Pathology of in-stent restenosis

Virmani, Renu; Farb, Andrew

doi:10.1097/00041433-199912000-00004

Cited by 218 publications

(142 citation statements)

References 39 publications

Supporting

Mentioning

132

Contrasting

Unclassified

Order By: Relevance

“…6,7 Our results suggest that SMCs are the main component of the neointima after both self-expanding stent and balloon overstretch injuries. They are in agreement with current views concerning the pathogenesis of stent-induced lesions, 8 whereas the pathogenesis of PTCA-induced lesions has up to now remained controversial. 6,7,[15][16][17] …”

Section: Discussionsupporting

confidence: 90%

“…4 It is conceivable that implantation of a self-expanding stent (Wallstent) into a porcine coronary artery leads to a chronic injury of the wall, resulting in the migration of medial SMCs into the intima. 8 Conversely, a balloon overstretch injury, resulting in complete rupture of the media and exposure of the adventitia to blood components, could lead (in addition to SMC stimulation) to activation and proliferation of adventitial fibroblasts, followed by their inward migration and participation in neointima formation. 6,7 To acquire more knowledge on the origin of cells responsible for neointima formation in both models, we studied chronologically the expression of well-established SMC differentiation markers, ie, ␣-smooth muscle (SM) actin, 9 SM myosin heavy chain (MHC) isoforms 1 and 2, 9 desmin, 9 and smoothelin, 10 in the arterial wall layers after stent implantation or PTCA.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Mechanisms of Neointima Formation and Remodeling in the Porcine Coronary Artery

et al. 2001

View full text Add to dashboard Cite

Background-To characterize the cells responsible for neointima formation after porcine coronary artery wall injury, we studied the expression of smooth muscle cell (SMC) differentiation markers in 2 models: (1) self-expanding stent implantation resulting in no or little interruption of internal elastic lamina and (2) percutaneous transluminal coronary angioplasty (PTCA) resulting in complete medial rupture and exposure of adventitia to blood components. Methods and Results-The expression of ␣-smooth muscle (SM) actin, SM myosin heavy chain isoforms 1 and 2, desmin, and smoothelin was investigated by means of immunohistochemistry and Western blots in tissues of the arterial wall collected at different time points and in cell populations cultured from these tissues. The expression of smoothelin, a marker of late SMC differentiation, was used to discriminate between SMCs and myofibroblasts. Both stent-and PTCA-induced neointimal tissues and their cultured cell populations expressed all 4 markers. The adventitial tissue underlying PTCA-induced lesions temporarily expressed ␣-SM actin, desmin, and SM myosin heavy chain isoforms, but not smoothelin. When placed in culture, adventitial cells expressed only ␣-SM actin. Conclusions-Our results suggest that SMCs are the main components of coronary artery neointima after both self-expanding stent implantation and PTCA. The adventitial reaction observed after PTCA evolves with a chronology independent of that of neointima formation and probably corresponds to a myofibroblastic reaction.

show abstract

Section: Discussionsupporting

confidence: 90%

mentioning

confidence: 99%

Mechanisms of Neointima Formation and Remodeling in the Porcine Coronary Artery

et al. 2001

View full text Add to dashboard Cite

show abstract

“…[7][8][9][10][11][12][13] Vessel injury by an angioplasty balloon or stent struts leads to the activation of platelets and mural thrombus formation. [13][14][15][16] The presence of vascular injury, mural thrombus, and a metallic foreign body activates circulating neutrophils and tissue macrophages.…”

