Ultrastructural study of proliferating and migrating smooth muscle cells at the site of PICA as an explanation for restenosis

Ohara, Takahiro; Nanto, Shinsuke; Hirayama, Atsushi; Asada, Shinji; Mishima, Masayoshi; Kodama, K.

doi:10.1016/0735-1097(91)90972-c

Cited by 7 publications

(6 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Restenosis is probably initiated within hours after PTCA [23,24]. While smooth muscle cell migration from the media to the intima occurs within the first 3-4 days following PTCA, the actual proliferation of these cells appears to begin somewhat later (at days 7-20) [50]. It is conceivable that a longer steroid course, including prolonged treatment prior to PTCA, may show benefit, though possibly with increased toxicity.…”

Section: Study Limitationsmentioning

confidence: 99%

A randomized trial of corticosteroids for the prevention of restenosis in 102 patients undergoing repeat coronary angioplasty

Stone

Rutherford

McConahay

et al. 1989

Cathet. Cardiovasc. Diagn.

View full text Add to dashboard Cite

To examine the effect of corticosteroid therapy on the development of restenosis following successful percutaneous transluminal coronary angioplasty (PTCA), we randomized 102 patients with restenosis following prior PTCA to receive high-dose steroids (n = 52) or no steroids (n = 50). The steroid regimen consisted of 125 mg methylprednisolone I.M. the night before and morning of the PTCA, and prednisone 60 mg p.0. Q.D. for 1 week Angiographic follow-up at 6 months was available in 27 steroid-treated patients (52%) and 27 controls (54%). The per lesion incidence of restenosis was similar in the two groups (36% vs. 40%, respectively, P = NS). Clinical follow-up was available in the remaining patients at a mean interval of 1.2 years. The clinical correlates of restenosis (incidence and severity of angina, positive treadmill exercise test, nonfatal infarction or death) were similar in the steroid treated and control groups (24% vs. 39%, respectively, P = 256). At late follow-up, 30 steroid-treated patients (58%) and 26 control patients (52%) had no clinical or angiographic evidence of restenosis (P = NS).In conclusion, a short course of high-dose corticosteroid therapy does not significantly reduce the frequency of restenosis following PTCA.

show abstract

Section: Study Limitationsmentioning

confidence: 99%

A randomized trial of corticosteroids for the prevention of restenosis in 102 patients undergoing repeat coronary angioplasty

Stone

Rutherford

McConahay

et al. 1989

Cathet. Cardiovasc. Diagn.

View full text Add to dashboard Cite

show abstract

“…Restenosis after coronary stenting is chiefly caused by inflammatory reactions due to injury to the vascular wall, resulting in cell proliferation and intimal hyperplasia 27–31 . The onset of these inflammatory reactions occurs soon after procedure at the molecular level, 40–43 resulting in reactions at the cellular level within a few days 44 . Therefore, we suspect that it is essential to suppress the inflammatory response to vascular injury as early as possible before diverging and spreading of inflammatory reactions.…”

Section: Considerationsmentioning

confidence: 99%

“…[27][28][29][30][31] The onset of these inflammatory reactions occurs soon after procedure at the molecular level, [40][41][42][43] resulting in reactions at the cellular level within a few days. 44 Therefore, we suspect that it is essential to suppress the inflammatory response to vascular injury as early as possible before diverging and spreading of inflammatory reactions.…”

Section: Considerationsmentioning

confidence: 99%

Hydrocortisone Reduces Restenosis After Stenting of Small Coronary Arteries

Kakio¹,

Matsumori²,

Ohashi³

et al. 2004

J Interven Cardiology

View full text Add to dashboard Cite

Stenting of small coronary arteries has been limited by high rates of restenosis, and restenosis after stenting has chiefly been attributed to inflammatory reactions resulting in cell proliferation and intimal hyperplasia. In order to suppress this inflammatory process, we examined the effects of hydrocortisone, an antiinflammatory agent, on restenosis after stenting in a nonrandomized retrospective registry. The study population consisted of 193 patients treated at two hospitals, who underwent stent implantations in coronary arteries of reference diameter <3 mm between February 1999 and September 2001. Target lesions included complex, restenotic, diabetic, or chronic total lesions and types of implanted stents were Multi-Link, S-series, and gfx stents. Effect of intravenous administration of hydrocortisone (200 mg) before stenting was compared to control patients who did not receive this treatment. There was no significant difference of early outcomes between the hydrocortisone group and the control group. On angiographic follow-up at 6 months after stenting, the rate of restenosis was significantly lower in patients treated with hydrocortisone as compared with control group (22.8% vs 37%, respectively; P < 0.05). The revascularization rate of target lesion at 6 months was also significantly lower in the treated group (16.5% vs 29%, respectively; P < 0.05). These results suggest that preprocedural intravenous administration of hydrocortisone reduces restenosis after stenting of small coronary arteries. Prospectively controlled trials will be necessary to confirm this preventive effect of hydrocortisone on coronary in-stent restenosis.

