PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Remodeling”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources

[Type and extent of vascular remodeling in significant coronary lesions: An intravascular ultrasound study].

The purpose of this study was to assess the dimension of regional vascular remodeling and its influence on lumen narrowing in vivo. Sixty-three patients with 68 coronary lesions were imaged by intravascular ultrasound before transcatheter therapy. Quantitative measurements of lumen area, vessel area, and plaque area were performed at the lesion site and at the proximal and distal reference site. Area stenosis was calculated as plaque area/vessel area. 100. The extent of remodeling was quantified by a remodeling index (RI = stenosis vessel area - mean reference vessel area/mean reference vessel area. 100). Additionally, three different groups of vascular remodeling were defined: 1) positive remodeling = stenosis vessel area > maximal reference vessel area; 2) intermediate remodeling = maximal reference vessel area >/= stenosis vessel area >/= minimal reference vessel area; 3) negative remodeling = stenosis vessel area < minimal reference vessel area. In 57% of lesions stenosis vessel area was not in between the proximal and distal reference area: 29% of lesions (20/68) had positive, 28% (19/68) negative, and 43% (29/68) intermediate remodeling. Overall remodeling index averaged -0.8+/-19.7%. In the negative remodeling group, reduction of vessel area contributed to 40+/-21% of lumen narrowing, in the positive remodeling group, stenosis vessel area was 21+/-12% enlarged (p<0.001). Lesions with negative remodeling exhibit a lesser plaque area, lesions with positive remodeling a larger than other vessels (8.2+/-2.4 mm(2), 13.8+/-3.7 mm(2), 10. 8+/-3.7 mm(2); p <0.001). Distinct vascular remodeling occurred in the majority of atherosclerotic lesions and is a bidirectional process. Overall, the extent and the frequency of positive and negative remodeling was almost balanced. In lesions with negative remodeling the plaque area was significantly lesser than in other lesions.

Adult↗

Correlation of coronary arterial remodeling determined by intravascular ultrasound with angiographic diameter reduction of 20% to 60%.

Negative remodeling is commonly observed in stenotic coronary lesions. It is unknown whether negative remodeling is an early or late event. This study was designed to elucidate when negative remodeling occurs in the development of coronary stenosis. Remodeling was assessed by preintervention intravascular ultrasound in 104 native coronary lesions with intermediate stenosis (20% to 60% of diameter stenosis measured by quantitative coronary angiography). Positive remodeling was defined as lesion external elastic membrane (EEM) cross-sectional area (CSA) greater than the proximal reference, intermediate remodeling as lesion EEM CSA between those of the proximal and distal references, and negative remodeling as lesion EEM CSA less than the distal reference. Positive, intermediate, and negative remodeling were observed in 18%, 32%, and 50%, respectively, of lesions with intermediate stenosis. Lesions with negative and intermediate remodeling had more hard plaque compared with those with positive remodeling (79% vs 70% vs 42%, p = 0.02). Calcium was more frequent in lesions with negative and intermediate remodeling than in those with positive remodeling (52% vs 55% vs 16%, p = 0.01). Lesions with negative remodeling had smaller EEM CSA (11.5 +/- 5.2 vs. 13.7 +/- 3.4 vs 14.5 +/- 5.6 mm(2), p = 0.03) and less plaque (7.9 +/- 4.6 vs 10.8 +/- 3.4 vs 10.8 +/- 4.9 mm(2), p = 0.004) compared with positive and intermediate remodeling lesions, although lumen CSA (3.7 +/- 1.7 vs 2.8 +/- 0.8 vs 3.6 +/- 1.3 mm(2), p = 0.1) and area stenosis (57 +/- 15% vs 59 +/- 14% vs 56 +/- 10%, p = 0.7) were similar. Negative remodeling is frequently observed in lesions with intermediate stenosis. This suggests that negative remodeling occurs early in lesion formation.

Aged↗

Impact of preinterventional arterial remodeling on neointimal hyperplasia after implantation of (non-polymer-encapsulated) paclitaxel-coated stents: a serial volumetric intravascular ultrasound analysis from the ASian Paclitaxel-Eluting Stent Clinical Trial (ASPECT).

