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placement) has significantly reduced mortality rate and complication incidence characteristics in of coronary stent restenosis on IVUS includ patients with myocardial infarction Nevertheless, the incidence of restenosis characteristics, in restenosis site, undeployment stent characterist stents (IRS) causing myocardial ischemia that requires target-injury reintervention characteristics, the characteristics of remodeling vascular remains high It usually presents with relatively stable clinical scenarios, undertakes however, a systematic review of the characteristics resten up to 20% of restenosis patients present with acute coronary syndrome resulting interventional in cardiologist to choose optimal the treatment st hemodynamic instability and even death, as demonstrated in variousrestenosis studies (balloon or stent or bypass surgery) Consequently, coronary stent restenosis hitherto is still a major concern A relatively of high proportion (60,5%) of restenosis injury in cardiologists with neointimal proliferation and stent abnormalities (stent un Percutaneous coronary angiography is routinely used to determine IRS; distortion, This stent malapposition, stent overlapping, stent fracture procedure, however, cannot exactly examine conditions of coronary stents the factors and contribute to coronary artery in stent restenosis vessels, as well as morphology of neointimal proliferation intimal hyperplasia was the dominant mechanism of ISR and s IntraVascular UltraSound (IVUS) provides accurate assessment of patterns the motivating of factor atherosclerosis plaque and coronary vessels, restenosis morphology andItstent should be noted that in this study, incidence of distal-end conditions Deep insights into characteristics of coronary stent post-intervention was higher than proximal-end, which is not consistent with restenosis including atherosclerosis plaque, stent conditions and associated requires factorsfurther investigation help reduce restenosis risk and offer appropriate management steps agaisnt We its hope that the results of this study will provide useful info causes cardiologist find optimal solutions during the intervention to li According to most updated recommendations worldwide and in Vietnam, prevent IVUS stent coronary restenosis is indicated to assess restenosis and its mechanism in order to guide treatment and Thesis structure: This thesis has 141 pages, divided management plan with grade IIa recommendation In Vietnam, there havechapters: been few Rationale (2 pages); Background (40 pages); Patient studies on stent restenosis, but no specific published study has pages), examined Results (32 pages); Discussion (38 pages); Results (2 p characteristics of stent restenosis using intravascular ultrasound Thereby, page) our study This thesis consists of 40 tables, figures and 32 charts “Characteristics and sevaral elements contribute to coronary arteryand in 111 stentof which are in Vietnamese and English respectively restenosis on intravascular ultrasound (IVUS)” was conducted and aimed to: (1) Describe characteristics of coronary artery in-stent restenosis on CHAPTER BACKGROUND intravascular ultrasound (IVUS) IVUS in assessment of IRS characteristics: (2) Determine factors associated with morphology of coronary artery in-stent IVUS is employed in assessment of: restenosis on intravascular ultrasound (IVUS) 1.1 IVUS in assessment of degree of restenosis: IVU The significance of thesis: accurately measure minimal luminal area (MLA) in restenosi Achile heel of coronary stent era is IRS Is causes serious consequences, even calculate percentage restenosis area death Although many efforts have been made to reduce restenosis and treatment, 1.2 IVUS in assessment of morphological characteristics o coronary IRS still occurs at a high rate Nonethelesss, along with its success comes Restenosis morphology in different types of in-stent res a phenomenon of coronary stent restenosis and devastating consequences,* even Restenosis morphology on IVUS is classified into four t death Despite various efforts in restenosis prevention and treatment, its incidence percutaneous coronary angiography, including focal and diffure is still high with a re-intevention rate of 50 - 70% in patients with recurring angina + Focal or localised restenosis: Restenosis length ≤ 10 mm and a subset of patients re-admitted due to fatal complications such as recurring reference artery adjacent to the injury It is one of the common causes leading to reintervention of the culprit artery 1.3 IVUS in assessment of characteristics of neointimal tissue proliferation: CHAPTER PATIENTS AND METHO Neointimal tissue proliferation is a response of vascular walls injured by 2.1 balloon Methods: A