Effects of alcohol on skeletal and cardiac muscle

Urbano-Márquez, Á; Fernández‐Solà, Joaquim

doi:10.1002/mus.20168

Cited by 115 publications

(153 citation statements)

References 123 publications

(237 reference statements)

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“…However, experimental and clinical studies have clearly demonstrated that ethanol itself is a direct noxious agent to heart in a progressive, cumulative, and dose-dependent manner, and its effects are independent of nutritional, vitamin, or mineral factors. According to current knowledge, the main relevant pathogenic mechanisms of alcohol-induced damage are due to interference in carbohydrate metabolism, protein synthesis, changes in oxidative status and mitochondrial function, disruption of transduction signals, and induction of apoptosis (Urbano-Márquez and Fernández-Solà, 2004). Alcohol alters the permeability of the sarcoplasmic reticulum to calcium ions and thus reduces the efficiency by which calcium activates muscle contraction, and it reduces the synthesis of cardiac proteins in both the contractile actin-myosin complex and in mitochondria, predominantly in alcoholics with high blood pressure.…”

Section: Alcoholmentioning

confidence: 99%

Drug-Induced Cardiomyopathies

Klimas¹

2012

Cardiomyopathies - From Basic Research to Clinical Management

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Section: Alcoholmentioning

confidence: 99%

Drug-Induced Cardiomyopathies

Klimas¹

2012

Cardiomyopathies - From Basic Research to Clinical Management

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“…Ethanol may cause both an acute myopathy with rhabdomyolysis as well as chronic skeletal muscle damage [32]. Ethanol may increase the susceptibility of skeletal muscle to other myotoxic substances by induction of CYP450 on skeletal muscle sarcoplasmic reticulum; this could account for the sporadic nature of alcohol-induced rhabdomyolysis [33].…”

Section: What Are the Possible Etiologies For Rhabdomyolysis In This mentioning

confidence: 99%

Case Files of the Medical Toxicology Fellowship at Drexel University

Vearrier

Curtis

2011

J. Med. Toxicol.

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A 28-year-old female was brought to the emergency department (ED) by her roommate after a suicide attempt, in which the patient took 29 capsules of an over-the-counter (OTC) sleep aid containing 50 mg of diphenhydramine (DPH) per capsule, for a total of 1450 mg, and consumed 100 ml of vodka. Her weight was 67 kg, yielding a dose of 22 mg/kg DPH. When a roommate arrived home from work several hours later, he noticed that the patient was walking aimlessly through the house and that "she was out of it." The patient subsequently informed the roommate of her suicide attempt, at which point he brought her by car to our ED. According to the patient, the ingestion occurred 9 h prior to arrival.In the ED, the patient complained of bilateral tingling and numbness in her legs and feet that had started within the last 4 h. She had a subjective sensation of inability to control the muscles in her legs and leg weakness. The patient denied any history of leg trauma, recent strenuous physical activity, or recent prolonged inactivity. Her medical history was significant for cervical dysplasia status post surgical excision and major depressive disorder. The patient denied taking any other prescribed or OTC medications, which her roommate corroborated.Physical examination revealed a young, disheveled female with normal body habitus. Initial vital signs included a temperature of 36.4°C, heart rate 123 beats/ min, respiratory rate 18 breaths/min, blood pressure 112/ 83 mm Hg, and pulse oximetry of 98% on room air. Pupils were 6 mm bilaterally and sluggishly reactive to light. Extraocular movements were intact. The mucous membranes of the oropharynx were dry. Cardiac examination was significant for a regular tachycardia, while the pulmonary examination was normal. Abdominal examination was significant for bowel sounds being present but decreased. The patient was alert and oriented to self and place, but not to time. She was able to answer simple questions, but was slow to respond. Strength, sensation, and deep tendon reflexes were normal. No ataxia or tremor was present. Extremity examination was significant for mottled skin color on the anterior legs bilaterally. Dorsalis pedis and posterior tibialis pulses were normal, as was sensation, strength, and capillary refill throughout the bilateral lower extremities. What is the Pharmacology of DPH?DPH is a first-generation H 1 antihistamine. It belongs to the ethanolamine subclass of antihistamines along with carbinoxamine, clemastine, dimenhydrinate, and doxylamine. Histamine receptors are categorized into four subtypes This case report was presented in poster form at the EAPCCT conference in 2009 in Stockholm, Sweden.

