Page 16 - Journal of Structural Heart Disease Volume 3, Issue 6

Original Research Article
172
mm for consistency of measurements), the pre-stent group showed only 44% (26–59) angiographic lu- minal diameter loss, whereas the single stent group showed 75% (62–85) luminal diameter loss (P = 0.007; Figure 5B).
Endothelialization and Exposed Stent Struts
There were no stent struts protruding into the lu- men of vessels in the pre-stent group (Figure 4 and 6), whereas numerous naked (i.e., non-endothelialized) stent struts were noted in the lumen of vessels in the single stent group (Figures 6G, 6H, and 6I). Accord- ingly, the degree of endothelialization was markedly higher in the pre-stent group (100% (89–100)) than in the single stent group (73% (56–96), P = 0.022; Table 2, Figure 5C).
Vessel Wall Injury
Similar degrees of vessel wall injury were noted in the pre-stent group and single stent group at the time of intentional fracture (i.e., short-term) with scores of 0.51 and 0.59, respectively. However, at mid-term evaluation, the injury score in the pre-stent group was signi cantly improved (decrease from 0.51 to 0.31, P = 0.046), whereas the injury score in the single stent group was unchanged (0.5, P > 0.05; Figure 5D), although the di erence between groups did not reach statistical signi cance (P = 0.067; Table 2, Figure 5D).
Lack of Injury to Adjacent Soft Tissue
Macroscopic examination of stented areas revealed a lack of external stent strut protrusion or transmural vessel injury in both the pre-stent and single stent groups (Figure 6). In both groups, the broken stent struts remained embedded in the vessel wall or ex- hibited inward protrusion due to the in-folding col- lapse of fractured stents (Figure 3, 4, and 6). There was no damage to the external part of the blood vessels or surrounding soft tissue (Figure 6C).
Microscopic examination of ve muscle groups in the hind limb, lymph nodes regional to the hind limbs and descending aorta, and multiple sections of brain, lung, each kidney, liver, heart, spleen, and spinal cord showed no important lesions and no evidence of thromboembolism or stent fragment displacement in any downstream (i.e., hind limb muscles/regional lymph nodes) or systemic tissues.
Discussion
Our study demonstrates the feasibility of inten- tional stent fracture of previously implanted stents with simultaneous pre-stenting in an in vivo piglet model. Additionally, pre-stenting appears to provide appropriate vessel patency, prevents vessel diameter loss, improves endothelialization rate, and prevents intraluminal protrusion of stent struts. Moreover, pre-stenting appears to be safe, with no damage to surrounding soft tissue and no signi cant vessel wall injury.
Stented vessel diameter and cross-sectional area were signi cantly improved by pre-stenting during simultaneous intentional stent fracture of previously placed stents compared with no pre-stenting. Inten- tional stent fracture causes a loss of stent integrity with a dramatic decline in radial sti ness and strength [4]. This decrease in radial sti ness and strength al- lows the blood vessel to recoil more than with an in- tact stent. Moreover, an irregular stent fracture pat- tern may result in an irregular vessel wall shape. Both recoil and irregular shapes of blood vessels lead to compromised vessel lumen with decreased vessel di- ameter and cross-sectional area, consistent with our ndings. As stent implantation is aimed at recovering areas of stenoses, it is of utmost importance that the stented vessel maintains appropriate patency. Simple stent fracture (i.e., unzipping) without the additional bene t of pre-stenting may not stabilize the vessel wall and may decrease vessel patency, thereby lead- ing to restenosis and a signi cant pressure gradient.
Endothelial coverage allows appropriate blood vessel function and prevents thrombus formation at the vessel wall [16]. Fractured and not pre-stented fragments may protrude into the vessel lumen and prolong or even prevent complete endothelializa- tion. Pre-stenting at the time of intentional fracture may prevent stent strut protrusion and thereby im- prove the chance of complete endothelialization with more rapid re-institution of physiologic vascular en- dothelial function.
Our observed vessel wall injury during pre-stent- ing was comparable to that after balloon angioplasty or single stent placement [6]. Incidental fracture of stents may cause severe vessel wall injury [17], and even intentional stent fracture in vivo (i.e., unzipping) may cause vessel wall damage due to an irregular
Journal of Structural Heart Disease, December 2017
Volume 3, Issue 6:165-175