The role of systemic inflammation in heart failure
- Authors: Khazova EV1, Bulashova OV1
-
Affiliations:
- Kazan State Medical University
- Issue: Vol 102, No 4 (2021)
- Pages: 510-517
- Section: Reviews
- URL: https://journals.rcsi.science/kazanmedj/article/view/65950
- DOI: https://doi.org/10.17816/KMJ2021-510
- ID: 65950
Cite item
Abstract
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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##article.viewOnOriginalSite##About the authors
E V Khazova
Kazan State Medical University
Author for correspondence.
Email: hazova_elena@mail.ru
ORCID iD: 0000-0001-8050-2892
SPIN-code: 7013-4320
Scopus Author ID: 57205153574
ResearcherId: O-2336-2016
Russian Federation, Kazan, Russia
O V Bulashova
Kazan State Medical University
Email: boulashova@yandex.ru
ORCID iD: 0000-0002-7228-5848
SPIN-code: 4211-2171
Scopus Author ID: 6507198087
Russian Federation, Kazan, Russia
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