Heart pathomorphological changes in the long-term alcohol consumption

Тертышный, С. И.; Shuliatnikova, T.; Zubko, M. D.

doi:10.14739/2310-1237.2020.2.212734

Cited by 3 publications

(1 citation statement)

References 16 publications

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“…It is thought that not only ethanol, but also the first metabolite acetaldehyde may directly interfere with cardiac muscle homeostasis. The possible pathogenesis of cardiac damage probably involves mitochondrial dysfunction [ 11 ], oxidative damage [ 4 , 12 ], and impaired calcium ion homeostasis due to the effect of ethanol and its metabolites. The treatment includes abstinence from alcohol, pharmacologic treatment for heart failure, and management of arrhythmia.…”

Section: Discussionmentioning

confidence: 99%

Detecting Concealing Heart Failure in a Young Alcohol-Related Liver Failure Patient Using the Most Basic Pathophysiological Principle

Lyu¹,

Miskovsky²

2022

Cureus

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Long-term alcohol abuse can cause alcohol-related liver injury (acute alcoholic hepatitis, acute liver failure, hepatic steatosis, fibrosis, or cirrhosis), as well as cardiac injury. Alcoholic cardiomyopathy is a severe consequence of chronic alcohol abuse. Incidence of alcoholic cardiomyopathy ranges from 1-2% of all heavy alcohol users. In the United States, excess alcohol consumption contributes to more than 10% of cases of heart failure. Here, we present a case of a 41-year-old male patient with severe alcohol abuse who presented with signs and symptoms of liver failure and was found to have severe left ventricular systolic dysfunction and dilated cardiomyopathy. More interestingly, the detection of heart failure in this patient was convoluted but also represented an amazing example of how the most basic pathophysiological principles help answer clinical questions in a perplexing scenario. The patient is a 41-year-old Caucasian male with severe alcohol abuse who presented with complaints of diffuse yellowish discoloration of skin, fatigue, and "feeling not like himself” for six weeks. A review of systems revealed mild exertional dyspnea and bilateral lower extremity swelling. Physical exam was remarkable for diffuse jaundice involving the whole body, tachycardia, and trace edema in the lower extremity bilaterally. Otherwise, lungs were clear to auscultation, normal heart sounds with regular heart rate and rhythm, no Jugular vein distention, and no carotid bruits were appreciated. Labs showed elevated total bilirubin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), ammonia, and lactate levels. Notably, venous blood gas (VBG) showed metabolic acidosis with compensating respiratory alkalosis with normal potential Hydrogen (pH). An electrocardiogram showed sinus tachycardia. Treatment was started for acute alcoholic liver failure, with intravenous fluids, intravenous prednisolone, and Clinical Institute Withdrawal Assessment for Alcohol (CIWA) protocol. The patient’s liver function markers went down stably. However, the patient’s mental status got worse and his lactate levels continued to rise. He was prescribed empirical antibiotics with a pan Computed tomography (CT) scan to look for any source of infection which revealed no meaningful positive findings. Surprisingly and interestingly, the venous blood gas pH started to trend up demonstrating alkalotic pH which contrasted the initial normal pH on admission. The metabolic acidosis was seemingly “over-compensated” by respiratory alkalosis. It was speculated that another underlying pathology existed to count for respiratory alkalosis. Chest X-ray (CXR) showed cardiomegaly but no pneumonia. An echocardiogram showed severe left ventricular systolic dysfunction with an Ejection Fraction of 20% and dilated left ventricle. The treatment direction was switched from treating liver failure to targeting heart failure with intravenous diuretics. The patient’s mental status improved remarkably after three days of diuresis and the patient wa...

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Section: Discussionmentioning

confidence: 99%

Detecting Concealing Heart Failure in a Young Alcohol-Related Liver Failure Patient Using the Most Basic Pathophysiological Principle

Lyu¹,

Miskovsky²

2022

Cureus

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Quantitative morphological analysis of age structural changes in prostate of experimental animals with ethanol poisoning

