ライフサイエンスコーパス: malapposition

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 m this study are important for understanding malapposition as a quantitative, rather than binary phen

16 t in a high frequency of late-acquired stent malapposition as a result of positive vessel remodeling.

17 Postintervention acute stent malapposition (ASM) occurred in 34.3% PES- and 40.3% BMS

18 SA, the greater the likelihood of persistent malapposition at follow-up and delayed healing.

19 no significant difference in the rate of SES malapposition between the groups.

20 angiography was identified in 4 of 14 cases, malapposition by OCT in 5 of 9 cases, strut discontinuit

21 omplete lesion coverage, underexpansion, and malapposition comprises the main pathomechanism for both

22 The area of late malapposition correlated directly with the increase in E

23 0.001), but not the maximal or average axial malapposition distance, was greater in thrombosed compar

24 Late stent malapposition has been reported to be an abnormal findin

25 ent underexpansion in 42% of patients, stent malapposition in 32%, incomplete lesion coverage in 20%,

26 struts in the lumen center was the cause of malapposition in cases 2 and 4.

27 n; 2) ostial and/or bifurcation stenting; 3) malapposition/incomplete apposition; 4) restenosis; and

28 pposed struts (1.2% versus 0.3%; P=0.02) and malapposition length (1.3 versus 0.4 mm; P=0.06) were al

29 Late stent malapposition (LSM) is only detected if intravascular ul

30 aximum area, length, volume, and arc of late malapposition measured 3.1+/-2.4 mm(2), 3.3+/-2.2 mm, 21

31 stent was identified, and the angle of late malapposition measured.

32 gs in VLST patients in descending order were malapposition, neoatherosclerosis, uncovered struts, and

33 Late malapposition occurs in 4% to 5% of slotted-tube bare-me

34 response, with resolution and development of malapposition, occurs through 9 months post-treatment.

35 ealed dissections, or late stent-vessel wall malapposition over the stented and adjacent references s

36 the proliferative reaction mainly occurs and malapposition resolves.

37 persensitivity was exclusive to SES, whereas malapposition secondary to excessive fibrin deposition w

38 tion, the proximal stent hoop tilted causing malapposition, the contralateral side of the stent from

39 Newly acquired malapposition was detected in 10.4% and 3.3% of 2.5-mm s

40 follow-up, a higher frequency of late stent malapposition was detected in PES-treated lesions (46.8%

41 Late acquired stent malapposition was due mainly to positive remodeling and

42 BMS-treated lesions, but late acquired stent malapposition was more common in PES-treated lesions.

43 Late stent-vessel wall malapposition was noted in one placebo patient and no (1

44 Extensive strut malapposition was the presumed cause for ScT in 1 case.

45 The location of late malapposition was the stent edge in 8 of 9 patients.

46 ndependent predictors of late acquired stent malapposition were plaque/thrombus protrusion (odds rati

47 There were 9 patients (4.4%) with late malapposition, which is separation of at least 1 stent s