BACKGROUND: This study used serial volumetric intravascular ultrasound (IVUS) to evaluate the effect of preinterventional arterial remodeling on in-stent intimal hyperplasia (IH) after implantation of non-polymer-encapsulated paclitaxel-coated stents. METHODS AND RESULTS: Patients were randomized to placebo or one of two doses of paclitaxel (low dose, 1.28 microg/mm2; high dose, 3.10 microg/mm2). Complete preinterventional, post-stent implantation, and follow-up IVUS were available in 18 low-dose and 21 high-dose patients. IH volumes were similar in low-dose and high-dose patients: 17.6+/-15.1 mm3 in low-dose patients and 13.1+/-13.3 mm3 in high-dose patients (P=0.3). Therefore, IVUS findings in low- and high-dose patients were combined. Preinterventional remodeling was assessed by comparing lesion site to proximal and distal reference arterial area: positive remodeling (lesion>proximal reference, n=13), intermediate remodeling (distal reference<lesion<proximal reference, n=13), and negative remodeling (lesion<distal reference, n=13). During follow-up, there was a decrease in lumen volume in positive remodeling lesions (from 106+/-30 to 90+/-27 mm3; P=0.0067) and in intermediate remodeling lesions (from 97+/-28 to 76+/-31 mm3; P=0.0004), but not in negative remodeling lesions (99+/-27 versus 92+/-32 mm3; P=0.15). The follow-up IH volume was lower in negative remodeling lesions (5+/-7 mm3) compared with positive remodeling (20+/-14 mm3; P=0.0051) and intermediate remodeling lesions (20+/-15 mm3; P=0.0043); however, IH volume was virtually identical in positive and intermediate remodeling lesions. Multivariate linear regression analysis determined that remodeling and inflation pressure were independent predictors of IH volume; variables tested in the model included diabetes, acute coronary syndromes, dose, remodeling, and preinterventional plaque burden. CONCLUSIONS: Preinterventional arterial remodeling, especially negative remodeling, influences neointimal hyperplasia suppression after implantation of non-polymer-encapsulated paclitaxel-coated stents.

Coronary Restenosis↗

Influence of differential vascular remodeling on the coronary vasomotor response.

OBJECTIVES: Arterial remodeling may increase or decrease the luminal encroachment of atherosclerotic plaques in the coronary circulation. However, the factors determining the nature and consequences of the remodeling process remain poorly characterized. The study aims were to assess whether the pattern of vascular remodeling influences the physical and vasomotor responses of the coronary arteries in vivo in man. METHODS: Coronary vessel area, distensibility and stiffness were determined in positively, negatively and non-remodeled arterial segments using intravascular ultrasound and Doppler flow measurement. Epicardial vasomotor responses were determined following intracoronary boluses of acetylcholine (10(-6) and 10(-4) M), adenosine (24-30 microg) and nitroglycerin (200 microg). RESULTS: Fifty-six coronary arterial segments were studied in 25 patients. In comparison to non- and positively remodeled segments, negatively remodeled segments had a higher stiffness index (67+/-16 vs. 33+/-5 and 38+/-8, respectively; P<0.02) and appeared to have lower compliance and distensibility (0.66+/-0.17 vs. 1.65+/-0.54 and 0.94+/-0.18/mmHg; P=NS). Non-remodeled segments had a greater change in vessel area with 10(-6) M acetylcholine (4.9+/-0.8%), compared to positively and negatively remodeled segments (0.6+/-1.8% and -4.9+/-1.8%, respectively, P<0.05). A significant degree of preservation of vasodilatation to 10(-6) M acetylcholine was evident in positively remodeled compared with negatively remodeled segments (P<0.05). Nitroglycerin caused greater vasodilatation in non-remodeled segments (7.2+/-3.8%) than either positively or negatively remodeled segments (4.7+/-0.9 and 3.7+/-0.6%, respectively, P<0.05). CONCLUSIONS: Vascular remodeling is an important and major determinant of local epicardial vasomotor responses. Both structural and functional abnormalities are associated with negative remodeling that may contribute to the adverse effects of such lesions.

Acetylcholine↗

Impact of different definitions on the interpretation of coronary remodeling determined by intravascular ultrasound.

