The Good, the Bad, and the Ugly with Alcohol Use and Abuse on the Heart

Walker, Robin K.; Cousins, Valerie; Umoh, Nsini; Jeffress, Miara; Taghipour, Delaram J.; AlRubaiee, Mustafa; Haddad, Georges E.

doi:10.1111/acer.12109

Cited by 67 publications

(43 citation statements)

References 47 publications

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“…The mechanisms of ACM development remain unclear [3,4,8,9]. An interesting hypothesis relates to the existence of a nonoxidative metabolic pathway for alcohol related to fatty acid metabolism in the heart, muscle, pancreas and brain [10,11].…”

Section: Mechanismsmentioning

confidence: 99%

Alcohol and cardiovascular diseases: where do we stand today?

2015

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Abstract. Klatsky AL (Northern California Kaiser Permanente, Oakland, CA, USA). Alcohol and cardiovascular diseases: where do we stand today?. (Review). J Intern Med 2015;278: 238-250.For centuries, multiple medical risks of heavy alcohol drinking have been evident with simultaneous awareness of a less harmful or sensible drinking limit. The increased risks of heavy drinking, defined as three or more standard-sized drinks per day, are both cardiovascular (CV) and non-CV. The CV risks include the following: (i) alcoholic cardiomyopathy (ACM), (ii) systemic hypertension, (iii) atrial arrhythmias, (iv) haemorrhagic stroke and, probably, ischaemic stroke. By contrast, modern epidemiological studies have shown lower morbidity and mortality amongst light-moderate drinkers, due mostly to a reduced risk of coronary artery disease (CAD), with contributions from ischaemic stroke and heart failure (HF). A low level of alcohol drinking has no clear relation to increased risk of any CV condition, except for haemorrhagic stroke. There is good evidence that supports the existence of mechanisms by which alcohol might protect against CAD, but the mechanisms for other alcohol-CV associations remain unclear. Interrelationships amongst the CV conditions affect the individual alcohol-disease relationships; for example, lower CAD risk in lightmoderate drinkers is to a large extent responsible for the reduced HF risk. International comparison data plus the presence of proposed beneficial nonalcohol components in wine (particularly in red wine) suggest that this beverage type might afford extra CAD protection. However, the effect of beverage choice is confounded by a healthier drinking pattern and more favourable risk traits in wine drinkers. Debate persists about methodological and public health issues related to the epidemiology of alcohol-related CV disease.

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Section: Mechanismsmentioning

confidence: 99%

Alcohol and cardiovascular diseases: where do we stand today?

2015

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“…Coincident with these observations, there are many reports showing that the direct exposure of cardiomyocytes to ethanol results in acute apoptotic cell death (Chen et al, 2000;Wang et al, 2015;Noritake et al, 2015). An enhanced generation of reactive oxygen species (ROS) has been proposed to be a crucial factor in ethanol cytotoxicity (Walker et al, 2013). On the other hand, structural collapse of the cytoskeleton in ethanol-exposed cells has not attracted much attention, although it was first reported several decades ago (French et al, 1987;Puszkin and Rubin, 1975;Iwata et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Restoration of YAP activation rescues HL-1 cardiomyocytes from apoptotic death by ethanol

et al. 2017

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-We reported previously that when mouse atrium-derived HL-1 cardiomyocytes undergo apoptosis upon exposure to 2% ethanol, the cellular cytoskeleton is severely disrupted and the anti-apoptotic transcriptional co-activator Yes-associated protein (YAP) is inactivated. Consistent with our previous observations, the expression of connective tissue growth factor (CTGF), an anti-apoptotic growth factor and a target of YAP, decreases in a time-dependent manner during exposure to 2% ethanol. The restoration of YAP activation rescues the cells from apoptosis: both the retrovirus-mediated expression of constitutively active YAP and the stabilization of the actomyosin cytoskeleton by jasplakinolide prevent cell death. In contrast, YAP inhibitors have no effect on cell death, confirming the inactivation of YAP in ethanol-exposed cells. Thus, a decrease in actin tension and YAP inactivation should be crucially involved in the cytotoxicity of ethanol on HL-1 cardiomyocytes.

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“…Various theories have been proposed to establish its causative effect and pathogenesis, but mainly it remains the thought that the toxic metabolites of ethanol disrupt cardiovascular metabolism and that there is increased cardiomyocyte loss secondary to oxidative damage [25].…”

Section: International Journal Of Cardiology J O U R N a L H O M E P mentioning

confidence: 99%

Psychiatric co-morbidities in patients with dilated cardiomyopathy

Rasoul

Potluri

Wong

et al. 2015

International Journal of Cardiology

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Various studies have investigated and reported on the association between physical and psychiatric conditions [1,2]. Recently, research focussing on the link between cardiovascular disease and psychiatric conditions has been on the rise [3]. Carter et al. [3] found that one in four psychiatric patients also suffered from a cardiovascular co-morbidity. Whether these links are causative, or not, there is a need to quantify this data to provide the evidence on which better targeted, holistic care-pathways can be based.It is well known that depression and anxiety are significant and commonly reported factors in heart failure [4] and it has been shown that patients with non-ischaemic heart failure, such as hypertrophic cardiomyopathy (HCM) [5,6] and dilated cardiomyopathy (DCM) [7] experience emotional stress, anxiety and in some cases depression and other psychiatric co-morbidities. This often attributed the fear of associated risk of sudden death and potential genetic risk to their own children [5,8]. In addition, recent studies [9] have shown an increasing trend in patients with psychiatric comorbidities alongside DCM, and have called for a lower threshold to both assess and detect these co-morbidities as they often go under-detected and under-diagnosed in hospital [10].In light of this and the increasing evidence of association between psychiatric conditions and cardiovascular disease, we investigated the prevalence of psychiatric co-morbidities and tendencies in patients with dilated cardiomyopathy (DCM) over a 14 year period. We do not believe any study has looked into DCM and the possible links to psychiatric conditions and tendencies over such a long period to date.We compiled an entirely anonymous database of adult patients diagnosed with dilated cardiomyopathy across seven hospitals in the North of England, UK during the period 01/01/2000 to 31/03/2013. We analysed the data for prevalence of firstly psychiatric co-morbidities such as; anxiety disorder, obsessive compulsive disorder, schizophrenia, schizoaffective disorder, bipolar disease, depression and dementia and secondly substance abuse and suicidal intent. We traced our patients with the ACALM (Algorithm for Co-morbidities, Associations, length of stay and Mortality) study protocol, which uses ICD-10 (International Classification of Disease, Version 10) and OPCS-4 (Office of population Censuses and Surveys Classification of Interventions and Procedures) procedure codes to correctly allocate patients for statistical analysis using SPSS Version 20.0. The prevalence data was assembled into five groups to aid analysis of trends over time. This methodology has been described by our group and others previously [1][2][3]9,[11][12][13][14][15][16][17][18][19][20][21][22][23].Between the years 2000 and 2013, 929,552 patients were admitted, 710 of which (0.08%) were labelled with a diagnosis of dilated cardiomyopathy. The majority of the population were made up of male patients (69%) and the mean age was 54.9 years ± 13.9 years (S.D.). The population consisted o...

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The Good, the Bad, and the Ugly with Alcohol Use and Abuse on the Heart

Cited by 67 publications

References 47 publications

Alcohol and cardiovascular diseases: where do we stand today?

Alcohol and cardiovascular diseases: where do we stand today?

Restoration of YAP activation rescues HL-1 cardiomyocytes from apoptotic death by ethanol

Psychiatric co-morbidities in patients with dilated cardiomyopathy

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