Electron microscopic observations in alcoholic heart disease.

Alexander, Carl S.

doi:10.1136/hrt.29.2.200

Cited by 110 publications

(32 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In 1917, it was shown that oxygen consumption is increased after even moderate ingestion of ethanol in some individuals (10). Over the past 20 yr, light and electron microscopic changes in mitochondrial structure and function have been documented in myocardium from animals (11,12) and human subjects (13,14) exposed to ethanol. After a lag period of ethanol exposure in vivo, mitochondria isolated from the heart exhibit impaired rates of oxygen consumption, diminished respiratory control, and reduced P/O ratios (15)(16)(17)(18).…”

Section: Methodsmentioning

confidence: 99%

“…Such changes could be due to alterations in mitochondrial function. Consumption of alcohol over several weeks leads to gross morphological changes in heart mitochondria in laboratory animals (11,12) and human subjects (13,14). Impairment of mitochondrial function has been noted as well and it includes diminished phosphate/oxygen ratios (P/O)' and respiratory control ratios (15)(16)(17)(18); these are changes that do not occur after exposure of mitochondria to ethanol in vitro.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Mitochondrial dysfunction induced by fatty acid ethyl esters, myocardial metabolites of ethanol.

Lange¹,

Sobel²

1983

J. Clin. Invest.

230

106

View full text Add to dashboard Cite

A B S T R A C T Mechanisms responsible for alcohol-induced heart muscle disease have been difficult to elucidate partly because of previously obscure, demonstrable cardiac metabolism of ethanol. Recently, fatty acid ethyl esters were identified in our laboratory and found to be myocardial metabolites of ethanol. In the present study, they have been shown to induce mitochondrial dysfunction. Incubation of isolated myocardial mitochondria with fatty acid ethyl esters led to a concentration-dependent reduction of the respiratory control ratio index of coupling of oxidative phosphorylation and decrement of maximal rate of oxygen consumption. Furthermore, fatty acid ethyl esters were demonstrated to bind to mitochondria in vitro, and, importantly, 72% of intracellularly synthesized ethyl esters were found to bind to mitochondria isolated from intact tissue incubated with ethanol. Protein binding of fatty acid ethyl esters was markedly less than that of fatty acids. Because uncoupling of mitochondrial oxidative phosphorylation correlated with the cleavage of fatty acid ethyl ester shown to be initially bound to mitochondria, with resultant generation of fatty acid, a potent uncoupler, in a locus in or near the mitochondrial membrane, fatty acid ethyl esters may contribute to a potentially toxic shuttle for fatty acid with transport from physiological intracellular binding sites to the mitochondrial membrane; direct effects of fatty acid ethyl esters may also be deleterious. Operation of this shuttle as a result of ethanol ingestion and subsequent accumulation of fatty acid ethyl esters may account for the impaired mitochondrial function and inefficient energy production associated with toxic effects of ethanol on the heart.

show abstract

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mitochondrial dysfunction induced by fatty acid ethyl esters, myocardial metabolites of ethanol.

Lange¹,

Sobel²

1983

J. Clin. Invest.

230

106

View full text Add to dashboard Cite

show abstract

“…Alkoholkardiomyopathie nicht spezifisch sind Alexander 1967;Alexander et al 1977). Bekanntlich kann Alkohol direkt kardiotoxisch wirken.…”

Section: Histologische Befundeunclassified

Zur Pathomorphologie chronischer alkohol-assoziierter Myokardver�nderungen

Ogbuihi

1989

Z Rechtsmed

View full text Add to dashboard Cite

Forensic cases of sudden cardiac death were reviewed from the point of view of a history of alcohol consumption. A group of known cases of chronic alcoholism and another group of cases known to have been normal social drinkers without evidence of chronic alcoholism were selected. Cases with evidence of hypertension, ischemic or coronary heart disease, as well as cases with positive toxicological findings, were excluded. Applying the same criteria, cases of sudden death from other causes without a known history of alcohol consumption were selected to form a control group. With particular reference to histological myocardial changes, which are often documented in association with alcohol consumption, no noteworthy differences were found between the two major groups despite the significantly much lower frequency in the control group.