prospective, observational, descriptive, cross-s angioplasty, stent placement and other equipments IVUS enables clinicians 2.2 Patients to assess characteristics of intra-stent neointimal proliferation such as echoluent 2.2.1 Inclusion or criteria: hypoechoic neointimal proliferation, echodense plaque, unstable or ruptured - Patients with history of coronary artery stent, suspected o plaque, thrombosis and eligible for percutaneous coronary angiography 1.4 IVUS in assessment of characteristics of in stent restenosis injury: -IVUS A diagnosis of in-stent restenosis was confirmed on imag is capable of assessing stent conditions after primary intervention incoronary a moreangiography detailed and explicit way than selective coronary angiography Clinicians can - IVUS not was indicated and successfully performed only measure stent parameters but also directly observe stent conditions such - Diagnositc as criterion of in-stent restenosis: Based on per stent underexpansion, stent malapposition, stent fracture, stent overlap, stent angiography: gap, A reduction in vascular lumen diameter at previo stent distortion (measured by QCA method) 1.5 IVUS in assessment of characteristics of post-stenting vascular - Criterion of successful IVUS: Restenosis image displa remodelling: Vascular remodeling is a phenomenon in which vascular sizeeligible changes for measuring parameters in this study over time due to fibroblast proliferation in the outer layer of vascular - wall, Criterion of failed IVUS: Restenosis image displayed transformation into muscular fibroblasts, outer layer thickening (or contraction) eligible and for measuring parameters in this study increased cellular density Negative remodelling is defined as a decrease 2.2.2 Exclusion in criteria: vascular size, and vice versa, positive remodelling is when vascular size expands Patients were excluded from this study if presented with o 1.6 Several combined factors on IVUS associated with in-stent restenosis:The criteria: - Hemodynamically instability radical reason for in-stent restenosis is neointimal proliferation However, various - Refusal to participate in this study or failed IVUS studies demonstrated that other factors combined with neointimal proliferation 2.3 Measurement can and assessments of in-stent restenos trigger restenosis, namely negative remodelling, stent underexpansion, percutaneous stent coronary angiography by QCA: Referenc malapposition, stent fracture, stent distortion These concomitant conditions Percentage at diameter restenosis, Percentage area restenosis, restenosis site can be detected on IVUS restenosis type Assess concurrent lesions: plaque, calcification, Several factors associated with restenosis morphology on IVUS 2.4 Measurement and assessments of in-stent restenosis par 2.1.Factors related to focal and diffuse restenosis on IVUS: Focal Locateand restenosis site, proximal reference site, distal reference diffuse restenosis are associated with prognosis of target-injury re-intervention analyse and the following parameters from three typical cross-secti choice of treatment method for restenosis injury size, vascular lumen, stent and intra-stent neointimal proli Factors related to restenosis morphology include patient characteristics, length, type of restenosis patterns (focal or diffuse), intra-stent resten stent, and technique of intervention Previous studies consistently showed marginthat restenosis patterns, stent conditions, remodelling negativ restenosis in bare-metal stents normally was diffuse restenosis (57% - 90.7%), 2.5 Data analysis: Data from this study was analysed by s while in drug-eluting stents mostly was focal (47-83.9%) on StataMP 14.2, with P < 0.05 yielding statistical significance In addition to previous factors, patient-related factors such as diabetes mellitus or cigarette smoking were linked to diffuse restenosis in some studies significantly different with p = 0,0001 when compared to mini medical history of coronary artery stent with a mean age of 66.9 ± 8.9 years old, of the reference vessel (9.8 ± 2.6 mm2) whom 60 patients (80%) were male Among their 91 restenosis lesions occuring in of restenosis on IVUS 62 drug-eluting stents, bare-metal stents and 21 stents with unknown 3.2.2 drugs,Characteristics 42 and 49 lesions were classified as moderate and severe restenosis, respectively 3.2.2.1 Characteristics of restenosis patterns on IVUS The mean duration of stent age was 53.8± 40.6 months Eight stents (8.8%) Outhas of 91 lesions on IVUS, 40 (44.0%) were focal resteno a life of less than 12 months, while the other 72 stents (91.2%) has a life of(56.0%) equal towere diffuse restenosis (type 2, 3, and 4) or greater than 12 months 3.2.2.2 Characteristics of neointimal proliferation 3.1.1 Cardiovascular risk factors of study