“Cytokine” Model of Pathogenesis of Chronic Heart Failure and the Opportunities of New Therapeutic Strategy in Decompensated Patients

Vasuk, A.; Dudarenko, P.; Uschuk, N.; Schkolnik, L.; Serova, K

doi:10.20996/1819-6446-2006-2-4-63-70

Cited by 6 publications

(7 citation statements)

References 42 publications

(51 reference statements)

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“…Systemic inflammation plays an important role in the pathogenesis and progression of CHF. Identification of the various biomarkers of inflammation has become the subject of intense study in both human and veterinary medicine [3,24,36,37]. Histological examination often reveals inflammatory infiltrates in the myocardium of dog with dilated cardiomyopathy [12,38].…”

Section: Discussionmentioning

confidence: 99%

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Immune-inflammatory concept of the pathogenesis of chronic heart failure in dogs with dilated cardiomyopathy

et al. 2019

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Background: Dilated cardiomyopathy is common in dogs. This form of cardiomyopathy is the main cause of death due to heart disease in dogs. Death can occur suddenly in clinically normal animals as a result of the progression of congestive heart failure (CHF). The pathogenesis of heart failure syndrome in dogs with dilated cardiomyopathy involves activation of the neurohumoral system and immune-mediated inflammation, which leads to further progression of the condition. Heart failure syndrome in dogs with dilated cardiomyopathy is caused by the progressive loss of cardiomyocytes, apoptosis, remodeling of the left ventricle, systolic and diastolic dysfunction, arrhythmias, reduced cerebral blood flow, the involvement of other key internal organs, and intestinal dysbiosis. Aim: This study aimed to determine the immunological and inflammatory mechanisms surrounding the development of heart failure syndrome in dogs with dilated cardiomyopathy. Materials and Methods: The subjects of this study were dogs with a dilated form of cardiomyopathy (n=159), complicated by various functional classes of heart failure syndrome. Evaluation of myocardial remodeling, systolic function, and systemic hemodynamics was performed using EMP-860 Vet and PU-2200V ultrasound scanners according to the standard technique. Electrocardiography was performed with all dogs in right lateral recumbency using the EK1T-04 Midas electrocardiograph (50 mm/s speed and 1 mV gain = 1 cm). Results: In some affected animals, especially in cases of compensated dilated cardiomyopathy, leukocytosis was noted. In patients with dilated cardiomyopathy complicated by heart failure syndrome of various functional classes, the number of neutrophils was significantly increased, and the number of lymphocytes was decreased by 1.9-2.1 times when compared with those in clinically normal animals. In dogs with dilated cardiomyopathy, neutrophilic leukocytosis develops with a simple regenerative shift to the left. The results of immunological studies indicate that dogs with dilated cardiomyopathy develop T lymphocytopenia as compared with clinically normal animals. Conclusion: The central component of heart failure syndrome in dogs with dilated cardiomyopathy is the activation of the neurohumoral system and immune-mediated inflammation. The development of CHF in dogs with dilated cardiomyopathy is caused by the progressive loss of cardiomyocytes, apoptosis, remodeling of the left ventricle, systolic and diastolic dysfunction, arrhythmias, reduced cerebral blood flow, involvement of other key internal organs, and intestinal dysbiosis.

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Section: Discussionmentioning

confidence: 99%

“…An important achievement over the past decade has been the development of the neurohumoral hypothesis for the progression of cardiovascular disease in humans and domestic animals [10,21,24,25]. We have established that dilated cardiomyopathy in dogs is widespread, and often familial.…”

Section: Discussionmentioning

confidence: 99%

Immune-inflammatory concept of the pathogenesis of chronic heart failure in dogs with dilated cardiomyopathy

et al. 2019

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“…Дисфункция эндотелия сосудов играет значимую роль в развитии и прогрессировании клинических проявлений ХСН и ИБС, а в одном из ранее проведенных исследований [1] показа-но влияние активации TLR2 при формировании дисфункция эндотелия в КА на фоне преходящей ишемии.…”

Section: результаты и обсуждениеunclassified

Association of the Individual Variable Sites TLRS Genes With the Severity of CHD in Younger Patients

Жидкова¹,

Понасенко²,

Kutikhin³

et al. 2016

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1НИИ комплексных проблем сердечно-сосудистых заболеваний, директор -д.м.н., проф. О.Л. Барбараш, 2 ГБОУ ВПО Кемеровская государственная медицинская академия Министерства здравоохранения РФ, ректор -д.м.н., проф. В.М. Ивойлов; кафедра кардиологии и сердечно-сосудистой хирургии, зав. ASSOCIATION OF THE INDIVIDUAL VARIABLE SITES TLRS GENES WITH THE SEVERITY OF CHD IN YOUNGER PATIENTS

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“…В настоящее время в дополнение к гемодинамической и нейрогуморальной концепциям развития хронической сердечной недостаточности (ХСН) широко обсуждают значение цитокиновой активации и иммунного воспаления [1,2]. Особенно это актуально для ХСН, обусловленной ишемической болезнью сердца вследствие атеросклероза.…”

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The role of systemic inflammation in heart failure

et al. 2021

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The discussion continues about the role of systemic inflammation in the pathogenesis of cardiovascular diseases of ischemic etiology. This article reviews the information on the role of C-reactive protein in patients with atherosclerosis and heart failure in risk stratification for adverse cardiovascular events, including assessment of factors affecting the basal level of highly sensitive C-reactive protein. Research data (MRFIT, MONICA) have demonstrated a relationship between an increased level of C-reactive protein and the development of coronary heart disease. An increase in the serum level of highly sensitive C-reactive protein is observed in arterial hypertension, dyslipidemia, type 2 diabetes mellitus and insulin resistance, which indicates the involvement of systemic inflammation in these disorders. Currently, the assessment of highly sensitive C-reactive protein is used to determine the risk of developing myocardial infarction and stroke. It has been proven that heart failure patients have a high level of highly sensitive C-reactive protein compared with patients without heart failure. The level of C-reactive protein is referred to as modifiable risk factors for cardiovascular diseases of ischemic origin, since lifestyle changes or taking drugs such as statins, non-steroidal anti-inflammatory drugs, glucocorticoids, etc. reduce the level of highly sensitive C-reactive protein. In patients with heart failure with different left ventricular ejection fraction values, it was found that the regression of the inflammatory response is accompanied by an improvement in prognosis, which confirms the hypothesis of inflammation as a response to stress, which has negative consequences for the cardiovascular system.

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“Cytokine” Model of Pathogenesis of Chronic Heart Failure and the Opportunities of New Therapeutic Strategy in Decompensated Patients

Cited by 6 publications

References 42 publications

Immune-inflammatory concept of the pathogenesis of chronic heart failure in dogs with dilated cardiomyopathy

Immune-inflammatory concept of the pathogenesis of chronic heart failure in dogs with dilated cardiomyopathy

Association of the Individual Variable Sites TLRS Genes With the Severity of CHD in Younger Patients

The role of systemic inflammation in heart failure

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