show abstract

“…Electron microscopic studies (7,8) of biopsies from patients with alcohol-induced cardiomyopathy have shown evidence of damage to the myofibres, including separation of filaments and loss of striation. In animal studies, loss of contractile proteins and defects in myocardial protein synthesis may partly explain the altered contractility.…”

Section: Have Demonstrated That If It Ismentioning

confidence: 99%

Acute reversible left ventricular dysfunction secondary to alcohol

Mahmoud¹,

Beauchesne²,

Davis³

et al. 2007

Canadian Journal of Cardiology

View full text Add to dashboard Cite

A 48-year-old woman presented to the emergency department with confusion and shortness of breath. She admitted to an eight-year history of the ingestion of more than 600 mL of vodka per day. Within the month before presentation, she had increased her alcohol intake by drinking a large glass of 70% ethanol per day.Before this medical admission, the patient had two previous admissions for acute pancreatitis due to ethanol abuse. On both occasions, she had normal cardiac enzyme levels and no evidence of cardiac dysfunction, and a chest x-ray revealed no cardiomegaly or pulmonary edema. Her most recent admission with pancreatitis had occurred four months before the present admission.The patient came to the emergency room with a decreased level of consciousness, hallucinations and convulsions after 24 h to 48 h of abstinence from alcohol. Her clinical assessment was consistent with the symptoms of delirium tremens.Her baseline laboratory evaluation showed pancytopenia, abnormal liver function tests (Table 1) and elevated cardiac enzyme levels ( Table 2). The toxicology screen was negative (Table 1). The initial chest x-ray revealed a normal cardiothoracic ratio and no evidence of heart failure. Her electrocardiogram showed sinus tachycardia, a nonspecific T-wave abnormality and right axis deviation. The right axis deviation was unchanged from a previous electrocardiogram. She received aggressive volume resuscitation, and 24 h after admission, she developed severe dyspnea. A subsequent chest x-ray after fluid resuscitation revealed pulmonary edema.An echocardiogram performed within 24 h of admission and reviewed by two independent echocardiographers demonstrated severe global left ventricular systolic dysfunction, with an ejection fraction of 20% by modified Simpson's biplane method. The left ventricle was not dilated, and the right ventricle had normal function. The end-systolic dimension was 4.1 cm and the end-diastolic dimension was 5.0 cm (Figure 1). The patient's delirium tremens was treated with benzodiazepines, and her congestive heart failure was treated with diuretics and an angiotensin-converting enzyme (ACE) inhibitor. After diuresis, her chest x-ray returned to normal. The pancytopenia and elevated liver enzyme levels resolved within a few days of hospital admission, with abstinence from alcohol. A dipyridamole stress test performed seven days after admission revealed no myocardial ischemia. The patient's ejection fraction was calculated at 58%, and she was discharged on a diuretic, an ACE inhibitor and a beta-blocker.After one month of abstaining from alcohol, the patient was asymptomatic. A repeat echocardiogram revealed normal left ventricular function, with an ejection fraction of 62% by modified Simpson's biplane method. The end-systolic dimension was 3.3 cm and the end-diastolic dimension was 4.8 cm (Figure 2). Her cardiac medications were subsequently discontinued. Chronic excess alcohol use is a well-established cause of dilated cardiomyopathy. The clinical features are variable because patients ma...

show abstract

Electron microscopic observations in alcoholic heart disease.

Cited by 110 publications

References 8 publications

Mitochondrial dysfunction induced by fatty acid ethyl esters, myocardial metabolites of ethanol.

Mitochondrial dysfunction induced by fatty acid ethyl esters, myocardial metabolites of ethanol.

Zur Pathomorphologie chronischer alkohol-assoziierter Myokardver�nderungen

Acute reversible left ventricular dysfunction secondary to alcohol

Contact Info

Product

Resources

About