The objective of this study was to compare the categorizations and determinants related to remodeling by the three definitions commonly used. Several morphological and intravascular ultrasound (IVUS) studies have demonstrated the fundamental importance of arterial remodeling in atherosclerosis. However, lack of consensus on how to define remodeling has led to conflicting analyses of factors that influence this process. Analysis of pre-interventional IVUS images of 514 lesions in native coronary arteries was performed. Arterial remodeling was defined as outward by definition 1, when [cross-sectional area (CSA) of the external elastic membrane (EEM) at the lesion site (EEM(lesion))]/[EEM CSA either at the proximal (EEM(prox ref)) or distal (EEM(distal ref)) reference site with the least amount of plaque] was > 1.05, intermediate when this ratio was between 0.95 and 1.05, and inward when < 0.95. Remodeling was defined as outward by definition 2 when EEM(lesion) > both EEM(prox ref) and EEM(distal ref), inward when EEM(lesion) < both EEM(prox ref) and EEM(distal ref), and intermediate when EEM(lesion) was intermediate between EEM(prox ref) and EEM(distal ref). By definition 3, vessel remodeling was defined as outward when EEM(lesion) > (EEM(prox ref) + EEM(distal ref))/2 and intermediate/inward when EEM(lesion) < or = (EEM(prox ref) + EEM(distal ref))/2. The frequency of outward remodeling was significantly higher by definitions 1 and 3 than by definition 2, whereas a higher frequency of inward remodeling was observed in definition 1, resulting in significantly different remodeling distributions between the three definitions (P < 0.0001). By multivariate logistic analysis, the only clinical determinants related to outward remodeling was younger age, and only by definition 3. IVUS determinants varied significantly between the three definitions. The only consistent determinants among the three definitions were smaller lumen CSA at the reference site and larger plaque + media CSA at the lesion site. This study demonstrates the significant impact of different remodeling definitions on the incidence and determinants of remodeling patterns. The marked variability in categorization of remodeling underscores the importance of developing a standard methodology.

Aged↗

Differential effects of Rho-kinase inhibition on artery wall mass and remodeling.

PURPOSE: Constrictive remodeling and new artery wall mass contribute to lumen narrowing in atherosclerosis and following injury. Rho-kinase, an important regulator of myosin phosphorylation and cytoskeletal reorganization, is critical to smooth muscle cell (SMC) growth and vasoconstriction, but its role in artery wall remodeling is poorly defined. We hypothesized that constrictive artery wall remodeling is dependent on Rho signaling so that blocking Rho-kinase would promote outward artery wall remodeling in response to intimal hyperplasia and thus limit lumen narrowing. METHODS: To test this hypothesis, we first studied the effects of the Rho-kinase inhibitor fasudil on SMC remodeling of collagen matrix in vitro. Mouse aortic SMCs were seeded into three-dimensional collagen gels with and without fasudil, and extent of contraction was measured at 24 hours. We then used the mouse carotid ligation model to study the effects of Rho-kinase inhibition on remodeling and intimal hyperplasia in vivo. C57B6/J mice were randomly assigned to fasudil (100 mg/kg per day) or vehicle and underwent unilateral carotid artery ligation or sham ligation. Remodeling and wall mass were measured after 28 days. RESULTS: Fasudil blocked SMC contraction of collagen gels in a dose-dependent manner. Complete inhibition of collagen gel remodeling was achieved between 10 and 30 micromol/L fasudil. In control mice, carotid ligation caused significant thickening of the adventitia, media, and intima (P <.01) and outward remodeling of the carotid wall. The external elastic lamina (EEL) area increased by 14% versus sham (P <.05), but this increase was insufficient to prevent lumen narrowing (-42% vs sham, P <.05). Fasudil treatment had favorable effects on wall mass, inhibiting neointimal (P =.04), medial (P =.03), and adventitial thickening (P =.07) versus controls. Opposite our hypothesis, however, fasudil did not enhance outward artery wall remodeling or improve lumen caliber. Rather, inhibiting Rho-kinase blocked outward remodeling in response to ligation. EEL area was significantly smaller in treated versus control animals (P =.04) and slightly smaller versus shams (P = NS). These data suggest that Rho activation contributes significantly to both hyperplasia and outward remodeling of the injured artery wall. Rho-kinase may prove an important target to limit intimal hyperplasia and prevent restenosis when remodeling is improved by other means (eg, stents).

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

Vascular remodeling in atherosclerotic coronary arteries is affected by plaque composition.