participants * Characteristics of neointimal proliferation - 87.5% of our patients had more than one cardiovascular risk factors, among which hypertension was identified in 91.2% of our patients, diabetes mellitus inTable 3.3 Atherosclerotic plaque and neointimal pr Mean ± 35%, cigarette smoking in 26.2% and obesity (BMI ≥ 23 kg/m2) in 40.7% Parameters 3.1.2 Percutaneous coronary angiography results P&M (mm2) 10.48 ± • Patients with lesions in ≥ coronary trunks: 50/80 (62.5%) % P&M (%) 75.8 ± • Percentage diameter restenosis on angiography:: 68.4 ± 12.5% (50-100%) Plaque residues (mm2) 5.43 ± 3.2 Characteristics of coronary in-stent restenosis on IVUS Intimal hyperplasia (IH) (mm2) 7.1 ± 10 3.2.1 Vessel and stent size at restenosis site and reference site (n =91) % Intimal hyperplasia (% IH) (%) 60.0 ± 3.2.1.1 Vascular and luminal size at restenosis site and reference site * Patterns of neointimal proliferation Table 3.1 Vascular and luminal cross-sectional size on IVUS Table 3.4 Patterns of neointimal proliferatio Parameters Proximal-end Restenosis Distal-end Mean Patterns n (Mean ± SD) reference site site reference site reference Echolucent Vascular size Echodense 49 EEMA (mm ) 17.1 ± 4.6 13.7±3.8* 10.9 ± 4.1 13.8±3.1* Mixed 25 EEMaD (mm) 4.8 ± 0.6 4.2 ± 0.6 3.7 ± 0.7 Unstable EEMD (mm) 4.4 ± 0.6 4.0 ± 0.6 3.5 ± 0.6 Luminal size Ruptured MLA (mm2) 11.6 ± 3.8 3.1 ± 0.9** 7.6 ± 2.9 9.8 ± 2.6 ** Thrombosis MLA < mm2 (n/%) (0) 77 (84.6) (8.8) (0.0) Calcified 37 MaLD (mm) 3.9 ± 0.6 2.0 ± 0.3 3.2 ± 0.6 - * Relationship between neointimal proliferation and dura MLD (mm) 3.5 ± 0.6 1.8 ± 0.3 2.9 ± 0.5 Table 3.5 Plaque patterns and duration of sten % Restenosis on IVUS 67.7 ± 9.0 Plaque patterns Mean durati * p > 0.05 ** p < 0.05 (mo Table 3.1: Vascular size at the restenosis site was similar to the reference vessel Echolucent plaque (n = 8) 25.9 ± 22.8 (3 -5 with no statistically significant difference (13.7 ± 3.8 vs 13.8 ± 3.1 mm , p > 0,05) Unstable plaque (n = 9) 49.4 ± 10.1 * (8 A high proportion (84.6%) of MLA at the restenosis site was less than mm Echodense/Mixed/Unstable plaque (n = 82) 58.5 ± 42.2 * (4 3.2.1.2 Stent size at restenosis site (* p < 0.05 in comparisons with duration of stent life of echo Table 3.2 Stent size at site of lesion 3.5 indicates that duration of stent age was associat Parameters Mean ± SD or n and Table % % restenosis on IVUS 68.9 ± 7.9 58.1 ± 11.8 luminal < 0.05 diameter (MLD) in the positive remodelling gr Minimal luminal area (mm2) 3.0 ± 0.9 3.6 ±1.1 < 0.05 significantly higher than the negative remodelling group (9.2 ± Minimal luminal stent area (mm2) 8.5 ± 2.3 7.0 ± 1.7 2.2> 0.05 mm2, and 1.9 ± 0.2 mm vs 1.8 ± 0.2 mm, respectively), Reference-vessel minimal luminal 9.9 ± 2.6 8.9 ± 7.5 > 0.05 of stent underexpansion (MLSA/MLAreference < 90% prevalence area (mm2) restenosis, however, were lower in those with positive remode Table 3.6: Patients with intimal hyperplasia had significantly with a higher negative remodelling (33.3% vs 61.1%, and 62.7 ± percentage of restenosis (68.9 ± 7.9 % vs 58.1 ± 11.8%, p < 0.05) and lower MLA all p < 0.05) respectively, (3.0 ± 0.9 mm vs 3.6 ± 1.1 mm, p < 0.05) compared to the other group 3.2.3 Several combined lesions in in-stent restenosis 3.2.2.3 Characteristics of stent at site of restenosis 3.2.3.1 Neointimal proliferation and stent underexpansion(MLS Table 3.7 Stent conditions at site of lesion Our study consisted of 81 lesions with %IH ≥ 50% and 10 Characteristics on IVUS n 3.9%describes frequency of combination between intimal hy Edge stent restenosis 53 58.2 underexpansion in in-stent restenosis Stent underexpansion (MLSA/MLAreference < 90%) 51 56.0 Table 3.9 Intimal hyperplasia (%IH ≥ 50%) and stent u Stent distortion 22 24.2 (MLSA/MLAreference < 90%) in in-stent resten Stent overlap 15 16.5 Intimal hyperplasia Stent under Stent malappostion 9.9 (n/%) (MLSA/MLA Inter-stent gap 1.1 Present Stent fracture 1.1 (n = 51) 3.2.2.4 Characteristics of vascular remodelling Present 46 (50.5) Table 3.8 Comparison of characteristics between two groups of negative and (IH ≥ 50%) (n= 81) Absent (IH < 50%) (n =10) (5.5) positive vascular remodelling Table 3.9 shows 35 restenosis lesions (38.5%) resulted Vascular, luminal, stent and Mean ± SD or n and % hyperplasia, 46 lesions (50.5%) from combination of these tw atherosclerotic plaque Negative Positive p from only stent underexpansion, and the other lesions (5.5%) parameters remodelling remodelling of these two factors, one of which was due to stent fracture (n = 54) (n = 21) 3.2.3.2 MLA (mm2) 2.9 ± 0.8 3.3 ± 0.8 > 0.05Stent conditions and sub-strut calcified plaque MLD (mm) 1.8 ± 0.2 1.9 ± 0.2 < 0.05 Table 3.10 Sub-strut calcified plaque and stent co Stent conditions (n/%) Sub-strut calcified MLSA (mm2) 7.9 ± 