Intrastent Restenosis: A Comprehensive Review

Abstract

The primary objective of this paper is to delineate and elucidate the contemporary advancements, developments, and prevailing trajectories concerning intrastent restenosis (ISR). We aim to provide a thorough overview of the most recent developments in this area, covering various aspects such as pathophysiological insights, therapeutic approaches, and new strategies for tackling the complex challenges of ISR in modern clinical settings. The authors have undertaken a study to address a relatively new medical challenge, recognizing its significant impact on the morbidity and mortality of individuals with cardiovascular diseases. This effort is driven by the need to fully understand, analyze, and possibly improve the outcomes of this emerging medical issue within the cardiovascular disease field. We acknowledge its considerable clinical implications and the necessity for innovative methods to mitigate its effects on patient outcomes. Therefore, our emphasis was directed towards elucidating the principal facets of the condition's prevalence, expounding upon the foundational mechanisms underscoring conspicuous restenosis, and delineating the risk factors relevant in shaping the contemporary landscape of diagnostic and therapeutic modalities. This thorough examination aims to provide a comprehensive understanding of the various dimensions of the condition, including epidemiological data, pathophysiological complexities, and clinical considerations critical for evaluating and enhancing current diagnostic and treatment approaches.

Keywords: angiography; bare-metal stents; coronary artery disease; drug-eluting ballons; drug-eluting stents; intrastent restenosis; intravascular imaging; pathophysiology; risk factors; treatment.

Figure 1

ISR physiopathology (adapted from an open–access source [32]). (Left): Coronary restenosis after conventional balloon angioplasty primarily arises from the phenomenon of elastic recoil of the arterial vessel wall. Moreover, the trauma inflicted on the coronary artery triggers the initiation of smooth muscle cell proliferation, their migration, and the deposition of an extracellular matrix. This cascade of events culminates in the formation of neointimal hyperplasia, which ultimately contributes to the pathogenesis of restenosis. (Center): The deployment of a BMS is associated with a heightened level of vascular injury, thereby augmenting the magnitude of neointimal hyperplasia and elevating the risk of in-stent restenosis. (Right): DESs dispense antiproliferative agents, effectively mitigating the extent of neointimal hyperplasia and correspondingly diminishing the susceptibility to in-stent restenosis.

Figure 2

Physiopathology of ISR: endothelial injury→ inflammatory response→ smooth muscle cell proliferation→ extracellular matrix formation→ neointimal hyperplasia→ lumen narrowing = ISR.

Figure 3

Angiographic classification of intrastent restenosis (adapted from an open-access source [65]). (a) Type I: there are four types of focal ISR described in the image above. (b) Type II: the observed lesions are confined strictly to the confines of the stent and do not exhibit any extension beyond its proximal or distal extremities. Type III: Diffuse, proliferative ISR. The identified lesions manifest a length exceeding 10 mm, exhibiting an extension that surpasses the boundaries of the stent at both its proximal and distal margins. Type IV: total occlusion of the stent resulting in no coronary perfusion.

Figure 4

OCT images used for optimal stent optimization. (A) Comprehensive three-dimensional intravascular reconstruction, vividly displaying instances of strut malposition; (B) Transversal section delineating the specifics of strut malposition, quantifying it at a length of 0.6 mm. This sectional view augments the understanding of the spatial irregularities within the stent deployment. (C) Longitudinal 3D reconstruction highlighting the stent along its entire length; significant malposition is observed at the distal end of the stent; D-Longitudinal reconstruction of the stent.