Abstract
Despite significant strides to mitigate the complications of acute coronary syndrome (ACS), this clinical entity still represents a major global health burden. It has so far been well-established that most of the plaques leading to ACS are not a result of gradual narrowing of the vessel lumen, but rather a result of sudden disruption of vulnerable atherosclerotic plaques. As most of the developed imaging modalities for vulnerable plaque detection are invasive, multiple biomarkers were proposed to identify their presence. Owing to the pivotal role of lipids and inflammation in the pathophysiology of atherosclerosis, most of the biomarkers originated from one of those processes, whereas recent advancements in molecular sciences shed light on the use of microRNAs. Yet, at present there are no clinically implemented biomarkers or any other method for that matter that could non-invasively, yet reliably, diagnose the vulnerable plaque. Hence, in this review we summarized the available knowledge regarding the pathophysiology of plaque instability, the current evidence on potential biomarkers associated with plaque destabilization and finally, we discussed if search for biomarkers could one day bring us to non-invasive, cost-effective, yet valid way of diagnosing the vulnerable, rupture-prone coronary artery plaques.
Highlights
Published: 14 June 2021Causing more than 1.8 million deaths a year worldwide, acute coronary syndrome (ACS) represents a major global health burden [1]
Unlike the former, matrix-rich lipid-poor plaques usually lack prominent macrophage collections and the main pathophysiologic mechanism that leads to ACS in these circumstances is superficial erosion, a poorly understood process not pertaining to pathogenetic mechanisms associated with plaque rupture [35,36,37,38]
Since atherosclerosis is an everlasting field of research worldwide, there is a multitude of biomarkers whose potential to indicate a vulnerable plaque has been tested
Summary
Causing more than 1.8 million deaths a year worldwide, acute coronary syndrome (ACS) represents a major global health burden [1]. The first step would be to adequately define vulnerable plaque in the clinical setting It has so far been well-established that most of the plaques leading to ACS are not a result of gradual narrowing of the vessel lumen, but rather as a result of disruption of an atherosclerotic plaque which most commonly did not cause a hemodynamically significant stenosis of the coronary artery lumen [4]. These plaques have certain “ominous” characteristics that make them prone to rupture, and were named vulnerable plaques [4]. In this review we present the available knowledge of pathophysiology behind vulnerable plaques, the current evidence on potential biomarkers reflecting plaque destabilization and we discuss if search for biomarkers could one day bring us to non-invasive, cost-effective, yet reliable way of diagnosing the rupture-prone coronary artery plaques
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