2.2 9.2 ± 2.1 < 0.05 Present Abse % restenosis 69.9 ± 7.7 62.7 ± 8.3 < 0.05 (n = 37) (n = IH (mm2) 5.9 ± 6.3 11.8 ± 18.4 < 0.05 % IH 61.2 ± 12.1 58.3 ± 18.7 Stent > 0.05 malapposition (44.4) (55 IH ≥ 50% 49 (90.7) 19 (90.5) > 0.05 Stent distortion 18 (81.8) (18 P&M(mm2) 9.7 ± 3.2 12.9 ± 3.4 < 0.05 Stent underexpansion 31 (60.8) 20 (39 % P&M 75.9 ± 7.2 78.9 ± 4.9 >Table 0.05 3.10 shows that the group with sub-strut calcif Plaque residues (mm2) 4.9 ± 2.8 7.0 ± 2.7 < 0.05 significantly higher rate of distorted stents than the statistically Duration of stent life 63.1 ± 45.8 43.9 ± 31.8 > 0.05 vs 18.2%, p < 0.05) Odds ratio of stent distortion in it (81.8% (months) strut calcified plaque was 11,8 (CI: 3.2 – 52.7; p < 0.0001) Stent normal conditions 26 (28.5) (2.2) 28 percentage of area of intimal hyperplasia due to higher MLSA Stent abnormal conditions 55 (60.5) (8.8) 63 5,0 ± 1,9 mm2, and 56.7 ± 17.5% vs 62.8 ± 11.4%), with all p < Total 81 10 91 - In the moderate group, MLSA was significantly lower com On the off chance that just intiamal hyperplasia was significant, it just group (8.9 ± 2.3 mm2 vs 7.8 ± 2.2 mm2), with p < 0.05 represented 28.1% in the investigation, while the intimal hyperplasia combined * Re-intervention in two groups of moderate restenosis w with stent abnormal conditions was up to 60.5% and MLA ≥ mm2 3.2.3.4 Vascular remodelling and intimal hyperplasia Table 3.13 Re-intervention and minimal lumina In 75 lesions eligible for remodelling calculations, we further categorized Re-intervention MLA < mm2 MLA ≥ into subgroups based on whether negative or positive remodelling, and presence (n=31) (n = 11 or absence of intimal hyperplasia (%IH ≥ 50%) 49 lesions (65.3%) were classified Yes (n/%) (n=15) (25.8%) (63.6% as negative remodelling with intimal hyperplasia; lesions (6.7%) as negative No (n/%) (n = 27) 23 (74.2%) (36.4% remodelling without intimal hyperplasia; 19 lesions (25.3%) as positive Total 31 (100%) 11 (100% remodelling with intimal hyperplasia; and lesions (2.7%) as positive remodelling Moderate restenosis with MLA < mm2 had a significantl without intimal hyperplasia intervention (74.2%) than moderate restenosis with MLA ≥ mm 3.2.4 Comparisons of restenosis characteristics between moderate and severe 3.2.4.2 Several factors associated with severe restenosis on IVU restenosis groups Table 3.14 Relationships between several lesion indices on 3.2.4.1 Comparisons of restenosis features on IVUS between moderate and severe in-stent restenosis (severe compared to moderat of coronary restenosis groups Mean ± SD or n/% Table 3.12 Comparisons of restenosis features between moderate and severe Factors Moderate Severe OR restenosis groups (n=42) (n=49) Parameter Moderate Severe p Reference-vessel minimal (n=42) (n = 49) 10.3 ± 2.8 9.4 ± 2.3 0.85 ( luminal area (MLAreference) (mm2) Reference-vessel minimal luminal area 10.4 ± 2.8 9.4 ± 2.3 > 0.05 MLAreference ≤ 9mm 2.4 (MLAreference) (mm2) 12 (28.5) 24 (48.9) Reference-vessel minimal luminal area ≤ mm 12 (28.6) 24 (48.9) < 0.05 EEMATT (mm ) 0.8 (n/%) 14.6 ± 3.9 12.9 ± 3.5 External elastic membrane area (EEMA) (mm2) 14.6 ± 3.9 12.9 ± 3.5 < 0.05 % IH< ≥0.05 50% 34 (80.9) 47 (95.9) 5.53( Minimal luminal area < mm2 (n/%) 31 (73.8) 46 (93.9) 2.7 P&M (mm2) 11.15 ± 3.7 9.90 ± Diffuse 3.3 > 0.05 restenosis 18(42.9) 33(67.3) % P&M 75.2 ± 7.3 76.4 ± 12.3 > 0.05 Duration of stent age (months) 57.6 ± 6.7 53.4 ± 5.9 0.99 Plaque residues (mm2) 5.81 ± 2.64 5.11 ± 2.07 > 0.05 MLSA (mm2) 8.9 ± 2.3 7.8 ± 2.2 0.79 Intimal hyperplasia (IH) (mm2) 9.6 ± 14.8 5.0 ± 1.9 < 0.05 MLSA < mm2 24 (57.1) 39 (79.6) 2.9 ( % intimal hyperplasia (%IH) 56.7 ± 17.5 62.8 ± 11.4 < 0.05 Minimal luminal stent area (MLSA) (mm ) 8.9 ± 2.3 7.8 ± 2.2 0.05 Stent Bare 0.05 metal stent (BMS) (n=8) (12.5%) (87 Intimal hyperplasia (%IH ≥ 50%) 9.7 (1.7-56.1) < Drug-eluting 0.05 stent (DES) (n=62) 32 (51.6%) 30 (4 Reference-vessel minimal luminal area 3.1 (1.02-9.6) < Total 0.05 33 (47.1%) 37 (5 (MLAreference) ≤ mm2 Diffusee restenosis was the primary pattern in bare-m Minimal luminal stent area < mm2 1.9 (0.7-5.9) >Meanwhile, 0.05 in drug-eluting stents, focal restenosis was more co Table 3.17 The difference in distribution of restenosis patterns Table 3.15 shows that only two factors on IVUS increased degree of restenosis, was statistically significant namely intimal hyperplasia (OR: 9.7; 95%CI: 1.7-56.1) and reference-vessel Table 2.18 ISR patterns in different generations of drug minimal luminal area (MLAreference) ≤ mm2 (OR: 3.1; 95% CI: 1.02-9.6) 3.3 Several factors related to coronary in-stent restenosis patterns on IVUS Stent type Tái hẹp điểm Tái hẹp l 3.3.1 Several factors related to focal and diffuse restenosis patterns (n/%) (n/% 3.3.1.1 Several patients-related factors associated with restenosis