Association Between Alcohol Intake and Cardiac Remodeling

Rodrigues, Patrícia; Santos‐Ribeiro, Samuel; Teodoro, Tiago; Gomes, Filipe Veloso; Leal, Inês; Reis, Jared P.; Goff, David C.; Gonçalves, Alexandra; Lima, João A.C.

doi:10.1016/j.jacc.2018.07.050

Cited by 34 publications

(35 citation statements)

References 32 publications

(36 reference statements)

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“…Further, we observed a trend towards an association between increasing amounts of alcohol consumption with a higher risk of incident LV systolic dysfunction (LVEF 50%) (P-for-trend 0.058), and with a higher risk of a clinically relevant decrease in LVEF (!10%) during follow-up (P-for-trend 0.012). Our findings are in contrast with the findings of a previous longitudinal population-based study, that reported no associations between alcohol consumption, LVEF and LV systolic dysfunction [10]. This study was composed of young adults, whereas our study is composed of older adults.…”

Section: Discussioncontrasting

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…Thus far, prospective studies that assessed the association of alcohol consumption and echocardiographic measures of cardiac structure and function are scarce [9,10]. These studies observed that higher alcohol consumption was associated with higher left atrial volume (LAV) [9], a measure of diastolic function, or with higher left ventricular mass index (LVMI) [10], a measure of cardiac remodelling, but no associations were observed between alcohol consumption and LVEF [10], a measure of systolic function. However, these studies are limited by their alcohol consumption assessment (at risk drinking versus no alcohol consumption) [9], or by their study population: relatively young to observe effects [10] or only composed of people with prior coronary heart disease [9].…”

Section: Introductionmentioning

confidence: 99%

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Moderate and heavy alcohol consumption are prospectively associated with decreased left ventricular ejection fraction: The Hoorn Study

Oort¹,

Beulens

Heijden

et al. 2020

Nutrition, Metabolism and Cardiovascular Diseases

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Section: Discussioncontrasting

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Moderate and heavy alcohol consumption are prospectively associated with decreased left ventricular ejection fraction: The Hoorn Study

Oort¹,

Beulens

Heijden

et al. 2020

Nutrition, Metabolism and Cardiovascular Diseases

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“…Alcoholic cardiomyopathy (ACM) is a specific heart muscle disease caused by chronic alcohol intake. Chronic alcohol intake tends to increase left ventricular mass and left ventricular dilatation and leads to heart failure (Rodrigues et al., ). Although there are multiple mechanisms causing ACM, excessive activation of the RAS is one of the most important mechanisms.…”

mentioning

confidence: 99%

(Pro)renin Receptor is Involved in Myocardial Damage in Alcoholic Cardiomyopathy

Xiong

Cao

Qiao

et al. 2019

Alcoholism Clin & Exp Res

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Background: (Pro)renin receptor (PRR), a novel member of the renin-angiotensin system, participates in various cardiovascular diseases. However, the role of PRR in alcoholic cardiomyopathy (ACM), which is caused by alcohol intake and manifests as myocardial damage and cardiac dysfunction, remains unclear.Methods: PRR gene silencing was achieved by transfecting recombinant adenovirus expressing anti-PRR short hairpin RNA (PRR-shRNA). In vitro, primary rat cardiac fibroblasts (CFs) were cultured with the stimulation of alcohol (200 mM), with or without PRR-shRNA and PD98059. Immunofluorescence, RT-PCR, and Western blot were used to measure the protein and messenger (mRNA) expression of PRR, fibrotic factors, and members of related signaling pathways. In vivo, Wistar rats were fed a diet containing 9% (v/v) alcohol or a normal diet for 3 months, with or without PRR-shRNA. Sirius Red staining, immunohistochemical staining, and toluidine blue staining were used to evaluate myocardial fibrosis, oxidative stress, and inflammation response.Results: Alcohol markedly increased PRR mRNA and protein expression in a time-and concentration-dependent manner in CFs. The increased expression of fibrotic factors induced by alcohol was prevented by PRR-shRNA and PD98059. Moreover, PRR-shRNA decreased the phosphorylation of extracellular regulated protein kinases (ERK) 1/2 in CFs. Furthermore, PRR-shRNA decreased cardiac fibrosis, reduced oxidative stress, and alleviated inflammation response in the myocardial tissue.Conclusions: Our results show that PRR-ERK1/2 signaling was involved in the development of ACM and that PRR could be a new target for the treatment of ACM.

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“…A study based on individual‐participant data for nearly 0.6 million consumers showed that even low alcohol consumption was associated with disease risks (Wood et al., ). Alcoholic cardiomyopathy (ACM) is characterized by myocardial degeneration caused by long‐term drinking, which causes the ventricle to dilate, and manifests as cardiac dysfunction (Iacovoni et al., ; Manthey et al., ; Rodrigues et al., ). Approximately one‐half of all cases of dilated cardiomyopathy are reported to be caused by alcohol (George and Figueredo, ; Li et al., ; Weintraub et al., ).…”

mentioning

confidence: 99%

AIN‐93 Diet as an Alternative Model to Lieber–DeCarli Diet for Alcoholic Cardiomyopathy

Cao

Zhang

et al. 2019

Alcoholism Clin & Exp Res

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Background: The Lieber-DeCarli alcoholic liquid diet is a classical method for establishing animal models of alcoholic cardiomyopathy (ACM). No study has reported whether the AIN-93 diet, which is widely used as a standard diet for both long-term and short-term studies with laboratory animals, could be used to construct the ACM animal model. The present study intended to investigate whether the AIN-93 diet could be used to establish a mouse ACM model.Methods: Twenty-four C57BL/6 male mice were randomly divided into 4 equally sized groups. In ethanol (EtOH)-fed groups, mice were fed a 4%-EtOH (w/v, 28% of total calories) alcoholic liquid diet of Lieber-DeCarli or the AIN-93 diet for chronic alcohol exposure for 180 days. In control-fed groups, mice were fed with non-EtOH liquid diets with the same calories as EtOH-fed groups. Morphological observations of the hearts and molecular investigation of the brain natriuretic peptide (BNP) were carried out by echocardiography, hematoxylin and eosin (H&E) and immunohistochemistry (IHC) staining, real-time quantitative polymerase chain reaction (qPCR), and enzyme-linked immunosorbent assay.Results: Echocardiography showed that mice fed with either the 4%-EtOH Lieber-DeCarli diet or the 4%-EtOH AIN-93 diet had dilated ventricles and poor cardiac function. IHC staining of BNP, qPCR of BNP mRNA, and plasma concentration of BNP showed an up-regulated expression in mice fed with both the 4%-EtOH Lieber-DeCarli and 4%-EtOH AIN-93 diets. Less fatty liver was also observed in mice fed the AIN-93 alcoholic diet than those fed the Lieber-DeCarli alcoholic diet.Conclusions: The AIN-93 alcoholic liquid diet can be used to establish ACM animal models, as with the conventional Lieber-DeCarli alcoholic liquid diet.

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Association Between Alcohol Intake and Cardiac Remodeling

Cited by 34 publications

References 32 publications

Moderate and heavy alcohol consumption are prospectively associated with decreased left ventricular ejection fraction: The Hoorn Study

Moderate and heavy alcohol consumption are prospectively associated with decreased left ventricular ejection fraction: The Hoorn Study

(Pro)renin Receptor is Involved in Myocardial Damage in Alcoholic Cardiomyopathy

AIN‐93 Diet as an Alternative Model to Lieber–DeCarli Diet for Alcoholic Cardiomyopathy

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