BACKGROUND: Narrowing of lumen in atherosclerotic lesions is determined not solely by accumulation of plaque but also by constrictive or expansive vascular remodeling. Underlying mechanisms and determinants of these bidirectional processes are not known. OBJECTIVES: To elucidate the response of vascular remodeling to progressive atherosclerosis by analyzing its potential association with composition of plaque. METHODS: Seventy patients with 77 de-novo coronary artery lesions underwent intravascular ultrasound imaging before coronary intervention. Target lesions were defined as soft, fibrous/mixed, and calcified plaques. Quantitative measurements of area of lumen (A(L)), total area of vessel (A(TV)) and area of plaque (A(P) = A(TV)-A(L)) were performed at the lesion site and at the proximal and distal reference sites. Remodeling was determined by using a remodeling index [I(R) = (stenosis of A(TV)/mean reference A(TV)) x 100]. RESULTS: Overall vascular remodeling was balanced with a mean remodeling index of 100.2+/-19.3% and a high interlesion range (60.2-152.4%). The remodeling index for soft lesions was significantly higher than those for fibrous/mixed and calcified lesions (110+/-18.8 versus 96.2+/-14.4 and 85.9+/-15.1%, P < 0.01). Calcified lesions exhibited lower remodeling indexes than did uncalcified lesions (85.9+/-15.1 versus 104.6+/-18.4%, P < 0.01). CONCLUSIONS: Processes involved in vascular remodeling are affected by composition of plaque insofar as there is a higher prevalence of constrictive remodeling among calcified plaques and a higher prevalence of expansive remodeling among soft lesions. These findings indicate that constrictive remodeling is a late manifestation in atherogenesis. Future studies are warranted in order to enhance the understanding of progression of atherosclerosis, and of mechanisms of vascular remodeling and their impacts on interventional therapy.

Coronary Artery Disease↗

Relation between coronary artery remodelling (compensatory dilatation) and stenosis in human native coronary arteries.

OBJECTIVES: To investigate the contribution of plaque size and vessel remodelling to coronary artery stenosis and to assess the role of vessel shrinkage (negative remodelling) across a wide range of lesions. DESIGN: Postmortem study of coronary remodelling in perfusion fixed hearts. SUBJECTS: 24 men and 24 women who died suddenly with coronary artery disease. MAIN OUTCOME MEASURES: Percentage stenosis, percentage plaque burden, percentage remodelling, and arc of normal vessel were measured and related to age, sex, smoking status, and history of hypertension. RESULTS: There was a positive relation between percentage stenosis and percentage plaque burden (r = 0.6, p < 0.0001) and an inverse relation between percentage stenosis and percentage remodelling (r = -0.4, p < 0.0001). Multilinear regression modelling showed that luminal stenosis = 1.0 (plaque burden) - 0.4 (vessel remodelling). Remodelling was greater in lesions that would not have been significant at angiography (</= 25% stenosis) than in the remaining lesions (25.9 (26)% v 10.0 (21.1)%, p < 0.0001, respectively) and was reduced in segments with circumferential plaques (12.7 (24.5)% v 20.7 (24.3)% in eccentric plaques, p = 0.001). Remodelling did not correlate with age, sex, or smoking. Negative remodelling was present in 62 lesions with a stenosis > 25% versus 10 lesions with </= 25% stenosis (p < 0.0001). Lesions with negative remodelling had greater plaque burden and luminal stenosis and a reduced arc of normal segment. CONCLUSION: Outward arterial remodelling negates the stenosing effect of increasing plaque size. Significant coronary stenoses arise from a failure of this outward remodelling in the face of a large plaque burden. Coronary arterial remodelling is unrelated to sex or smoking and is plaque specific.

Adult↗

Relationship between coronary artery remodeling and plaque vulnerability.

BACKGROUND: In vivo studies with intravascular ultrasound have shown that complex plaque anatomy and plaque rupture are more frequent in the presence of marked outward remodeling. A large lipid core and a high macrophage count are recognized histological markers for plaque vulnerability. The link between plaque vulnerability in terms of these markers and remodeling in coronary arteries has not been explored. METHODS AND RESULTS: In 88 male subjects who died suddenly with coronary artery disease, 108 plaques were studied. The percent remodeling was calculated. Lesions with remodeling > or = 0% were considered to have positive remodeling, and those in which remodeling was < 0% were considered to have negative remodeling. Percent lipid core and macrophage count at the plaque were assessed. Of 108 plaque sites, 64 (59.2%) had undergone no remodeling or positive remodeling, and 44 (40.7%) had negative remodeling (vessel shrinkage). Lesions with positive remodeling, compared with lesions with vessel shrinkage, had a larger lipid core (percent mean lipid core was 39.0 +/- 21.0% versus 22.3 +/- 23.1%, respectively; P < 0.0001) and a higher macrophage count (mean macrophage count was 15.6 +/- 12.3 versus 8.9 +/- 11.6, respectively; P = 0.005). CONCLUSIONS: We have shown that coronary artery plaques with positive remodeling have a higher lipid content and macrophage count, both markers of plaque vulnerability. These results may explain why plaque rupture is often apparent at sites with only modest luminal stenoses (but marked positive remodeling).

