Abstract and Introduction
Abstract
New advances in image and signal processing have allowed the development of numerous invasive and noninvasive imaging modalities that have revealed details of plaque pathology and allowed us to study in vivo the atherosclerotic evolution. Recent natural history of atherosclerosis studies permitted us to evaluate changes in the compositional and morphological characteristics of the plaque and identify predictors of future events. The idea of being able to identify future culprit lesions and passivate these plaques has gradually matured, and small scale studies have provided proofs about the feasibility of this concept. This review article summarizes the recent advances in the study of atherosclerosis, cites the current evidence, highlights our limitations in understanding the evolution of the plaque and in predicting plaque destabilization, and discusses the potentiality of an early invasive sealing of future culprit lesions.
Introduction
The miniaturization of medical devices, technological innovations, new developments in image and signal processing, and advances in biological and molecular imaging have provided us with a variety of imaging modalities that permit detection of local inflammation and detailed evaluation of changes in atheroma burden and its composition. These techniques demonstrated that coronary atherosclerosis has focal and eccentric manifestations that evolve in an independent manner, which is affected by the composition of the plaque, the presence of inflammation, and the local hemodynamic environment. Prospective natural history of atherosclerosis studies shed light into the mechanisms involved in this process and allowed us to identify predictors of future culprit lesions. The idea of being able to predict plaque development has gradually evolved and recently the Shield Evaluated at Cardiac Hospital in Rotterdam for Investigation and Treatment of TCFA study has been reported, which examined the feasibility of sealing non–flow-limiting lesions that have features associated with increased vulnerability (Figure 1).
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Figure 1.
Stent implantation in a high-risk plaque leads to neointimal formation and increases the thickness of the tissue that covers a lipid core (LC) (A) resulting in the potential passivation of the plaque (B). Imaging data acquired at baseline from a patient recruited in the SECRITT study: palpography demonstrated high strain (C), radiofrequency analysis of the backscattered intravascular ultrasound signal showed a lipid-rich plaque, which, however, did not cause luminal obstruction (D), whereas optical coherence tomography demonstrated a TCFA (cap thickness 40 μm) (E). The results of the study are summarized in panel (F): at 6-month follow-up, the thickness of the fibrous cap was increased by 170 μm, there was a minor reduction in the mean lumen area, minimal malapposition, and most of the struts were fully covered. Panel A and B were obtained with permission from Moreno.
The aim of this review article is to summarize the technological advances in the study of atherosclerosis, cite the current evidence, and discuss the potentiality of an invasive passivation of future culprit lesions.