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1 ited by endoleak caused by inflow or outflow malapposition.
2 MS also resulted in more late-acquired stent malapposition (29.6% versus 7.9%; P=0.0005) resulting fr
3 lated to (1) stent underexpansion, (2) strut malapposition, (3) edge dissection(s), and (4) residual
4 ) mainly because of more late acquired stent malapposition (30.8%) compared with BMS-treated lesions.
5        The most frequent findings were strut malapposition (34.5%), neoatherosclerosis (27.6%), uncov
6 icularly associated with late acquired stent malapposition (36.8% versus 15.4% compared with nonatten
7 er, the "background" frequency of late stent malapposition after bare-metal stent implantation is not
8 dence and mechanisms of acute and late stent malapposition after primary stent implantation in ST-seg
9 ated to incomplete healing, leading to stent malapposition and incomplete reendothelialization.
10 laque is associated with late acquired stent malapposition and related less target lesion revasculari
11 -term hazards related to late-acquired stent malapposition and thus stent thrombosis.
12  stent thrombosis (ST) are stent uncoverage, malapposition, and neoatherosclerosis.
13 ) bioresorbable vascular scaffolds, avoiding malapposition, and revealing a single connector fracture
14                          Late acquired stent malapposition area correlated to the decrease of peri-st
15  tissue thickness, tissue coverage area, and malapposition area were automatically quantified.
16 m this study are important for understanding malapposition as a quantitative, rather than binary phen
17 t in a high frequency of late-acquired stent malapposition as a result of positive vessel remodeling.
18                 Postintervention acute stent malapposition (ASM) occurred in 34.3% PES- and 40.3% BMS
19 SA, the greater the likelihood of persistent malapposition at follow-up and delayed healing.
20 her side branch scaffolding length and lower malapposition (at bifurcation core and distal MV) with P
21 no significant difference in the rate of SES malapposition between the groups.
22 angiography was identified in 4 of 14 cases, malapposition by OCT in 5 of 9 cases, strut discontinuit
23 omplete lesion coverage, underexpansion, and malapposition comprises the main pathomechanism for both
24                             The area of late malapposition correlated directly with the increase in E
25 0.001), but not the maximal or average axial malapposition distance, was greater in thrombosed compar
26                                   Late stent malapposition has been reported to be an abnormal findin
27 ent underexpansion in 42% of patients, stent malapposition in 32%, incomplete lesion coverage in 20%,
28  struts in the lumen center was the cause of malapposition in cases 2 and 4.
29  is used to assess stent tissue coverage and malapposition in stent evaluation trials.
30 n; 2) ostial and/or bifurcation stenting; 3) malapposition/incomplete apposition; 4) restenosis; and
31 pposed struts (1.2% versus 0.3%; P=0.02) and malapposition length (1.3 versus 0.4 mm; P=0.06) were al
32                                   Late stent malapposition (LSM) is only detected if intravascular ul
33 aximum area, length, volume, and arc of late malapposition measured 3.1+/-2.4 mm(2), 3.3+/-2.2 mm, 21
34  stent was identified, and the angle of late malapposition measured.
35 gs in VLST patients in descending order were malapposition, neoatherosclerosis, uncovered struts, and
36                                         Late malapposition occurs in 4% to 5% of slotted-tube bare-me
37 response, with resolution and development of malapposition, occurs through 9 months post-treatment.
38 ealed dissections, or late stent-vessel wall malapposition over the stented and adjacent references s
39 the proliferative reaction mainly occurs and malapposition resolves.
40 persensitivity was exclusive to SES, whereas malapposition secondary to excessive fibrin deposition w
41                                           No malapposition, stent fracture or late strut discontinuit
42 tion, the proximal stent hoop tilted causing malapposition, the contralateral side of the stent from
43                               Newly acquired malapposition was detected in 10.4% and 3.3% of 2.5-mm s
44  follow-up, a higher frequency of late stent malapposition was detected in PES-treated lesions (46.8%
45                          Late acquired stent malapposition was due mainly to positive remodeling and
46 BMS-treated lesions, but late acquired stent malapposition was more common in PES-treated lesions.
47                       Late stent-vessel wall malapposition was noted in one placebo patient and no (1
48                              Extensive strut malapposition was the presumed cause for ScT in 1 case.
49                         The location of late malapposition was the stent edge in 8 of 9 patients.
50                     Stent underexpansion and malapposition were found in 74% and 22% of vessels, resp
51 ndependent predictors of late acquired stent malapposition were plaque/thrombus protrusion (odds rati
52 dences of focal lesions, underexpansion, and malapposition were similar between both cohorts, minimal
53       There were 9 patients (4.4%) with late malapposition, which is separation of at least 1 stent s