Cell Count↗

[Comparison of the occurrence of positive and negative vascular remodeling in patients with stable vs unstable angina pectoris].

BACKGROUND: The vascular remodelling refers to the increase or decrease in EEM (external elastica membrane) area that occurs during development of atherosclerosis. The positive remodeling, which was thought only as a compensatory factor during atheroma development, was also found as a one of the main features of unstable plaque. The intravascular ultrasound is very good tool to measure different type of arterial remodelling. These findings correlate with histologic post-mortem specimen with excellent results. AIM OF THE STUDY: To correlate the remodelling index from patients suffered from stable angina pectoris (SAP) and from patients suffered from unstable angina (UA). METHOD: We performed IVUS in 51 patients. In the group of patients with unstable angina were included patients with worsening angina symptoms in last six weeks or with angina in rest. We used IVUS--endosonics In-Vision with 30 MHz probe Awanar with mechanical pull-back. We studied the occurrence of positive remodelling, negative remodeling (an index that describes remodeling is expressed as: lesion EEM CSA/reference EEM CSA. If the lesion EEM area is greater than the reference EEM area, positive remodelling has occurred, and the index will be > 1.0. If the lesion EEM area is smaller than the reference EEM area, negative remodelling has occurred, and the index will be < 1.0). RESULTS: We performed the intravascular ultrasound in 51 patients, 22 patients (43.1%) with unstable angina (UA) and in 29 patients (56.9%) stable angina (SAP). The positive remodelling was found in 14 patients (63.6%) in UA group vs. 5 patients (17.2%) in group with SAP, p < 0.05. The negative remodelling was found in 6 patients (27.3%) in UA group vs. 23 patients (79.3%) in SAP group, p < 0.05. CONCLUSION: Positive remodelling is more often found in patients with UA vs. in patients with SAP. Positive arterial remodelling is therefore one of the features of unstable atherosclerotic plaque.

Angina Pectoris↗

Mechanisms of atrial remodeling and clinical relevance.

PURPOSE OF REVIEW: Atrial fibrillation usually occurs in the context of an atrial substrate produced by alterations in atrial tissue properties referred to as remodeling. Remodeling can result from cardiac disease, cardiac arrhythmias, or biologic processes such as senescence. Recent advances in understanding remodeling have allowed for insights into mechanisms underlying atrial fibrillation that have been transferred from experimental models to humans. This paper reviews recent progress in understanding atrial remodeling, as well as the consequent clinical insights into atrial fibrillation pathophysiology and treatment. RECENT FINDINGS: Two principal forms of remodeling have been described in animal models of atrial fibrillation: ionic remodeling, which affects cellular electrical properties, and structural remodeling, which alters atrial tissue architecture. Atrial tachycardias (particularly rapid tachyarrhythmias such as atrial flutter and atrial fibrillation) cause ionic remodeling, which decreases the atrial refractory period and promotes atrial reentry. Congestive heart failure produces atrial interstitial fibrosis, which promotes arrhythmogenesis by interfering with atrial conduction properties. Recent animal studies have provided insights into the pathways involved in remodeling, and have indicated the pathophysiological role of remodeling in specific contexts. In addition, work in animal models has provided information about pharmacological interventions that can prevent the development of remodeling. Clinical studies have shown that novel approaches to remodeling prevention identified in animal work have potential therapeutic value in man. SUMMARY: Understanding atrial remodeling has the potential to improve our appreciation of the pathophysiology of clinical atrial fibrillation and to allow for the development of useful new therapeutic approaches.

Action Potentials↗

[Intravascular ultrasound study of coronary remodeling and determination of matrix metalloproteinase and hypersensitive C-reactive protein].

