Malignant ventricular arrhythmias in alcoholic cardiomyopathy

Guzzo-Merello, Gonzalo; Domínguez, Fernándo; González-López, Esther; Cobo‐Marcos, Marta; Gómez‐Bueno, Manuel; Fernández‐Lozano, Ignacio; Millán, Isabel; Segovia, Javier; Alonso‐Pulpón, Luis; García‐Pavía, Pablo

doi:10.1016/j.ijcard.2015.07.029

Cited by 29 publications

(24 citation statements)

References 23 publications

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“…Ethanol intake ≥24 g per day in females and ≥36 g per day in males has been found to cause hypertension; therefore, hypertension frequently contributes to LV dysfunction in cases of cardiomyopathy (6). Excessive alcohol intake is responsible for one-third of newly emerging atrial fibrillation cases, and malignant ventricular arrhythmias are common when the LV ejection fraction is <40% (7,8). However, arrhythmia was not detected in our patient.…”

Section: Discussionmentioning

confidence: 55%

A Case of Ischemic Cerebellar Stroke with Alcoholic Cardiomyopathy

Akinci¹,

Özer²,

Urgun³

et al. 2017

tnd

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Section: Discussionmentioning

confidence: 55%

A Case of Ischemic Cerebellar Stroke with Alcoholic Cardiomyopathy

Akinci¹,

Özer²,

Urgun³

et al. 2017

tnd

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“…MFN1 plays a key role in regulating mitochondrial fusion and maintaining the dynamic balance of mitochondrial morphology and promotes the mutual combination of mitochondria mainly in the early stage of fusion. When the expression level of MFN1 is insufficient, the efficiency of mitochondrial fusion is decreased, mitochondrial fragmentation is increased, mitochondrial mobility is weakened, and mitochondrial morphology also changes significantly 31 . By analyzing the specific mechanism of ethanol-induced damage to the mitochondrial function of cardiomyocytes, it was found that the protein and mRNA levels of MFN1 in ethanol-treated cardiomyocytes were decreased.In order to further confrm whether MFN1 serves a role in ethanol-induced cardiomyocyte mitochondrial function, the expression levels of MFN1 in ethanol-treated AC16 cardiomyocytes were upregulated via plasmid transfection, and then mitochondrial morphology, MMP and the ROS contents were analyzed respectively.As a result, mitochondria morphology basically returned to normal, MMPs were recreased, the ROS contents were decreased,which manifested mitochondrial function in ethanol-treated cardiomyocytes may be restored following upregulation the MFN1 expression.Therefore,MFN1 may inhibit ethanol-induced cardiomyocyte mitochondrial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-488-3p is expressed highly in ethanol-induced cardiomyocytes and regulates mitochondrial function via target gene MFN1

Liu

Song

2020

Preprint

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Objective To confirm ethanol-induced mitochondrial dysfunction in AC16 cardiomyocytes and the relationship with the ethanol concentration and duration. to investigate the nol. To study miR-488-3p promoted ethanol-induced mitochondrial dysfunction by regulating target gene MFN1. Methods The changes of mitochondrial morphology in cardiomyocytes were observed by fluorescence microscopy using mitotracker scanning. Mitochondrial membrane potential(MMP) and reactive oxygen species (ROS) contents were analyzed by flow cytometry. The expressions of miR-488-3p and MFN1 were detected by Real-time quantitative PCR or Western blot analysis, respectively.The interaction between miR-488-3p and MFN1 was explored by bioinformatics analysis and Luciferase reporter gene experiment. Results Ethanol intake damaged the mitochondrial morphology and function in AC16cardiomyocyte and there was the dependency upon ethanol concentration and duration. Mitochondrial dysfunctions in cells were manifested in abnormal mitochondrial morphology,decreasing MMPs, and increasing ROS contents. Ethanol intake upregulated expression levels of miR-488-3p,downregulated expression levels of MFN1 in AC16 cardiomyocytes and there was the dependency upon ethanol concentration and duration.Downregulation the expression level of miR-488-3p or upregulation expression levels of MFN1 after ethanol-induced cardiomyocytes, the damage to mitochondrial dysfunction can be reduced. miR-488-3p promoted ethanol-induced mitochondrial dysfunction by downregulating the expressions of MFN1. Conclusion 1.Ethanol can induce mitochondrial dysfunction in cardiomyocytes which is positively correlated with ethanol concentration and duration.2.The expression levels of miR-488-3p are decreased and the expression levels of MFN1 are recreased in AC16 cardiomyocytes after ethanol intake, which were positively correlated with ethanol concentration and duration.3. MFN1 is a direct target gene for miR-488-3p and together regulate mitochondrial function in AC16 cardiomyocytes. Key words: cardiomyocyte;alcoholic cardiomyopathy; mitochondrial dysfunction;mitochondrial membrane potential;reactive oxygen species;microRNA-488-3p; mitochondrial fusion protein 1

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“…Even moderate alcohol consumption represents a risk factor for atrial fibrillation 43. Left bundle branch block suggests increased risk of sudden cardiac death 44. The function of the left ventricle can improve after abstinence, and even if the dysfunction persists, the signs and symptoms of heart failure can improve 40.…”

Section: Alcoholic Heart Disease and Alcoholic Liver Cirrhosismentioning

confidence: 99%

Cardiac manifestations in alcoholic liver disease

Milić

Lulić

Štimac

et al. 2016

Postgraduate Medical Journal

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Alcoholic liver disease is the most prevalent cause of progressive liver disease in Europe. Alcoholic cirrhosis occurs in 8%-20% of cases of alcoholic liver disease. It has significant influence on cardiovascular system and haemodynamics through increased heart rate, cardiac output, decreased systemic vascular resistance, arterial pressure and plasma volume expansion. Cirrhotic cardiomyopathy is characterised by systolic and diastolic dysfunction and electrophysiological abnormalities, if no other underlying cardiac disease is present. It is often unmasked only during pharmacological or physiological stress, when compensatory mechanisms of the heart become insufficient to maintain adequate cardiac output. Low-to-moderate intake of alcohol can be cardioprotective. However, heavy drinking is associated with an increased risk of cardiovascular diseases, such as alcoholic cardiomyopathy, arterial hypertension, atrial arrhythmias as well as haemorrhagic and ischaemic stroke. Alcoholic cardiomyopathy is characterised by dilated left ventricle (LV), increased LV mass, normal or reduced LV wall thickness and systolic dysfunction.

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Malignant ventricular arrhythmias in alcoholic cardiomyopathy

Cited by 29 publications

References 23 publications

A Case of Ischemic Cerebellar Stroke with Alcoholic Cardiomyopathy

A Case of Ischemic Cerebellar Stroke with Alcoholic Cardiomyopathy

MicroRNA-488-3p is expressed highly in ethanol-induced cardiomyocytes and regulates mitochondrial function via target gene MFN1

Cardiac manifestations in alcoholic liver disease

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