patterns 1st-generation DES (n=38) 16 (42.1) 22 (57 Several patients-related factors associated with focal and diffuse restenosis 2nd-generation DES (n= 24) 16 (66.7) (33 patterns are illustrated in Table 3.16 Total 32 (51.6) 30 (48 Table 3.16 Several patients-related factors associated with restenosis patternsSecond-generation DES had a higher rate of focal re Factors Mean ± SD or n/% generation stents (66.7% vs 33.3%), albeit without statistical sig Focal Diffuse Table 3.19 Univariate logistic regression of some stent-re OR: (95% CI) p (n =40) (n =51) association with restenosis patterns Age (yrs) 66.8 ± 7.2 67.5 ± 9.8 1.01 (0.96-1.05) > 0.05 Mean ± SD or n Women (35.0) 13 (65.0) 1.61 (0.52 - 5.3) Factors > 0.05 Focal Diffuse OR Hypertension 37 (44.6) 46 (55.4) 0.74 (0.11 - 413) > 0.05 (n = 40) (n =51) Diabetes mellitus 11 (32.4) 23 (67.6) 2.1 (0.82 - 5.85) Duration > 0.05 of stent life (months) 53.4 ± 38.3 57.3 ± 44.7 1.0 ( Dyslipidemia 26 (51) 25 (49.0) 1.04 (0.32 - 3.3) Bare > 0.05 metal stent (2.5) (13.7) 8.53( Cigarette smoking 14 (56.0) 11 (44.0) 0.51 (0.18 - 1.43) Total > 0.05 stent length (mm) 47.8 ± 26.7 45.3 ± 17.9 0.99 ≥ CV risk factors 20 (50.0 ) 20 (50.0) 0.64 (0.25 - 1.61) Stent > 0.05 length ≥ 40 mm 28 (46.7) 32 (53.3) 0.72 Glucose 6.9 ± 3.0 7.2 ± 3.3 1.03 (0.89 - 1.18) MLSA > 0.05 < mm2 23 (36.5) 40 (63.5) 2.67 Creatinine 97.7 ± 24.3 90.5 ± 26.2 0.99 (0.97 -1.0) Stent > 0.05 underexpansion 21 (41.2) 30 (58.8) 1.29 ≥ multivessels disease 14 (35.9) 25 (64.1) 1.95 (0.7 - 5.16) Stent > 0.05 distortion 12 (54.5) 10 (45.5) 0.57 Table 3.16 indicates that diabetes mellitus prevalence in patients with diffuse Stent malapposition (66.7) (33.3) 0.35 restenosis was higher than in those with focal restenosis (67.6% vs 32.2%) with an In univariate analysis of some factors related to restenosis OR of 2.1; this difference, however, was not statistically significant stents had a higher risk of diffuse restenosis compared to drug-e 3.3.1.2 Several stent-related factors associated with restenosis patterns 8.53; 95%CI: 1.01-390.1; p < 0.05) * Stent types and instent restenosis patterns 3.3.2 Edge stent restenosis (ESR) and its associated factors 62 and lesions occurred in DES and BMS, respectively Fisher’s 3.3.2.1 exact test Prevalence of Edge stent restenosis was employed to compare two proportions in two groups with expected53 cell lesions (58.2%) had Edge stent restenosis (alone or co frequency ≤ 5, yielding the following table: body restenosis), of which had margin stenosis at both proxim adding up to a total of 58 sites of Edge stent restenosis investiga Edge stent Proximal Distal p Edge stent restenosis Body stent restenosis Edge Edge (n=58) (n=3 (n=58) (n=20) (n=38) MLSA (mm2) 8.0 ± 2.3 8.9 ± External elastic membrane area (EEMA) (mm2) 13.0 ± 3.9 14.2 ± 3.4 12.3 ±MLSA 4.1 > 0.05 < mm2 46 (79.3) 21 (5 Minimal luminal area (MLA) (mm ) 3.2 ± 0.9 3.3 ± 0.9 3.2 ±MLA 1.0 reference > 0.05 (mm2) 9.6 ± 2.7 10.2 ± Minimal luminal stent area (MLSA) (mm2) 7.6 ± 2.3 8.5 ± 2.0 7.2 ±Stent 2.3 < 0.05 underexpasion 37 (63.8) 19 (5 MLSA < mm2 46 (79.3) 12 (60.0) 34 (89.5) < 0.05 IH ≥ 50% 42 (72.4) 34 (8 Intimal hyperplasia (IH) (mm2) 4.4 ± 1.8 5.2 ± 1.9 4.0 ± 1.7 Compared < 0.05 to stent body restenosis, Edge stent restenosis h % intimal hyperplasia (%IH) 56.3 ± 10.5 59.5 ± 11.2 54.7 ±and 9.9 a>lower 0.05 rate of % IH ≥50% (72.4% vs 89.5%, p < 0.05) 3.3.2.6 Several factors related to stent margin restenosis on IVU % IH ≥ 50% (%) 42 (72.4) 16 (80.0) 26 (68.4) > 0.05 Table 3.23 Several parameters on IVUS associated Calcified intimal hyperplasia 16 (26.7) 10 (50.0) (15.8) < 0.05 OR (95% C 1.4 ± 3.5 1.09 ± 0.3 1.6 ± Parameters 4.3 > 0.05 on IVUS Remodelling index (RI) Intimal hyperplasia (IH ≥ 50%) 0.6 (0.07-1 (n=52) (n=18) (n=34) Stent>underexpansion (MLSA/MLAreference < 1.7 (0.7-4.4 Stent malapposition (8.6) (10.0) (7.9) 0.05 90%) Stent size at proximal edge was greater than at distal edge (8.5 ± 2.0 vs 7.2 ± Minimal luminal stent area < mm2 3.1 (1.1 - 2.3 mm2, p < 0.05) Prevalence of intimal hyperplasia (%IH ≥ 50%) in Edge stent Negative remodelling 0.7 (0.2- restenosis was 72.4%, with similar %IH at both proximal and distal ends (59.5 ± Drug-eluting stent 5.4 (0.9-58 11.2% vs 54.7 ± 9.9 %, p > 0.05) Restenosis at proximal margins had a higher In rate univariate analysis of some risk factors of Edge stent res of calcified plaques compared to distal margins (50% vs 15.8%, p < 0.05).mm Minimal was associated with an increased risk (OR = 3.1; 95%CI: luminal stent area < mm2 was identified in 79.3% of Edge stent restenosis lesions Distal edge restenosis had a higher prevalence of minimal luminal stent area < mm2 than proximal edge restenosis (89.5% vs 60%, p < 0.05), as illustrated in CHAPTER DISCUSSION Table 3.20 4.1 General