LAUSR

Alcoholic cardiomyopathy (ACM) is a condition of toxic origin that causes gradual changes in the structure and function of the heart, resembling those seen in idiopathic dilated cardiomyopathy (CMP). ACM occurs in persons who consume large amounts of alcohol (>100 g/d in men, > 80 g/d in women) over a long period of time (at least 5 years, usually around 15 years) in the absence of other significant heart disease. In western countries, this condition accounts for approximately one third of all cases of acquired dilated CMP. ACM may affect up to one third of all consumers of large amounts of alcohol. As the overall alcohol consumption of the Spanish population has not decreased in recent years, neither has the incidence of ACM, and alcohol intake continues to be an important risk factor for both ACM and cardiovascular disease. Moreover, the harmful effects of alcohol may be added to those of other cardiovascular risk factors, such as hypertension, diabetes mellitus, and hypercholesterolemia. It has also been reported that, because of the toxic systemic effect of alcohol and its metabolites, other organic diseases related to alcohol use, such as liver cirrhosis, alcoholic dementia, and protein-calorie malnutrition, increase the risk of developing ACM. For many years, the potential reversibility of ACM has been a subject of medical interest. Already in the IV century BC in Greece, Hippocrates observed that patients with ‘‘hydropsy’’, the clinical equivalent of congestive heart disease, improved when they stopped drinking alcohol, a recommendation that has persisted to this day. However, we need to look back to the XIX century in German beer drinkers to find clear clinical descriptions of ACM reversibility with abstinence from alcohol. In t, for a very long time people doubted that alcohol consumption, in itself, was the cause of dilated CMP. It was suggested that contaminants in the beer such as cobalt and arsenic used as defoaming agents brought about this condition, and not the ethanol. Another proposal was that ACM could be caused by the protein-calorie malnutrition, thiamine deficiency (western Beriberi), or the deficits in selenium, magnesium, or phosphorus that are often associated with chronic alcohol consumption. Some 30 years ago, several clinical and experimental studies verified that ethanol was the cause of this toxic dilated CMP, and that there was a clear dose-dependent effect related to the cumulative alcohol consumption over the lifetime of each person. This generated the concept of total lifetime alcohol intake (LAI) per kilogram of body weight as an approach to better estimate the personal risk of developing ACM. Thus, the natural history of ACM has been defined as a chronic disease that initiates with a subclinical phase in which the only change observed is left ventricular diastolic dysfunction. This is followed by the systolic dysfunction phase, with a gradual decrease in left ventricular ejection fraction (LVEF). In this phase, events related to congestive heart failure and arrhythmias appear, and there is a clear increase in mortality in persons who continue to consume large amounts of alcohol. Binge drinking is particularly detrimental over the course of ACM, as it can trigger acute cardiac events of this type (holiday heart syndrome). It was also seen that women are more prone to develop ACM than men and that some genetic polymorphisms such as angiotensin-converting enzyme DD genotype increase the risk of developing this condition. With regard to the pathogenesis of ACM, it is currently considered to be a direct toxic effect of alcohol through multifactorial and synergistic mechanisms. These include Cadependent signal transduction changes affecting myocardial contractility, the antioxidant and proinflammatory effects of alcohol and acetaldehyde, changes in the synthesis of structural and contractile proteins, and apoptosis induction, with consequent cardiomyocyte loss and replacement by subendocardial and interstitial fibrosis (Figure 1). Furthermore, alcohol inhibits cardiomyocyte repair and replication mechanisms, which worsens myocardial remodeling. Finally, a recent study suggested that certain myokines (FGF-21, METRNL, IGF-1, myostatin) may play a role in modulating ethanol-induced myocardial injury and myocardial repair mechanisms. Based on these data, it is it is reasonable to conclude that all ACM patients should completely abstain from alcohol.However, in general, these patients have an elevated LAI (> 20 kg of ethanol/ kg of body weight) and are alcohol-dependent. Despite undergoing specific detoxification programs, not all patients achieve lasting alcohol abstinence. Around one third continue drinking large amounts of alcohol despite recommendations to abstain, which leads to high mortality, at an annual rate of more than 10%. Another subgroup (30%-40%) is only able to reduce previous alcohol consumption to moderate doses (<60 g/d). In ACM patients who persistently abstain from alcohol intake, a fast, significant improvement has been observed in LVEF. However, patients with Rev Esp Cardiol. 2018;71(8):603–605