OBJECTIVE: To investigate remodeling characteristics of coronary lesions in patients with acute coronary syndromes (ACS) versus stable angina pectoris (SA) using intravascular ultrasound (IVUS), and to explore the relationship between arterial remodeling and clinical presentation or matrix metalloproteinase (MMPs) or hyper-sensitive C-reactive protein (hs-CRP). METHODS: We studied culprit lesions of 38 patients with ACS and 18 patients with SA using IVUS before coronary intervention. The lesion site and a proximal or distal reference site including the external elastic membrane (EEM) area and lumen area were analyzed. Plaque area and remodeling index (RI) were calculated, and directions of arterial remodeling were determined. Positive remodeling was defined as RI > 1.05 and negative remodeling as RI < 0.95. We analyzed the culprit lesion qualitatively, identified high risk plaque and compared them in each group. The blood level of MMP-2, MMP-9 and hs-CRP in each group were also determined. RESULTS: The plaque area at culprit lesions in patients with ACS was significantly larger (11.94 +/- 4.90 versus 9.17 +/- 3.36 mm2; P = 0.035), and also the RI in ACS group was significantly greater than that of patients with SA (0.972 +/- 0.222 versus 0.796 +/- 0.130; P = 0.003). The distribution of remodeling in these two groups was different: positive remodeling was more frequent in ACS group than in SA group (34.2% versus 5.6%, P = 0.047), whereas negative remodeling was more frequent in SA group (52.6% versus 88.9%, P = 0.003). There was higher incidence of high risk plaque in ACS group compared to SA (76.3% versus 50.0%, P = 0.040). The level of serum MMP-2 in ACS group was higher than that of SA group (250.65 +/- 47.97 microg/L versus 214.21 +/- 47.20 microg/L, P = 0.029). The same applied for plasma MMP-9 (84.26 +/- 9.78 microg/L versus 68.46 +/- 22.82 microg/L, P = 0.038) and serum hs-CRP (3.62 +/- 3.37 mg/L versus 1.48 +/- 1.52 mg/L, P = 0.041). CONCLUSIONS: Positive remodeling, larger plaque area and higher incidence of high risk plaque are associated with ACS, whereas negative remodeling is more common in patients with SA. This association between the extent of remodeling and clinical presentation may reflect a greater tendency that plaques with positive remodeling can cause ACS. The change of level of MMP-2, MMP-9 and hs-CRP in ACS patients may be helpful in investigating vulnerable plaques.

Adult↗

Mandibular remodeling after bilateral sagittal split osteotomy for prognathism of the mandible.

PURPOSE: To describe the postoperative remodeling changes in the mandible after bilateral sagittal split osteotomy to correct mandibular prognathism. PATIENTS AND METHODS: Twenty patients who underwent bilateral sagittal split osteotomy for the correction of mandibular prognathism were studied for postoperative remodeling changes within the mandible. The 6-week, 1-year, and long-term postoperative cephalometric mandibular tracings of 12 patients were superimposed using the fixation wires as the stable reference points to demonstrate the specific locations of the intrabony remodeling. RESULTS: There was a general direction of remodeling at the condylion and gonion anteriorly and superiorly, while the B point and pogonion did not show much change in remodeling. At the condylion, 60% and 40% of the cases showed significant horizontal and vertical remodeling, respectively. At the gonion, 50% and 55% of the cases showed significant horizontal and vertical remodeling, respectively. No correlation was found between the remodeling changes at condylion and gonion and the surgical movement or relapse at B point and pogonion. There was a significant correlation between the observed horizontal relapse at gonion and the horizontal remodeling changes at this point showing that the postoperative displacement of this point is a result of both positional translocation and remodeling changes. CONCLUSION: The results of this study show that there are intrabony remodeling changes that occur in the mandible after sagittal split osteotomy and that these continue for a long period of time in some patients. This remodeling occurred more in the condylar and gonial areas, while the chin remained relatively stable.

Adolescent↗

Preintervention arterial remodeling as a predictor of intimal hyperplasia after intracoronary stenting: a serial intravascular ultrasound study.