characteristics of study participants 3.3.2.3 Vascular remodelling at Edge stent restenosis 4.1.1 Cardiovascular risk factors Two out of 20 proximal and four out of 38 distal edge of restenosis were ineligible to Cardiovascular risk factors in this study were primarily hy calculate remodelling index for lack of proximal or distal reference Prevalence of dyslipidemia (75%) and diabetes mellitus (35%) Mean age o negative and positive remodelling at Edge stent restenosis was respectively was71.1% over 65 years old These figures partially reflect an increas (37/52 lesions) and 8.9% (15/52 lesions) and metabolic diseases in Vietnam An astonishing increas 3.3.2.4 Stent type and Edge stent restenosis hypertension was reported by Vietnam Hypertension Associa Table 3.21 compares prevalence of Edge stent restenosis in two groupsincrease of drug-was attributable to salt-rich diets and daily-life str people Prevalence of type diabetes mellitus in our study was eluting stents and bare-metal stents previous studies such as E-SIRIUS study (19%), a study by Table 3.21 Edge stent restenosis in BMS and DES Stent type Edge stent restenosis Body stent restenosis (16%), p while consistent with another study by Byoung- Keuk Ki 4.1.2 Characteristics of ISR on percutaneous coronary angiograph DES (n/%) (n=62) 40 (64.5) 22 (35.5) Multivessel disease (≥ vessels) was identified in approxim < 0.05 BMS (n/%) (n=8) (25.0) (75.0) our patients (62.5%) It was shown to be an independent p Total 42 (60.0) 28 (40.0) 70 in other previous studies restenosis Parameter Minimal luminal stent area (MLSA) < mm2 was found in 63 out *ofRelationship 91 between neointimal hyperplasia and de restenosis lesions (69,2%) MLSA ≥ mm2 on IVUS is generally considered minimal as theluminal area, minimal luminal stent area and refere criterion of optimal post-intervention stent size to reduce risks of restenosis luminal andarea target-injury re-intervention months later In fact, optimal stent size is Restenosis not severity and minimal luminal area (MLA) in l achieved in all patients at the time of intervention In a study investigating 50% were significantly lower than in those with %IH < 50% intervention outcomes using IVUS by Johansson B, only 38% of stents achieved 58.1% ±a 11.8%, and 3.0 ± 0.9 mm vs 3.6 ± 1.1 mm, all p < luminal area ≥ mm2 In our study at the time of restenosis, MLSA < mm groups, could however, showed no significant differences in minima be attributable to initial small size of stent in order to be compatible with and small referencec-vessel minimal luminal area Studying co intervened vessels, stent underexpansion or chronic stent contraction neointimal proliferation and stent size on 221 Palmaz-Schatz st 4.2.2 Characteristics of restenosis on IVUS lesion with a follow-up duration of months, Hoffmann 4.2.2.1 Restenosis patterns neointimal hyperplasia thickness was independent of stent size In this study, focal restenosis (type 1) was presented in 40 lesions of onneointimal IVUS proliferation from stent size explains a high rate o (44.0%), while diffuse restenosis (type 2, and 4) in 51 lesions (56.0%) stents: Among with a same process of intimal hyperplasia, lumen of sm those with focal restenosis, 13 lesions (14,3%) had more than one affected susceptible site to stenosis than large vessels This pattern of multifocal restenosis in 13 lesions was all presented in DES 4.2.2.3 Characteristics of stents at site of restenosis 4.2.2.2 Characteristics of neointimal proliferation In our study on in-stent restenosis lesions, minimal luminal * Neointimal proliferation in in-stent restenosis restenosis (MLSA) (8.3 ± 2.3 mm2) was significantly lower th In our study, mean area of intimal hyperplasia (IH) was 7.1 mm area ; mean at site of reference vessel (MLAreference) (9.8 ± 2.6 mm2) percentage intimal hyperplasia (%IH) was 60.0% These findings are consistent Minimal luminal stent area (MLSA) < mm2 was found in with other studies examining intimal hyperplasia burden on restenosis using sites IVUS Investigating 49 restenosis lesions on IVUS, Marco T Castagna showedAnalysing that IVUS parameters on a large number of patien intimal hyperplasia burden (%IH) was 67.0 ± 9%, while another study Shunji by Kang Kasaoka proved that stent length, small reference-vess published a percentage of 65.9 ± 16.1% luminal area were prognostic factors of restenosis, with a In previous studies by Gary S Mintz, Soo-Jin Kang, Marco T Castagna, nearly 20% in stents with minimal luminal stent area (MLSA) intimal hyperplasia with % IH ≥ 50% played a significant role in mechanisms to 40% of in those with MLSA < mm2 coronary in-stent restenosis 89% of restenosis lesions in our study had %IH In our ≥ investigation, stent margin restenosis occurred with 50% In an investigation of Kang revealed