Potential biomarkers to detect inflammation leading to coronary artery disease

Abstract

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 plaques in 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.