BACKGROUND: The impact of vascular remodeling pattern on intimal hyperplasia (IH) after coronary stenting is unknown. HYPOTHESIS: The preintervention remodeling pattern of the lesion might be associated with IH after the coronary stenting procedure. METHODS: Serial (pre-, post-stent implantation, and follow-up) intravascular ultrasound (IVUS) images were obtained in 58 patients with single-stent implantation (GFX stents in 41 and NIR in 17). The matching IVUS image slices at the preintervention lesion site were selected for serial comparisons. The remodeling index (RI) was defined as lesion/proximal reference external elastic membrane cross-sectional area (CSA) at preintervention lesion site. Adequate remodeling was defined as a RI > 0.95 and inadequate remodeling as a RI < or = 0.95. Vessel stretching, percent vessel stretching, and percent IH CSA, as well as pre- and postintervention IVUS variables were evaluated according to the remodeling pattern. RESULTS: The percent IH CSA was 31% in adequate remodeling (n = 29, mean RI = 1.05) and 41% in inadequate remodeling (n = 29, mean RI = 0.88) (p = 0.049). Percent vessel stretching was 15% in adequate remodeling and 22% in inadequate remodeling (p = 0.007). The RI inversely correlated with percent vessel stretching (r = -0.435, p = 0.001). CONCLUSIONS: Compared with preintervention adequate remodeling, inadequate remodeling was associated with increased percent IH CSA, which might be related with more vessel stretching.

Adult↗

Elevated homocysteine levels might be associated with coronary artery remodeling in patients with stable angina: an intravascular ultrasound study.

BACKGROUND: The relationship between plasma biologic markers and coronary artery remodeling is unknown. HYPOTHESIS: Plasma biologic markers are associated with coronary artery remodeling. METHODS: Preintervention intravascular ultrasound images were obtained in 44 patients with chronic stable angina. Plasma samples were collected 24 h before coronary intervention. The biologic markers included total cholesterol, low-density lipoprotein (LDL) cholesterol, triglyceride, high-density lipoprotein (HDL) cholesterol, lipoprotein(a) [LP(a)], C-reactive protein (CRP), and homocysteine. The remodeling index (RI) was defined as a ratio of the (lesion/proximal reference) external elastic membrane cross-sectional area. Positive remodeling was defined as an RI > 1.05, negative remodeling as an RI <0.95, and intermediate remodeling as an RI between 0.95 and 1.05. RESULTS: Total cholesterol level (r = 0.092, p = 0.557), LDL cholesterol level (r = 0.123, p = 0.426), triglyceride level (r = 0.020, p = 0.901), HDL cholesterol level (r = 0.042, p = 0.789), LP(a) level (r = 0.062, p = 0.729), and CRP level (r = 0.266, p = 0.089) did not significantly correlate with the RI. However, the plasma homocysteine level positively correlated with the RI (r = 0.398, p = 0.008). The plasma homocysteine level was significantly lower in the lesions with negative remodeling and higher in the lesions with positive remodeling (10.8 +/- 0.7 micromol/l in negative remodeling, 13.1 +/- 0.6 micromol/l in intermediate remodeling, and 18.1 +/- 2.8 micromol/l in positive remodeling, p = 0.021). CONCLUSIONS: Elevated homocysteine levels might be associated with coronary artery remodeling in patients with stable angina.

Analysis of Variance↗

Oxidized low-density lipoprotein and high-density lipoprotein cholesterol modulate coronary arterial remodeling: an intravascular ultrasound study.

BACKGROUND: Oxidized low-density lipoprotein (oxLDL) not only plays an important role in plaque formation, but also impairs the endothelium-dependent relaxation. Constrictive remodeling rather than intimal hyperplasia mainly contributes to restenosis after balloon angioplasty. Probucol (powerful antioxidant) reduced restenosis rate by improving constrictive remodeling. Thus, oxLDL may modulate coronary arterial remodeling. HYPOTHESIS: The study was designed for using intravascular ultrasound to test the hypothesis that arterial constrictive remodeling (CR) was associated with oxLDL in patients with coronary artery disease. METHODS: Intravascular ultrasound was performed in 36 patients with de novo atherosclerotic coronary. Remodeling was defined and evaluated as follows: remodeling index (RI) = lesion vessel area (VA)/(proximal reference VA + distal reference VA)/2. Constrictive remodeling (CR) was defined as remodeling index (RI) < 0.9. Neutral and expansive remodeling (NER) was defined as RI > or = 0.9. The level of plasma ox-LDL was measured by sandwich ELISA using the monoclonal antibody (DLH3)-recognized oxidatively modified lipoproteins and the antihuman apoprotein B monoclonal antibody. RESULTS: Neutral and expansive remodeling was found in 24 lesions, and CR in 12 lesions. Remodeling index was significantly lower in the CR group than in the NER group (0.8 +/- 0.1 vs. 1.0 +/- 0.1, p < 0.001). The level of oxLDL in the CR group was significantly higher than that in the NER group (24.0 +/- 12.1 vs. 16.4 +/- 6.2 U/ml, p < 0.05). The level of high-density lipoprotein-cholesterol (HDL-C) in the CR group was significantly lower than that in the NER group (40.5 +/- 4.8 vs. 46.2 +/- 10.6 mg/ml, p < 0.05). There was a statistically significant correlation between the value of HDL-C/ ox-LDL and the RI (r = -0.48, p < 0.005). CONCLUSIONS: Oxidized LDL and HDL-C were associated with arterial remodeling in de novo atherosclerotic lesions.