after implantation at 348 DES ourInstudy this (58.2%) Besides, stent underexpansion was als study, %IH ≥ 50% was identified in 93% of restenosis sites abnormal condition in our study with a rate of 56% Stent disto * Characteristics of intra-stent neointimal proliferation on IVUS 24.2% of all lesions Our study also noted other stent abnormal Recently-formed neointimal hyperplasia was noted in 8.8% of restenosis later stent malapposition, stent fracture or stent gap lesions, echodense atherosclerotic plaques in 53.9%, mixed plaques in 4.2.2.4 27.5%, Characteristics of vascular remodelling calcified plaques in 40.6%, and unstable plaques in 9.9% Notably, ruptured * Prevalence of vascular remodelling in the study plaques and intra-stent thrombosis were found in 4.4% and 2.2% of lesions, Negative vascular remodelling is a phenomenon of vascu respectively times It was presented in a majority of restenosis lesions (72 In-stent restenosis is considered as a relatively stable clinical syndrome; study bya Khong Nam Huong reported that negative remodelli subset of patients with in-stent restenosis, though, present with clinical scenarios coronaryof artery injuries with a prevalence of 84% In ano acute coronary syndrome in various studies Acute coronary syndrome coronaryisartery injuries by Hoang Van Sy, negative remodellin apparently associated with formation of fresh atherosclerotic plaques of 59.1% remodelling In our study, restenosis was determined to be caused by sten Compared to in negative remodelling lesions, MLSA and MLD inMLSA/MLA positive reference < 90% and IH < 50%; by neointim remodelling lesions were significantly higher (9.2 ± 2.1mm2 vs 7.9 ± 2.2 MLSA/MLA mm2, and reference ≥ 90% and IH ≥ 50%; and by a combined 1.9 ± 0.2 mm vs 1.8 ± 0.2mm, all p < 0.05) Stent underexpansion were neointimal less proliferation and stent underexpansion if MLSA/ML common in positive remodelling than in negative remodelling (33.3% vs IH 61.1%, > 50% p 35 restenosis lesions (38.5%) were only hyperplas < 0.05) Moreover, positive remodelling lesions also experienced a lower 50%); degreeover of a half of lesions (50.5%) resulted from a combinat restenosis than negative remodelling lesions (62.7 ± 8.3% vs 69.9 ± 7.7, pwhile < 0.05) only lesions (5.5%) were underexpansion-induced Interestingly, positive remodelling had higher extra-stent atherosclerotic 4.2.3.2 plaque Stent conditions and sub-strut calcified plaques residues than negative remodelling (7.0 ± 2.7 vs 4.9 ± 2.8 mm2, p < Studies 0.05) have shown that plaque calcification also facilitates s Compared to negative remodelling, positive remodelling also contribute, In ourtostudy, a four out of 37 lesions with sub-strut calcification ( certain extent, to a reduction in restenosis risk, but an elevation in risks of of54latelesions without sub-strut calcification (9.3%) thrombosis and stent malapposition, as shown in previous studies onmalapposition vascular This difference, though, was not statistically s remodelling 0,05, which may be attributable to a small sample size in our stu As noted earlier, stent underexpansion was presented in 61.1% of negative * Stent distortion: remodelling lesions, nearly two-fold higher than in positive remodelling (33.3%), Studies have proved that eccentric or calcified atheroscle with p < 0.05 This index was also used by Giancarla to determine chronic induce stent stent under-deployment, and therefore, stent distortion underexpansion caused by negative vascular remodelling In this case, both lesions stent of stent distortion had sub-strut atherosclerotic plaque underexpansion and negative remodelling contribute together in mechanisms phenomenon of inof calcification in extra-stent plaques elevated risk stent restenosis or under-deployment with an OR of 11.8 (95% CI: 3.2 - 52.7; p 4.2.3 Common combinations of restenosis characteristics on IVUS 4.2.3.3 Neointimal hyperplasia and stent abnormal conditio 4.2.3.1 Neointimal hyperplasia and stent underexpansion Neointimal hyperplasia combined with abnormal stent condi According to MUSIC criteria, stent is considered as in a post-intervention in a high rate in our study (60,5%) This finding highlights th optimal condition on IVUS if minimal luminal stent area is ≥ 90% of referencefrom not only neointimal proliferation but also other combin vessel minimal luminal area Hence, stent underexpansion was defined in abnormal this study stent conditions that could trigger activation of neointi as a ratio of MLSA at site of restenosis and MLA at site of reference 4.2.3.4 Vascular remodelling and neointimal hyperplasia (MLSA/MLAreference) < 90% Neointimal hyperplasia combined with negative remodel The prevalence of stent underexpansion in this study was 56% common Stentpattern in this study (65.3%), while positive