Table of Contents    
Year : 2020  |  Volume : 11  |  Issue : 1  |  Page : 1-2  

Potential biomarkers to detect inflammation leading to coronary artery disease

Editor in Chief, Journal of Natural Science, Biology and Medicine, University College Dublin, Dublin, Ireland

Date of Submission14-Feb-2020
Date of Decision15-Feb-2020
Date of Acceptance16-Feb-2020
Date of Web Publication11-Mar-2020

Correspondence Address:
Arun H.S Kumar
Editor in Chief, Journal of Natural Science, Biology and Medicine, University College Dublin, Dublin, Ireland

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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0976-9668.280267

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How to cite this article:
Kumar AH. Potential biomarkers to detect inflammation leading to coronary artery disease. J Nat Sc Biol Med 2020;11:1-2

How to cite this URL:
Kumar AH. Potential biomarkers to detect inflammation leading to coronary artery disease. J Nat Sc Biol Med [serial online] 2020 [cited 2020 Sep 26];11:1-2. Available from:

Coronary artery disease (CAD) remains the leading cause of morbidity and mortality globally. Myocardial infarction (heart attack) is a common manifestation of CAD. Despite the contributions of CAD to cardiovascular complications being well known, the causative factors triggering the development of CAD are continued to be explored. A complex interplay between genetic, environmental, and lifestyle factors are suggested to be responsible for the development of CAD. The early phase of CAD is believed to be initiated by endothelial cell dysfunction, which consequently leads to reduced smooth muscle cell tone, eventually resulting in compromised vascular anatomy triggering vascular remodeling. Collaterally, the vascular remodeling is also associated with the influx of lipoproteins and inflammatory cells leading to the build-up of atherosclerotic plaques. The development of atherosclerotic plaques is also observed in the arteries as a consequence to natural aging process. Besides aging, unhealthy diet, smoking, sedentary lifestyle, and diseases such as hypertension, diabetes, and obesity are well known to hasten the development of atherosclerotic plaques. The presence of atherosclerotic plaques is not a problem; however, the uncertainty of how and when the atherosclerotic plaques can compromise the arterial function is a clinically challenging question, which has remained unanswered. The uncertainty in understanding the behavior of atherosclerotic plaques is due to several reasons. (1) We do not know how exactly the atherosclerotic plaques begin to develop. (2) Despite several known histological features of unstable atherosclerotic plaques, we are not certain on the features of the atherosclerotic plaquesin vivo which predispose them to rupture. (3) Atherosclerotic plaque burden can be in a single blood vessel or multiple blood vessels and we do not know if atherosclerotic plaques have a communication network between them which can trigger or influence some plaques to become more prone to rupture.

Besides these uncertainties with the atherosclerotic plaques, they are not the exclusive contributors to CAD. Several patients without any atherosclerotic plaques burden or evidence of plaque rupture are also reported to have CAD and its consequences (myocardial infarction). In contrast, plaque rupture is also reported in patients without any symptoms of myocardial infarction. Oxidative stress and inflammation are seen has interdependent hallmark of CAD. Several studies examining the role of oxidative stress and/or inflammation in predisposing the atherosclerotic plaques to rupture have reported a range of associated biomarkers including interleukin-1 (IL-1) beta, IL-18, C-reactive protein (CRP), activated T cells, myeloperoxidase levels, toll-like receptor 2, CD44, and glycosaminoglycan. However, the utility of these biomarkers to identify vulnerable plaque seem to have a low predictive value. Included in this issue is a study reporting the validity of high-sensitivity CRP (hs-CRP) as a biomarker for the severity of CAD. While inflammation is very likely a driver of CAD and atherosclerotic plaque development, whether inflammation can trigger plaque rupture is a clinically vital question which remains inconclusive. Indeed, plaque rupture is also reported in a considerable proportion of patients with normal levels of CRP (a marker of inflammation). Considering that systemic inflammation is differently manifested compared to local inflammation, should atherosclerotic plaques with inflammation be treated differently than atherosclerotic plaques not associated with inflammation? If so, can hs-CRP be used as a sole biomarker to differentiate these two categories of atherosclerotic plaques? The differential features of systemic versus local inflammation with a specific focus on atherosclerotic plaques remains a vital research questions which should be answered. Further, the cellular and biochemical features of atherosclerotic plaques with or without inflammation which eventually leads to plaque rupture need better clarity. Several studies evaluating the genetic loci associated with CAD have indicated IL6R and CXCL12 as potential markers of vascular wall inflammation. It will be interesting to see if a combination of IL6, CXCL12, and hs-CRP will be useful as a personalized medicine strategy to identify atherosclerotic plaques associated with inflammation.



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