Restenosis and in-stent restenosis

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Chapter 13 Restenosis and in-stent restenosis

PATHOPHYSIOLOGY

Vascular injury during coronary intervention, leads to a complex reparative process that may become excessive and cause restenosis. Renarrowing after PCI develops over weeks to months post-procedure, in contrast to de novo coronary lesions, which develop over years, likely reflecting the difference in the underlying mechanisms and the extent of inflammation involved with each lesion type. The process of restenosis can be broadly categorized into four interrelated facets:

2. Thrombus formation, before or after angioplasty, contributes to restenosis by lumen occupation. Furthermore, activated platelets within the thrombus secrete a host of substances from their alpha-granules (Fig. 13.1), which promote vasoconstriction, chemotaxis, mitogenesis, and activation of neighboring platelets, mediating the growth of fibromuscular tissue (neointima). Use of proper antiplatelet agents and anticoagulation therapy during PCI should limit this mechanism of restenosis, though no supportive data exist to establish a role for anti-thrombotics to reduce restenosis.
4. Arterial remodeling during the reparative process can result in an increase, decrease, or no change in the cross-sectional area of the artery lumen. This so-called Glagov phenomenon (Fig. 13.2)1, combined with neointimal hyperplasia, represents the final wave of the restenotic process. The restenotic process is usually complete within 3–6 months after balloon angioplasty and atherectomy, but can extend up to 6–12 months following stent placement. As such, the time course for restenosis after stents is delayed, relative to that for balloon angioplasty, by 1–3 months. Hence, patients who are free of restenosis at nine months after coronary stent placement are likely to have long-term patency within the index lesion. DES contain a polymeric coating that allows sustained (several weeks) release of anti-inflammatory and antiproliferative drugs, which inhibit neointimal growth.
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Figure 13.1 Mechanisms of restenosis following PCI.

Source: Chan AW and Moliterno DJ, Clinical Evaluation of Restenosis. In Atherothrombosis and Coronary Artery Disease, edited by V. Fuster, EJ Topol, and EG Nabel, p. 1416 (Figure 93.2).

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Figure 13.2 Vascular remodeling following PCI.

Source: Chan AW and Moliterno DJ, Clinical Evaluation of Restenosis. In Atherothrombosis and Coronary Artery Disease, edited by V. Fuster, EJ Topol, and EG Nabel, p. 1417 (Figure 93.3).

While elastic recoil and thrombus formation can lead to acute vessel closure and acute restenosis, the concept of restenosis primarily refers to neointimal hyperplasia and vascular remodeling over months, which result from an inflammatory reparative processes following PCI-induced vascular injury.

DEFINITIONS OF RESTENOSIS

Angiographic restenosis

Various definitions for angiographic restenosis have been used. 50% or greater dichotomous diameter stenosis at follow-up angiography is a widely used criterion in clinical trials. However, reporting of the minimum luminal diameter (MLD) may avoid variation of restenosis rates reported in clinical trials due to inconsistent definitions of angiographic restenosis. The difference between pre-procedural MLD and immediate post-procedural MLD is defined as acute gain, and the difference between post-procedural MLD and MLD at follow-up is termed to late loss. Acute gain is lowest with PTCA, followed by atherectomy, and stenting (highest acute gain). Late loss is usually proportional to acute gain, such that the late loss index, defined as late loss divided by the acute gain, is similar after revascularization with PTCA, atherectomy, or stents (Fig. 13.3).

While visual methods of assessing angiographic stenosis severity are prone to interobserver and intraobserver variability, the use of quantitative coronary angiography (QCA) is highly reproducible, and is the standard technique employed in most contemporary research trials. QCA is usually unreliable for assessing bifurcation lesions and in the absence of disease-free reference segments.

PREDICTORS FOR RESTENOSIS

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