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“…One one hand, there is a pleasant tonic and healthy cardiovascular effect when consumed at occasional low doses in a social context, decreasing, for instance, cardiovascular morbidity and mortality [1]. On the other hand, alcohol is a toxic able to induce a variety of noxious cardiac and vascular effects when consumed in binges or at a high-cumulated lifetime consumption, increasing cardiovascular morbidity and mortality [2,3].…”

Section: Introductionmentioning

confidence: 99%

“…In fact, the total lifetime dose of alcohol consumed by a subject was the most relevant parameter related to the development of LV dysfunction (low ejection fraction) and alcoholic cardiomyopathy (ACM). Chronic ACM is developed over a long period of time of usually more than 10 years and thus, usually starts between the third to fifth decades of [3,9]. Binge drinking is also an additional negative factor that may increase chronic alcoholmediated heart damage and/or induce acute exacerbations of ventricular dysfunction, malignant arrhythmias and potential cardiac arrest [2,3].…”

Section: Introductionmentioning

confidence: 99%

“…Chronic ACM is developed over a long period of time of usually more than 10 years and thus, usually starts between the third to fifth decades of [3,9]. Binge drinking is also an additional negative factor that may increase chronic alcoholmediated heart damage and/or induce acute exacerbations of ventricular dysfunction, malignant arrhythmias and potential cardiac arrest [2,3]. susceptibility factors or other additional noxious factors such as tobacco and cocaine use [10,11].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Alcoholic Cardiomyopathy: Old and New Insights

Fernández‐Solà¹,

Riba²

2017

J Alcohol Drug Depend

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Alcohol cardiomyopathy (ACM) is a chronic dilated heart disease with decreased left ventricular ejection fraction that may be detected in one-fourth of high-dose alcohol consumers. It causes progressive diastolic and systolic dysfunction, supra and ventricular arrhythmias leading to heart failure and increased mortality. The main etiological factor for ACM is ethanol consumption that affects the myocardium in a dose-dependent manner. The mechanisms of ACM are diverse, synchronic and synergistic. Alcohol alters the channel and receptor structure of the cell membrane, decreases intracellular calcium transients, increases oxidative and inflammatory damage, decreases structural protein synthesis and interferes with excitation-contraction coupling mechanisms. Subjects with excessive alcohol consumption may have a subclinical cardiomyopathy with atrial and LV diastolic dysfunction measured by echocardiography or cardiac MR. Subclinical LV dysfunction may progress and later appear clinical features of heart failure. Cardiac myocytes adapt to ethanol aggression by cell and nuclear hypertrophy and dilatation of heart chambers. Progressive myocyte structure disarray and apoptosis produce myocyte loss, hypertrophy of the remaining cells, subendocardial and interstitial fibrosis and low-degree myocyte regeneration. In addition, ethanol also interferes with cardiac repair and adaptation mechanisms. Thus, local cardiomyokines (FGF-21) and growth factors (myostatin, IGF-1, leptin) are modified by ethanol, limiting cardiac remodeling and myocyte regeneration, and leading to abnormal hypertrophy and eccentric ventricle dilatation. This imbalance between aggression and protection mechanisms induces progressive myocyte loss and heart dysfunction. Alcohol abstention is the main goal in ACM, although control drinking (<-60 g/day) may allow recovery of LV function. Monitoring of systemic mediated alcohol-damage, and correction of vitamin and ion deficiencies is needed. Heart failure in ACM should be treated similar to other dilated cardiomyopathies. Heart transplantation is limited to subjects without other organ damage who are able to abstain from alcohol. New preventive and therapeutic strategies are under development to decrease alcohol-mediated myocyte damage and increase heart protective and repair mechanisms.

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Effects of alcohol on skeletal and cardiac muscle

Cited by 115 publications

References 123 publications

Drug-Induced Cardiomyopathies

Drug-Induced Cardiomyopathies

Case Files of the Medical Toxicology Fellowship at Drexel University

Alcoholic Cardiomyopathy: Old and New Insights

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