Perspective - Journal of Cholesterol and Heart Disease (2023) Volume 7, Issue 4
Inflammatory biomarkers in the pathogenesis and prognosis of acute coronary syndrome.
Olivier Maite *
Department of Emergency medicine and critical care nursing, Wollo University, Ethiopia
- *Corresponding Author:
- Olivier Maite
Department of Emergency medicine and critical care nursing
Received: 05-Aug-2023, Manuscript No. AACHD-23-112269; Editor assigned: 07-Aug-2023, PreQC No. AACHD-23-112269 (PQ); Reviewed: 21-Aug-2023, QC No. AACHD -23-112269; Revised: 24-Aug-2023, Manuscript No. AACHD-23-112269 (R); Published: 31-Aug-2023, DOI: 10.35841/aachd-7.4.160
Citation: Maite O. Inflammatory biomarkers in the pathogenesis and prognosis of acute coronary syndrome. J Cholest Heart Dis 2023;7(4):160
Acute Coronary Syndrome (ACS) is a critical cardiovascular condition that encompasses a spectrum of ischemic heart diseases, including unstable angina, non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). Inflammation plays a crucial role in the initiation, progression, and prognosis of ACS. This article aims to provide a comprehensive overview of the role of inflammatory biomarkers in the pathogenesis and prognosis of ACS, highlighting their potential as diagnostic tools and therapeutic targets .
In recent years, extensive research has demonstrated the intricate interplay between inflammation and ACS. Inflammatory biomarkers, such as C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and various cellular adhesion molecules, have emerged as valuable indicators of the underlying inflammatory processes in ACS. This article explores the mechanistic insights into how these biomarkers contribute to the pathogenesis and prognosis of ACS. The initiation of ACS involves atherosclerotic plaque destabilization, leading to plaque rupture or erosion and subsequent thrombus formation. Inflammation plays a pivotal role in each stage of this process. Inflammatory biomarkers, such as CRP and IL-6, reflect the presence and intensity of systemic inflammation and are associated with endothelial dysfunction, plaque vulnerability, and thrombus formation. Moreover, activated immune cells release cytokines and chemokines that further perpetuate the inflammatory response, contributing to the progression of ACS .
Inflammatory biomarkers not only provide insights into the pathogenesis of ACS but also serve as important prognostic indicators. Elevated levels of CRP, IL-6, and TNF-α have been associated with adverse outcomes, including recurrent myocardial infarction, cardiovascular death, and heart failure in ACS patients. These biomarkers not only reflect the extent of myocardial injury but also indicate the ongoing inflammatory response, which can promote adverse remodeling, ventricular dysfunction, and subsequent cardiovascular events. The use of inflammatory biomarkers in clinical practice has shown promise in the diagnosis, risk stratification, and therapeutic management of ACS. High-sensitivity CRP has been incorporated into risk assessment algorithms, such as the Framingham Risk Score, to improve risk prediction. Additionally, targeted anti-inflammatory therapies, such as monoclonal antibodies against IL-1β and IL-6 receptors, have demonstrated potential in reducing cardiovascular events in ACS patients [3,4].
Inflammatory biomarkers provide valuable insights into the pathogenesis and prognosis of ACS. Their involvement in the inflammatory cascade, plaque destabilization, thrombosis, and adverse cardiac remodeling underscores their importance as diagnostic and prognostic tools. Furthermore, targeting the inflammatory pathways implicated in ACS holds promise for the development of novel therapeutic interventions that may improve patient outcomes and reduce the burden of this life-threatening condition. Further research is warranted to elucidate the precise mechanisms by which inflammatory biomarkers contribute to ACS and to explore their full potential in clinical practice .
- Guyton JR, Klemp KF. Development of the lipid-rich core in human atherosclerosis. Arterioscler Thromb Vasc Biol. 1996;16(1):4-11.
- Kruth HS. Localization of unesterified cholesterol in human atherosclerotic lesions. Demonstration of filipin-positive, oil-red-O-negative particles. Am J Pathol. 1984;114(2):201.
- Burke AP, Kolodgie FD, Farb A, et al. Morphological predictors of arterial remodeling in coronary atherosclerosis. Circulation. 2002;105(3):297-303.
- Castellani C, Angelini A, de Boer OJ, et al. Intraplaque hemorrhage in cardiac allograft vasculopathy. Am J Transplant. 2014;14(1):184-92.
- Barger AC, Beeuwkes III R, Lainey LL, et al. Hypothesis: vasa vasorum and neovascularization of human coronary arteries: a possible role in the pathophysiology of atherosclerosis. N Engl J Med. 1984;310(3):175-7.