benefits, and thus, it was not performed. However, given the characteristic rise and fall of cardiac enzyme levels, this supports the diagnosis of acute alcohol-induced myocardial damage. Improvement in left ventricular function has been observed as early as six months after abstinence from alcohol, and complete recovery can http://rumeds.ru/22890-internat-dlya-psihicheski-nepolnocennyh-lyudey.html be achieved in 18 months (5,6). In an echocardiographic study of 13 patients with alcohol-induced cardiomyopathy, five demonstrated the normalization of left ventricular function after total abstinence for six months (6). Although the severity of histological alterations on endomyocardial biopsy correlates with the degree of heart failure in one of our studies, biopsy is not in common use for prognostic purposes 117. Even the recovery after abstinence of alcohol is hard to predict based on morphometric evaluation of endomyocardial biopsies 118.

Is there an immediate risk of alcohol intake?

• Various pathophysiological mechanisms have been postulated in the development of cardiomyopathy however one key factor undergoing active research is the role of genetic mutation and susceptibility to develop cardiomyopathy.
• In the mid-1960s, another unexpected heart failure epidemic among chronic, heavy beer drinkers occurred in two cities in the USA, in Quebec, Canada, and in Belgium.
• In 1819 the Irish physician Dr. Samuel Black, who had a special interest in angina pectoris described what is probably the first commentary pertinent to the ”French Paradox“ 91.
• They aim to control oxidative damage, myocyte hypertrophy, interstitial fibrosis, and persistent apoptosis.

Finally, it should be noted that McKenna and co-workers, in one of the most frequently cited papers in the ACM field, reported an incidence of 40% in 100 individuals suffering from idiopathic DCM, but in this case the consumption threshold used was only g/d8. Data on the amount of alcohol consumption required to cause ACM are limited and controversial. Moreover, ranolazine prevents ethanol-induced atrial arrhythmias both in vitro and in vivo by blocking the late sodium current, which is activated by CaMKII.112 Its effect on preventing the decrease of LVEF in AC is currently unknown. Alcohol-induced cardiomyopathy treatment includes a combination of lifestyle modifications, pharmacological treatment, management of arrhythmia, and supportive care. This review will provide an updated view of this condition, including its epidemiology, pathogenesis, diagnosis, and treatment (Graphical Abstract).