remodel underexpansion was presented in 20% of restenosis lesions with a criterion neointimal of hyperplasia less than 50% was presented in only MLSA/MLATCTB < 80% in a study on 49 restenosis lesions by Marco T Castagna restenosis lesions (2.7%) Notwithstanding no statistically signi Examining sirolimus-eluting in-stent restenosis on 28 lesions months percentage after intimal hyperplasia in both groups of negative and p stenting using IVUS, Byoung-Keuk Kim reported stent underexpansion in negative 48% ofremodelling lesions still had a higher degree of resten total lesions and a proportion of 33% of lesions with only neointimal hyperplasia that vascular shrinkage, in combination with neointimal hyp and no mechanistic causes such as stent underexpansion, stent margin restenosis contributes or to in-stent restenosis stent gap 4.2.4 Characteristics of moderate and severe restenosis Analysis mechanisms of restenosis in DES on IVUS, Kang proved that 4.2.4.1 drugSeveral characteristics of two groups of moderate and s eluting in-stent restenosis was primarily caused by neointimal proliferation IVUS Nevertheless, stent underexpansion and stent undersize were other mechanistic Compared to moderate restenosis lesions, reference-vesse factors contributing to in-stent restenosis Stent underexpansion, in that study, area ≤was mm2 was significantly more common in severe resten mm2, p < 0.05) These figures illustrate that not intimal hyperplasia itself among but its which a study by Chang examined clinical, procecdure burden (%IH) depends on stent size related factors associated with diffuse restenosis on 173 resten Among 42 moderate restenosis lesions on percutaneous coronary angiography, patients Among those patient-related factors investigate 31 lesions (73.8%) had MLA < mm2 on IVUS, 27 of which (64.3%) hypertension were lowered risk of diffuse restenosis with an OR subsequently re-intervened Using IVUS, we identified an addition of 1.025-4.103, 64.3% of p = 0.0420 lesions requiring re-intervention that would be otherwise missed on percutaneous Patients with multivessels disease (≥2 vessels) have an in coronary angiography times in IRS risk compared to those with only one vessel diseas The re-intervention rate in moderate restenosis lesions in our study was CI: in 1.266–6.745; line p =0.012), as demonstrated in a study by Zhao with rates of intervention in coronary moderate stenosis reported by Khong restenosis-associated Nam factors in 417 patients with in-stent reste Huong (73.7%) or Fernandes (68%) coronary angiography 12 – 48 months after stenting procedure Moderate restenosis lesions with MLA < mm2 had a significantly higer 17.5rate ± of 10.2 tháng) with degree of restenosis of 72.3 ± 16.7% re-intervention than those with MLA ≥ mm2 (74.2% vs 36.4%, p < 0.05) 100%) In In a 2018, Wang assessed 368 patients with diabetes, resu meta-analysis study on significance of IVUS in guidance of coronary intervention 20% Among risk factors such as age, smoking, medical treatm by Gary, the majority of studies established a threshold for intervention as IRS MLA was< similar between the groups with or without resten mm2 at left main and < mm2 at other sites This threshold was shown diffuse to be restenosis was significantly higher in patients with highly correlated with myocardial ischemia assessed by FFR as well as compared clinical to those with only one vessel disease (59.5% vs 40.8% symptoms Several studies on Asian patients published a lower threshold of study, MLAalthough < injuries involving ≥ multivessels disease nea mm2 In a study by Khong Nam Huong at National Heart Institute, MLAdiffuse < mm restenosis (OR: 1.95; 95%CI: 0.7 – 5.16), it was not stat was a risk factor associated with an increased severity of angina pectorispossibly on CCSdue to a limited sample size scale 4.3.1.2 Stent-related factors associated with restenosis patterns 4.2.4.2 Several factors related to severe restenosis on IVUS * Stent types and restenosis patterns In univariate analysis, reference-vessel minimal luminal area (MLAreferenceAssessing ) 0.05) (3) Inclusion of both statistical bare- significance though Nonetheless, when categorizing metal and drug-eluting stents in our study by MLSA < mm2, we noted a significantly higher prevalence 4.3.2.2 Characteristics of Edge stent restenosis at restenosis stent margins group compared to restenosis stent Edge stent restenosis is supposedly a result of stent margin injury induced vs 55.2%, by p < 0.05) Additionally, restenosis lesions at stent balloon inflation pressure Some authors proposed that proximal ends significantly formed a lower rate of intimal hyperplasia than at stent bod greater angle than distal ends, which predisposed them to injury duringp
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