Microparticles in patients undergoing transcatheter aortic valve implantation (TAVI)

Abstract

Degenerative aortic stenosis (AS) is the most frequent form of acquired valvular heart disease. AS is known to entail endothelial dysfunction caused by increased mechanical shear stress leading to elevated circulatory levels of microparticles. Endothelial and platelet microparticles (EMP and PMP) are small vesicles that originate from activated cells and thrombocytes. We sought to evaluate whether transcatheter aortic valve implantation (TAVI) procedure would elicit effects on circulating EMP and PMP. 92 patients undergoing TAVI procedure for severe AS were included in this study. Samples were obtained at each visit before TAVI, 1 week post-procedure and at 1, 3 and after 6 months after TAVI and were evaluated using flow cytometry. A 12 month clinical follow-up was also performed. CD62E+ EMP concentration before TAVI was 21.11 % (±6.6 % SD) and declined to 20.99 % (±6.8 % SD) after 1 week, to 16.63 % (±5.4 % SD, p < 0.0001) after 1 month, to 17.08 % (±4.6 % SD, p < 0.0001) after 3 months and to 15.94 % (±5.4 % SD, p < 0.0001) after 6 months. CD31+/CD42b−, CD31+/Annexin+/− EMP remained unchanged. CD31+/CD41b+ PMP evidenced a slight, but statistically significant increase after TAVI and remained elevated during the entire follow-up. Apart from a procedure-related improvement in echocardiographic parameters, TAVI procedure led also to a decline in CD62E+ EMP. The reduction in pressure gradients with less hemodynamic shear stress seems also to have beneficially affected endothelial homeostasis.Electronic supplementary materialThe online version of this article (doi:10.1007/s00380-016-0885-z) contains supplementary material, which is available to authorized users.

Platelet Activation Is Limited during Transcatheter Aortic Valve Implantation in Patients on Aspirin Monotherapy and without per Procedural Clinical Complications

“…The association between shear stress and hemostatic activation has been demonstrated in vitro and in vivo in various clinical conditions, severe aortic stenosis being one of the best documented. Increased levels of sCD40L or sGPVI 14,15 in conjunction with a reduction of surface GPIba or GPVI, 16 platelet-derived chemokines 17 and serotonin 18 in platelet-free plasma, or of circulating platelet-derived microparticles [19][20][21] and platelet-monocyte aggregates 22 in whole blood have been reported in these patients. Platelet generation of eicosanoids resulting from the oxidative transformation of arachidonic acid through cyclooxygenase 1 (COX-1) and lipoxygenase (LOX) pathways is an early response to platelet activation.…”

“…12-HETE (ng/mL) median [IQ ] 9 . 0 [7][8][9][10][11][12][13][14][15][16][17][18][19][20][21] 2.6 [1.5-3.9] <10 3…”

“…In contrast, they were not correlated with serotonin levels at any time (p ¼ 0.89 and 0.93, respectively). Membrane exposure of CD62-P (MFI : 33 and 38 before and after, respectively, p ¼ 0.67), or CD63 (27 [23][24][25][26][27][28][29][30][31][32] and 30 [17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32] , p ¼ 0.36) did not vary and remained low.…”

Research update for articles published in EJCI in 2016

“…Of note, the TAVI procedure also led to a significant decline in EMP levels, likely via reduction in pressure gradients and consequently reduced turbulent flow. 87 What has come more in the focus is what is stored inside microparticles as potential additional messengers. Micro-RNAs have been in the centre of investigation in a broad spectrum of diseases (eg, diabetes) and might shed new light on endothelial signalling mechanisms in these disease conditions.…”

Mechanisms of Platelet Dysfunction in Patients with Implantable Devices

“…67 In patients treated with medical devices, a recent study has also demonstrated increased concentrations of procoagulant PMPs in patients post-TAVI even though endothelial cell-derived microparticles were decreased. 78 There is a persistent rise in PMPs and consequent increase in cellular adhesion molecule expression and inflammatory cytokines in VAD patients, potentially contributing to a perpetual cycle of vascular injury and perturbed hemostasis. 79,80 There was also a significant increase in phosphatidylserine-expressing procoagulant microparticles in patient subgroups with severe hemostatic complications.…”