show abstract

“…Histologicamente, a hiperplasia da íntima difere significativamente da placa aterosclerótica, quanto à arquitetura celular e ao conteúdo lipídico. Estudos utilizando microscopia eletrônica 8 e imuno-histoquímica 9,10 têm demonstrado que a neo-íntima é formada fundamentalmente por célu-las musculares lisas envoltas em matriz extracelular. O espessamento da íntima não se vincula, necessariamente, à presença de reestenose 11 .…”

Section: A Hiperplasia Da íNtimaunclassified

“…A CML vascular em estado proliferativosintético é particularmente difícil de ser diferenciada de fibroblastos, sendo algumas vezes referida como miofibroblasto 17 . Vários meses após a angioplastia, as células musculares revertem do fenótipo proliferativo-sintético para o contrátil 8,11 . Como o processo aterosclerótico representa um estímulo para a ativação da CML vascular [18][19][20] , é possível que a dilatação de lesões que possuam células musculares ativadas possa facilitar o desenvolvimento da hiperplasia da íntima 21,22 .…”

Section: A Hiperplasia Da íNtimaunclassified

Reestenose pós-angioplastia. Fisiopatogenia

Caramori¹,

Yamamoto²,

Zago³

1997

Arq. Bras. Cardiol.

View full text Add to dashboard Cite

A angioplastia coronária transluminal percutânea (ACTP), desde sua introdução por Andreas Grüntzig 1 , adquiriu papel destacado no manejo da cardiopatia isquêmica. Atualmente, grande parte das lesões coronárias obstrutivas são passíveis de tratamento percutâneo, com um índice de sucesso primário -lesão residual <50% e ausência de complicações maiores ->90%. Entretanto, reestenose ou recorrência da lesão persiste, sendo a principal limitação dos procedimentos coronários intervencionistas, ocorrendo em 20 a 40% das obstruções inicialmente dilatadas com sucesso 2,3 . A necessidade de procedimentos diagnósticos e terapêu-ticos repetitivos determina um marcante prejuízo à evolução dos pacientes que desenvolvem reestenose e eleva, significativamente, os custos globais do tratamento. A despeito de que múltiplas alternativas tenham sido avaliadas, poucas abordagens têm se mostrado promissoras na tentativa de reduzir a incidência de reestenose. O implante de próteses endocoronárias ou stents é a única intervenção que determina redução clinicamente significativa da reestenose 2,3 . Entretanto, seu uso implica elevados custos. Além disso, os efeitos da permanência a longo prazo de um corpo estranho na parede coronária ainda não foram totalmente definidos.A reestenose desenvolve-se, fundamentalmente, nos primeiros meses após a angioplastia, tendo o pico de incidência entre o 3º e o 6º mês após o procedimento 4,5 . Sua fisiopatologia é complexa e multifatorial, não estando completamente entendida. Observa-se que a redução no diâme-tro luminal coronário que leva a reestenose pós-angioplastia pode se estabelecer de forma precoce ou tardia. Nas primeiras horas após a angioplastia, pode haver redução do lúmen coronário por formação de trombo mural ou por retração elástica. A trombose mural muitas vezes está vinculada a eventos agudos e à oclusão arterial, especialmente na angioplastia no infarto agudo do miocárdio ou angina instável. Quando subclínica, é provável que esteja associada à redução tardia do lúmen coronário. Por sua vez, a retração elástica que provavelmente é causada pela elasticidade do segmento não aterosclerótico da parede vascular, freqüentemente, ocorre de maneira assintomática e parece ser um importante determinante dos resultados a longo prazo, principalmente da angioplastia por cateter-balão 4 . Os eventos que ocorrem tardiamente ao procedimento -após os primeiros dias -são os principais determinantes da reestenose, independentemente da técnica utilizada: cateter-balão, aterectomia direcionada ou rotacional, laser ou stent. Neste artigo, são discutidos os dois mecanismos fundamentais de reestenose, que são a hiperplasia da íntima e o remodelamento geométrico negativo ( fig. 1). A HIPERPLASIA DA ÍNTIMAEm praticamente todos os pacientes submetidos a ACTP ocorre algum grau de hiperplasia da camada íntima, ou formação de neo-íntima. Este espessamento intimal é uma característica da resposta da parede vascular à injúria e ocorre independentemente da técnica de angioplastia utilizada 6,7 . Histologicamente, a hipe...

show abstract

Ultrastructural study of proliferating and migrating smooth muscle cells at the site of PICA as an explanation for restenosis

Cited by 7 publications

References 0 publications

A randomized trial of corticosteroids for the prevention of restenosis in 102 patients undergoing repeat coronary angioplasty

A randomized trial of corticosteroids for the prevention of restenosis in 102 patients undergoing repeat coronary angioplasty

Hydrocortisone Reduces Restenosis After Stenting of Small Coronary Arteries

Reestenose pós-angioplastia. Fisiopatogenia

Contact Info

Product

Resources

About