Section: Pathophysiology Of In-stent Restenosismentioning

confidence: 99%

Coated Stents for the Prevention of Restenosis: Part I

2002

View full text Add to dashboard Cite

O ver the past decade, the use of endoluminal metallic stents has become common practice during percutaneous coronary intervention (PCI), especially after clinical trials showed evidence of decreased restenosis rates when compared with balloon angioplasty alone. [1][2][3] Although stents significantly reduce restenosis when compared with balloon angioplasty, restenosis rates in patients who receive stents are still 20% to 40% at 6 months. [1][2][3][4][5][6] Recently, the concept of using stents coated with agents that could potentially inhibit neointimal hyperplasia has emerged. These agents include biocompatible materials, anticoagulants, corticosteroids, and antimitotic agents. This 2-part article reviews animal studies, human observational studies, and results from randomized clinical trials investigating coated stents. Part I discusses the pathophysiology of in-stent restenosis, as well as animal studies investigating coated stents. Part II discusses human studies investigating coated stents. Pathophysiology of In-Stent RestenosisIn-stent restenosis is primarily due to neointimal hyperplasia. [7][8][9][10][11][12][13] Vessel injury by an angioplasty balloon or stent struts leads to the activation of platelets and mural thrombus formation. [13][14][15][16] The presence of vascular injury, mural thrombus, and a metallic foreign body activates circulating neutrophils and tissue macrophages. 12,13,17,18 These cellular elements release cytokines and growth factors that activate smooth muscle cells. 19 -23 Upregulation and expression of genes such as c-myc that regulate cell division ensues, leading to cell proliferation. 24,25 Production of matrix metalloproteinases is also upregulated, leading to remodeling of the extracellular matrix, and initiating smooth muscle cell migration. 26 -28 The end result of this cascade of events is the uncontrolled proliferation of smooth muscle cells around the vessel intima and the deposition of extracellular matrix material, which often lead to significant luminal narrowing 3 to 6 months after PCI (Figure 1). Coated StentsThe systemic administration of a variety of agents has not had a significant impact on post-PCI restenosis rates. 29 -34 Although there is some evidence that controlling mural thrombus formation may decrease neointimal hyperplasia, [35][36][37] antiplatelet agents have not reliably resulted in reductions in restenosis rates in clinical trials. 29,30 Similarly, the systemic administration of corticosteroids aimed at controlling the inflammatory process has not shown decreased restenosis rates. 31 The lack of effect of systemically administered agents may be due to inadequate drug concentrations at the site of stent insertion. The limited success of these agents in decreasing rates of in-stent restenosis, coupled with side effects, prompted the development of coated stents.Stent coatings can be divided into 2 categories, biocompatible materials and drug-eluting coatings (Table 1). Biocompatible materials currently under investigation are thought to be less th...

show abstract

“…Neointimal hyperplasia inside the stent is the major contributor in restenosis [1] . Clinical and laboratory data show that local inflammatory process takes role in neointimal hyperplasia process [2] .…”

Section: Introductionmentioning

confidence: 99%

Comparison of the Effects of Bare Metal Stents and Drug Eluting Stents on C- Reactive Protein Levels

Özyüncü¹

2015

JHC

View full text Add to dashboard Cite

Aim: It's suggested that drug eluting stents (DES) may have systemic anti inflammatory properties and this can play a role in decreased restenosis rates. We aimed to compare bare metal stents (BMS) and DES on their effects on C-reactive protein (CRP) levels, a good marker of systemic inflammation. We also aimed to investigate the relation between the inflammation levels and myonecrosis and adverse cardiac events. Methods: Patients undergoing elective stent implantation were grouped as BMS (n = 70) and DES (n = 42). Basal and 24th hour postprocedural CRP and CKMB levels were measured and the difference (Δ) was compared between the groups. The patients were followed up for adverse cardiac events for one year. Results: Mean age was 62 ± 11 and 75% were males. There was significant CRP rise in both groups at 24 th hour, but the ΔCRP was 2.1 (0.5-6.2) mg/L in BMS and 2.3 (0.2-5.2) mg/L in DES group, the difference wasn't statistically significant (p = 0.703). ΔCKMB and adverse cardiac event rates were similar between the two groups (p = 0.897 and p = 0.785). There was no correlation between ΔCRP and ΔCKMB (r = -0.090 and p = 0.459 for BMS, r = 0.158 and p = 0.318 for DES). The effect of ΔCRP on the incidence of adverse cardiac events was not significant (p = 0.349 for BMS, p = 0.135 for DES). Conclusion: Our findings reveal that patients with BMS and DES implantation exhibit similar grade of systemic inflammation after the procedure. At similar levels of systemic inflammation, the local anti-inflammatory properties of DES can play a role at decreased restenosis rates.

show abstract

Pathology of in-stent restenosis

Cited by 218 publications

References 39 publications

Mechanisms of Neointima Formation and Remodeling in the Porcine Coronary Artery

Mechanisms of Neointima Formation and Remodeling in the Porcine Coronary Artery

Coated Stents for the Prevention of Restenosis: Part I

Comparison of the Effects of Bare Metal Stents and Drug Eluting Stents on C- Reactive Protein Levels

Contact Info

Product

Resources

About