Antikardiyolipin antikorların stent implantasyonu sonrası gelişen restenoza etkisi

Abstract

ÖZET ANTİKARDİYOLİPİN -ANTİKORLARIN STENT IMPLANT ASYONU SONRASI GELİŞEN RESTENOZA ETKİSİ Koroner stentler, yalnızca PTCA sırasında oluşan akut komplikasyonları tedavi etmek için değil, aynı zamanda, PTCA sonrası restenoz oranım azaltmak amacıyla da kullanılmışlardır. Stentlerin restenoz insidansını azalttığı gösterilmiştir; bununla beraber kesin olarak ortadan kaldıramamıştır. Restenoz, balon veya stent sonrası meyadana gelen arteriyel fiziksel zedelenme ile başlar. Bundan sonra inflamatuar ve trombotik mekanizmaları, neointimal hiperplaziyi ve damar rekoilini içeren kompleks bir olay başlar. Trombogenezde rol alan çeşitli faktörlerin restenoza etkisi olduğu da gösterilmiştir. ACL antikorların, SLE gibi otoimmün bir hastalığı olanlarda tromboz riskini arttırdığı da gösterilmiştir. Bu çalışmanın amacı, antikardiyolipin antikorlarının stent restenozuna etkisinin olup olmadığının araştırılmasıdır. Bu çalışmada, Ocak 1997 ile Şubat 1998 tarihleri arasında stent implante edilen 31 hastada aCL IgM ve IgG seviyeleri tesbit edildi. Enfeksiyöz ve otoimmün hastalığı olanlar çalışma dışı bırakıldı. Takip anjiografisi stent implantasyonu sonrası yaklaşık 6 ay sonra yapıldı. Restenoz, takipte koroner arter çapının %50'den fazla daralması olarak tanımlandı. Lezyon darlığının derecesi görsel tahminle belirlendi. Serimiz, restenoz tesbit edilmeyen 19 hasta, A grubu ve restenoz tesbit edilen 12 hasta, B grubu olmak üzere iki gruba ayrıldı. Tıbbi anemnez, laboratuvar bulgular ve stent ve lezyon özellikleri açısından iki grup arasında kıyaslama yapıldı. Restenozlu hastalarda aCL IgM, restenoz göstermeyen gruba göre daha fazla artış gösterdi. ACL IgG her iki grupta artış göstermesine rağmen iki grup arasında istatistiki bir fark göstermedi. Bunun yanında hem aCL IgM hem de IgG seviyeleri ile herhangi vasküler risk faktörleri ve laboratuvar bulgular arasında korrelasyon tesbit edilmedi. Sonuç olarak, stent sonrası aCL IgM'nin restenoz riski açısından bağımsız bir gösterge olduğu görülmüştür. Bizim çalışmamız, restenozda otoimmün ve trombojenik mekanizmaların da rol oynayabileceğini düşündürmüştür. -47-SUMMARY THE EFFECT of ANTİCARDIOLIPIN- ANTIBODIES ON RESTENOSIS AFTER STENT IMPLANTATION Coronary stents are used not only to treat acute complications during PTCA but also to reduce the restenosis rate after successful PTCA. Stents have been shown to reduce the incidence of restenosis; however, they are not a cure. Restenosis begins with the arterial physical injury created by balloon or stent. Thereafter, a complex cascade begins involving inflammatory and thrombotic mechanisms, neointimal hyperplasia, and vessel recoil. Several factors, which are involved in the trombogenesis, were shown their influence on restenosis. It was also shown that aCL -antibodies increase the rsik of thrombosis in patients with autoimmune disease such as SLE. The aim of this study is to investigate if there is the effect of aCL antibodies on stent restenosis. In this study, aCL IgM and IgG levels were determined in 3 1 patients undergoing stent placement between January 1997 and February 1998. Patients with autoimmune and infectious diseases were excluded from the study. Follow-up coronary angiography was performed approximately 6 months after stent placement; restenosis was defined as > 50 % reduction in diameter of the coronary vessel. The degree of lesion stenosis was determined by visual estimation. The series compromised 2 groups: 19 patients with restenosis (group A) and 12 patients without restosis (group B). Medical history, laboratory findings and stent and lesion properties were compared between two groups. In patients with restenosis, aCL IgM were more often increased than were those in patients without restenosis. ACL IgG increased in both groups but no difference between two groups. Furthermore, there was no correlation between any vascular risk factors or laboratory findings, or both with both aCL IgM and IgG levels. In conclusion aCL IgM appears to be an independent indicator for an increased risk for restenosis after stent placement. Our study suggest that autoimmune mechanism and thrombogenesis may also have a role in restenosis. -48-

SUMMARY THE EFFECT of ANTİCARDIOLIPIN- ANTIBODIES ON RESTENOSIS AFTER STENT IMPLANTATION Coronary stents are used not only to treat acute complications during PTCA but also to reduce the restenosis rate after successful PTCA. Stents have been shown to reduce the incidence of restenosis; however, they are not a cure. Restenosis begins with the arterial physical injury created by balloon or stent. Thereafter, a complex cascade begins involving inflammatory and thrombotic mechanisms, neointimal hyperplasia, and vessel recoil. Several factors, which are involved in the trombogenesis, were shown their influence on restenosis. It was also shown that aCL -antibodies increase the rsik of thrombosis in patients with autoimmune disease such as SLE. The aim of this study is to investigate if there is the effect of aCL antibodies on stent restenosis. In this study, aCL IgM and IgG levels were determined in 3 1 patients undergoing stent placement between January 1997 and February 1998. Patients with autoimmune and infectious diseases were excluded from the study. Follow-up coronary angiography was performed approximately 6 months after stent placement; restenosis was defined as > 50 % reduction in diameter of the coronary vessel. The degree of lesion stenosis was determined by visual estimation. The series compromised 2 groups: 19 patients with restenosis (group A) and 12 patients without restosis (group B). Medical history, laboratory findings and stent and lesion properties were compared between two groups. In patients with restenosis, aCL IgM were more often increased than were those in patients without restenosis. ACL IgG increased in both groups but no difference between two groups. Furthermore, there was no correlation between any vascular risk factors or laboratory findings, or both with both aCL IgM and IgG levels. In conclusion aCL IgM appears to be an independent indicator for an increased risk for restenosis after stent placement. Our study suggest that autoimmune mechanism and thrombogenesis may also have a role in restenosis. -48-