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Alcohol and the heart: the good, the bad and the worse in heart failure
  1. Luis Eduardo Rohde1,2,
  2. Luis Beck-da-Silva1,2
  1. 1 Serviço de Cardiologia, Hospital de Clinicas de Porto Alegre, Porto Alegre, Brazil
  2. 2 Programa de Pós-Graduação em Cardiologia e Ciências Cardiovasculares, Faculdade de Medicina da Universidade Federal do Rio Grande do Sul
  1. Correspondence to Dr Luis Eduardo Rohde, Hospital de Clinicas de Porto Alegre, Porto Alegre, RS 90035-903, Brazil; rohde.le{at}gmail.com

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There is a general acceptance among researchers, physicians and even the general population that the consumption of moderate amounts of alcoholic beverages may have beneficial effect in the heart. A large number of experimental, clinical and epidemiological studies presumably give scientific support to this perception. There have been reports on favourable effects of different alcoholic beverages on several surrogate end-points of atherosclerosis, such as blood lipoproteins, clotting and fibrinolytic factors, endothelin and oxidative stress. Wine is the prototype beverage associated to cardioprotection, with additional positive consequences in the cardiovascular system allegedly attributed to the presence of natural polyphenols, particularly resveratrol. The mechanisms involved in the potential cardioprotective effects of polyphenols are numerous and include antioxidant, vasodilator, anti-inflammatory, antifibrotic, antiapoptotic and anti-ischaemic properties. Recent experimental data also demonstrate that polyphenols can exert its cardioprotective effect via the activation of several powerful prosurvival cellular pathways.1 Unfortunately, all these persuasive data must be interpreted with great caution in the clinical arena for several reasons. Data from observational studies have intrinsic methodological pitfalls and are far from consensual. Analysis of the Atherosclerosis Risk in Communities (ARIC) study has suggested that the risk/benefit ratio of alcohol ingestion might be directly related to race and gender strata. African-American moderate drinkers, for instance, were shown to be at unexpected increased risk of incident coronary artery disease, while women who were rare drinkers were at the lowest risk.2 Fuchs and Chambless3 have elegantly postulated that a great part of the attributed benefit of moderate alcohol ingestion could be explained by a lower prevalence of other risk factors and by an indication of a healthier behaviour (and not a real protective mechanism), implying that the real association between the consumption of alcoholic beverages and the incidence of coronary artery has not yet been fully appreciated. It seems that the postulated ‘good’ might indeed not be that good for the heart.

In this controversial ‘double-edged sword’, it is undeniable that at least one side is considerably sharper than the other. There is a well-established relation between lifetime alcohol consumption and major structural and functional myocardial abnormalities.4 In this scenario, the aforementioned prosurvival pathways are indeed shifted to a prodamage venue, with intense inflammation, extracellular fibrosis, intracellular organelle injury, that might evolve to cardiomyocyte necrosis and cellular death. In addition, convincing data indicate that alcohol impairs mitochondria function assessed by membrane potential and respiratory chain activity.5 Markers of oxidative stress and myocardial apoptosis are also adversely affected by alcohol consumption, an effect that might be gender dependent, being worse in women. Besides ethanol’s direct toxicity, acetaldehyde and ethyl esters, its principal metabolites, are able to impair cardiac function uncoupling excitation-contraction, promoting oxidative damage and lipid peroxidation.6 The bad news is in fact real: alcohol can irreversibly damage the heart in a dose-dependent and time-dependent fashion. Noteworthy for doctors and patients, however, is the salutary effect of quit drinking over the failing myocardium.

Unfortunately, the worse is yet to come. In their Heart paper, Manthey et al published disturbing findings on the worldwide mortality due to alcoholic cardiomyopathy (ACM), incorporating data from death registries for more than 100 countries.7 In 2015, there were more than 27 000 deaths from ACM and this translated into close to 8% of all global deaths from cardiomyopathy being caused by alcohol. Despite the intrinsic expected drawbacks of an analysis based on registries and administrative data sets, their findings are intriguing and troublesome. They observed a large regional asymmetry with regard to alcohol-attributable fractions, with the vast majority of the mortality observed in Eastern Europe and Central Asia. Although there is some uncertainty about the internal validity of the results because of under-reporting in several countries and over-reporting in others (such as those from Eastern Europe), the global burden of alcohol-related diseases and mortality is astounding, considering that this is a completely preventable disease.

The current findings should help us deal with this important healthcare problem in several ways. First, a great effort should be made to accurately report deaths that are related to alcohol ingestion worldwide, as the vast majority of countries in the current analysis clearly under-reported their events. Second, preventive strategies should be promoted to decrease the incidence of ACM itself, particularly in regions where the burden of ACM mortality is greater. Third, affected patients with ACM must be intensively and continuously advised to significantly reduce their drinking levels or fully abstain from drinking, the best proven strategy to reduce risks and improve prognosis. Finally, new research is needed to unravel if the burden of ACM is related only to patterns of drinking or is it also (or mostly) dependent on genetically mediated predisposition.4 The uttermost question, unfortunately, still remains: is it really safe to drink moderate amounts of alcoholic beverages, and can it really work as a remedy? Until this conundrum is not fully addressed (and we are far from solving these dilemmas), no policy or recommendation on cardioprotective drinking should be ever made.

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Footnotes

  • Funding No funding related to this paper.

  • Competing interests None declared.

  • Patient consent Not required.

  • Provenance and peer review Commissioned; internally peer reviewed.

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