Hnatiuk,

Nesteruk,

Fedoniuk

et al. 2024

Wiad Lek

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Aim: To find out the age remodeling of the structural components of the prostate gland at alcohol poisoning using quantitative morphological analysis. Materials and Methods: The structure of the prostate gland of 4 white male rats groups were morphologically investigated. The 1 group included 30 control intact animals aged 8 months, the 2-nd group – 30 rats aged 24 months, the 3-rd group – 30 8-month-old animals with ethanol intoxication, and the 4-th group included 30 24-month-old rats with the specified simulated pathology. Ethanol intoxication was modeled by intragastric administration of 30% ethyl alcohol solution at a dose of 20 ml/kg once daily for 28 days. Rats were euthanized by bloodletting under general thiopental anesthesia 28 days after the beginning of the experiment. The area of glands, the height of glandular epithelial cells, the area of their nuclei and cytoplasm, the nuclear-cytoplasmic ratio in these cells and the stromal-parenchymal ratio in the organ were studied using light microscopy and were determined morphometrically. Morphometric parameters were processed statistically. Results: It was established that with age in the intact prostate of laboratory sexually mature white male rats, the area of glands, the height of glandular epitheliocytes, the area of their nuclei and cytoplasm, with the stability of nuclear-cytoplasmic ratios in the epithelial cells of the glands, significantly decreases, and the stromal-parenchymal ratio in the organ under study increases. Long-term ethanol poisoning leads to pronounced structural changes in the prostate, which is characterized by pronounced atrophy of the glandular epithelium, a decrease in the area of the glands, a decrease in the height of epithelial cells, a violation of nuclear-cytoplasmic relations in them, an increase in stromal-parenchymal ratio, and a prominent growth of the muscle-elastic stroma. The revealed structural changes of the studied components of the prostate dominated in 24-month-old experimental animals. Conclusions: Morphological analysis of the prostate gland established that morphometric and morphological changed significantly according to the age and were depend on the ethanol poisoning.

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Morphometric assessment of age-related structural changes in the vessels of the microcirculatory bed of the prostate gland under conditions of ethanol intoxication

Hnatjuk,

Nesteruk,

Tatarchuk

et al. 2023

BMBR

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Vessels of the microcirculatory bed ensure the full trophism of the body at the level of capillary-tissue relations and are the first to respond to various functional and pathological conditions of organs. At the same time, morphological changes in prostate microvasculature with age under conditions of prolonged ethanol poisoning have been understudied. The purpose of this study was to determine the age-related remodelling of the prostate vessels of the microcirculatory bed in case of prolonged alcohol intoxication. Injection, histological, morphometric, and statistical methods were used. The microvasculature of the prostate gland of 80 sexually mature white male rats of different ages was studied, 40 animals served as controls, and 40 rats were injected daily for 28 days with a 30% ethanol solution at a dose of 20 ml/kg intragastrically. Morphometric analysis indicated that chronic ethanol poisoning in white rats significantly reduces the lumens of arterial microvessels and hemocapillaries, while expanding the venous vessels in the microcirculatory bed of the prostate gland. When venous congestion occurs, the density of microvessels decreases, and microcirculation bed is disturbed. This disruption is accompanied by atrophic, dystrophic, and necrobiotic changes in endotheliocytes, epithelial cells, muscle cells, stromal structures, infiltration, and sclerosing. Intragastric 28-day administration of a 30% ethanol solution at a dose of 20 ml/kg to laboratory mature white male rats leads to pronounced structural changes in the microvasculature of the prostate microcirculatory bed: constriction of arterioles, precapillary arterioles and hemocapillaries, dilation of the capillary venules and venules, which is complicated by significant venous haemorrhage, development of atrophy, dystrophy, necrosis of vascular endothelial cells, glandular epithelial cells, muscle cells, connective tissue structures, cellular infiltration, and sclerosis. Vessels of the microcirculatory bed play a leading role in ethanol-induced damage of prostate structures, which dominate in 24-month-old experimental animals

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Heart pathomorphological changes in the long-term alcohol consumption

Cited by 3 publications

References 16 publications

Detecting Concealing Heart Failure in a Young Alcohol-Related Liver Failure Patient Using the Most Basic Pathophysiological Principle

Detecting Concealing Heart Failure in a Young Alcohol-Related Liver Failure Patient Using the Most Basic Pathophysiological Principle

Quantitative morphological analysis of age structural changes in prostate of experimental animals with ethanol poisoning

Morphometric assessment of age-related structural changes in the vessels of the microcirculatory bed of the prostate gland under conditions of ethanol intoxication

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