Association of Adventitial Vasa Vasorum and Inflammation With Coronary Hyperconstriction After Drug-Eluting Stent Implantation in Pigs In Vivo

Abstract

Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jpIn order to reduce the adverse effects of the first-generation DES, many efforts have been made, including the development of a newer biocompatible DES. 9 Biolimus-A9 eluting stent (BES) is one of the new-generation DES with unique characteristics, such as biodegradable polymers that are absorbed into the arterial wall approximately 6 months after stent implantation. 9-11 Although BES has recently been shown to preserve ex-vivo coronary vasomotion as compared with SES in the short-term observations in pigs 12 and humans, 7 its mechanism remains largely unknown.We have previously demonstrated that Rho-kinase activation is a central molecular mechanism of coronary spasm in he widespread utilization of drug-eluting stents (DES) has remarkably reduced the risk of re-stenosis and of repeated revascularization. 1 However, the first-generation DES with durable polymers, such as sirolimus-eluting stents (SES), have no beneficial prognostic effects as compared with bare metal stents 2 or even cause unfavorable effects, such as stent thrombosis 3,4 and coronary hyperconstricting responses, 5-8 not only to acetylcholine, 5 but also to exercise 6 and atrial pacing. Background: The importance of adventitial inflammation has been implicated for the pathogenesis of coronary artery disease. However, the roles of adventitial changes in drug-eluting stent (DES)-induced coronary hyperconstriction remain largely unknown. In the present study, this issue in pigs in vivo with a special reference to adventitial vasa vasorum (VV) formation and Rho-kinase activation, a central mechanism of coronary vasospasm, was examined.

Pericyte-Specific Ninjurin1 Deletion Attenuates Vessel Maturation and Blood Flow Recovery in Hind Limb Ischemia

“… 36 Abnormalities in microvasculature, vasa vasorum in adventitial or perivascular fat of relatively bigger vessels including coronary arteries may contribute to atherosclerosis and functional spastic disorder. 37 , 38 Microvascular dysfunction in cardiac tissues also critically contributes to transition from compensative cardiac hypertrophy to heart failure. 39 It is well documented that vascular immaturation in tumor is associated with pathogenesis of tumor, including their growth and metastasis, and abnormalities in pericytes and their interaction with tumor ECs contribute to tumor vascular immaturation.…”

Two-year results after coronary stenting of small vessels in Japanese population using 2.25-mm diameter sirolimus-eluting stent with bioresorbable polymer: primary and long-term outcomes of CENTURY JSV study

“…Although these outcomes were largely satisfactory, over a prolonged period, the remaining polymer has been shown to induce inflammation associated with excessive coronary artery contractions and the development of vasa vasorum. It has been suggested that these long-term events may be preventable using a bioresorbable-polymer DES, which eventually becomes a BMS, because inflammation due to the polymer is reduced after the polymer disappears [15, 16]. Regarding outcomes for bioresorbable-polymer DESs, Wöhrle et al have reported the results of vessels ≤ 2.5 mm in diameter as a subgroup analysis of the CENTURY II trial.…”

“…2 Comparison of clinical outcomes at 9 months and 2 years with RESOLUTE φ2.25 mm Fig. 3 Comparison of clinical outcomes at 9 months and 2 years with other sizes of Ultimaster DES the polymer is reduced after the polymer disappears [15,16]. Regarding outcomes for bioresorbable-polymer DESs, Wöhrle et al have reported the results of vessels ≤ 2.5 mm in diameter as a subgroup analysis of the CENTURY II trial.…”

Vasospastic angina: pathophysiology and clinical significance

“…Кроме того, в КА, вовлеченных в спазм, увеличивается содержание молекул адгезии, например, P-селектина [29]. Исследования на животных продемонстрировали, что имплантация стента с лекарственным покрытием может усиливать воспаление адвентиции КА и вызывать их констрикцию посредством активации ROCK [30]. Доказано, что при ВС эпи-кардиальная и периваскулярная жировая ткань также вовлечены в патогенез неспецифического воспаления [31].…”