Vulnerable Plaque and Inflammation: Potential Clinical Strategies

Abstract

Although enormous progress has been made in the prevention and treatment of cardiovascular disease, it still remains the leading cause of death worldwide. During the last decades, advances in the understanding of the pathophysiology of vulnerable plaque progression, coupled with novel diagnostic and therapeutic approaches, created a new opportunity for progress against cardiovascular disease. It has been demonstrated that inflammation, implicated in all stages of atherosclerosis, is an integral part of vulnerable plaque development and progression, leading eventually to plaque instability. Thus, new diagnostic modalities have been proposed for the detection of local plaque inflammation. Moreover, treatments such as stenting, photodynamic therapy, and novel pharmaceutical agents are under consideration as methods to stabilize the vulnerable plaques by inhibiting inflammation. This review provides an overview of the inflammatory process leading to atherosclerotic cardiovascular disease and the potential clinical strategies that may substantially decrease the incidence of events. We will mention the major impact of local and systemic inflammation on plaque advancing and destabilization, the imaging techniques for early detection of vulnerable plaques and the potential therapeutic strategies.

Inhibitory effect of apolipoprotein A-I on matrix metalloproteinase-2 expression <italic>in vivo</italic> and <italic>in vitro</italic>

“…The atherosclerotic plaque is the complex lesion composed of distinct morphological features, including fibrous cap, shoulder area and lipid core. Rupture is associated with the breakdown of the ECM in the shoulder region of such plaques, and the risk of plaque rupture is influenced by specific characteristics of the plaque structure [24]. Indeed, the plaque with thin fibrous cap and large lipid core is more vulnerable to rupture.…”

Pentraxin 3 and atherosclerosis among type 2 diabetic patients

“…It is worthwhile to know that atherosclerosis is not only a result of hyperglycemia but many other factors among others insulin resistance, dyslipidemia, and hypercoagulability. These are cardiovascular diseases (CVD) that still remain leading causes of death worldwide despite tremendous progress in their prevention and treatment [1]. One can assess the cardiovascular risk in patients with diabetes using the risk scores for general population (e.g Systematic COronary Risk Evaluation (SCORE) or less popular scales dedicated for individuals with diabetes (i.e.…”

USNCTAM perspectives on mechanics in medicine

“…Interface 11: 20140301 diagnosed and/or acutely treated with drugs delivered locally to rupture prone plaques using NPs in order to promote rapid plaque stabilization and/or passivation. In addition to the size of the necrotic lipid core, the extent and location of plaque inflammation appear to be key factors in determining plaque instability [120,121]. Along with immune cell activation, inflammation contributes to the loss of collagen in the fibrous cap, a prelude to fibrous cap rupture.…”

“…Inflammation is also known to induce differential surface expression of specific vascular molecules such as ICAM-1, intravascular cell adhesion molecules and selectins. Bloodborne NPs, conjugated with targeting ligands and loaded with therapeutic and/or imaging agents, can potentially recognize and use these molecules as vascular docking sites, thereby helping to detect VPs and/or deliver site-specific acute therapy [121,122].…”