Chi-Square Distribution↗

Association of plaque characterization by intravascular ultrasound virtual histology and arterial remodeling.

Positive remodeling is more often observed in lesions of patients who have acute coronary syndromes or vulnerable (rupture-prone) plaques. However, there are few data that correlate plaque morphology, composition, and arterial remodeling in vivo. We evaluated coronary plaque characterization of lesions with positive remodeling using intravascular ultrasound (IVUS) radiofrequency data analysis. Seventy-seven nonbifurcation native coronary lesions (in 50 patients) were imaged in vivo using 30-MHz IVUS transducers. Lesions were classified into 4 plaque types, fibrous, fibrofatty, dense calcium, and necrotic core, by using processing of the radiofrequency signal validated in vitro. The remodeling index was calculated as the lesion external elastic membrane area divided by the proximal reference external elastic membrane area. Lesions were divided into 2 groups: positive remodeling (remodeling index>1.0, 26 lesions) and intermediate/negative remodeling (remodeling index<or=1.0, 51 lesions). Total plaque volume and the volume of each plaque type were averaged over the length of the lesion. Reference segment plaque compositions were similar. Mean lesion fibrofatty plaque area was significantly larger in lesions with positive remodeling than in lesions with intermediate/negative remodeling (1.2+/-0.7 vs 0.8+/-0.4 mm2, p=0.001; 26.3+/-6.6% vs 19.8+/-5.7%, p<0.001, of total plaque volume). The same results were obtained at the minimum lumen site and in the subgroup of patients who had acute coronary syndromes. Further, there was a linear relation between remodeling index and fibrofatty plaque area (r=0.26, p=0.02). In conclusion, in vivo IVUS radiofrequency data analysis demonstrates that positive remodeling occurs in lesions with more fibrofatty plaque.

Coronary Artery Disease↗

Arterial remodeling in the left coronary system: the role of high-density lipoprotein cholesterol.

OBJECTIVES: We sought to evaluate the plaque and patient variables related to arterial remodeling responses of early, de novo atherosclerotic lesions involving the left coronary artery. BACKGROUND: Coronary artery remodeling is a lesion-specific process involving either enlargement or shrinkage of atherosclerotic coronary arteries. There are little histologic data available correlating plaque morphologic and patient clinical characteristics with the degree and type of arterial remodeling in early atherosclerosis. METHODS: We studied 736 serial arterial sections from the left coronary system of 97 autopsy cases (mean age 33 +/- 11 years) by correlating the arterial remodeling response to plaque with demographic, serologic and histologic variables. Using the most proximal section as a reference, and considering the expected degree of internal elastic lamina tapering, remodeling was classified as positive (including neutral remodeling or compensatory enlargement) or negative. RESULTS: Remodeling was classified as positive in 84.3% (compensatory in 30.6%) and negative in 15.7% of sections with an overall mean luminal stenosis of 10.4 +/- 9.9%. In the lesions with the greatest arterial cross-sectional narrowing from each case, compensatory enlargement was associated with higher high-density lipoprotein (HDL) cholesterol (59.4 +/- 27.2 mg/dl) compared with either neutral (49.3 +/- 15.5 mg/dl) or negative remodeling (30.4 +/- 5.2 mg/dl; p = 0.019). In subjects with advanced atherosclerosis (maximum American Heart Association histologic grade 5 atherosclerosis), there was a modest linear relationship between higher HDL cholesterol and the propensity for positive remodeling (r2 = 0.37; p = 0.025). On multivariate analysis, only HDL cholesterol was related to the arterial remodeling response. CONCLUSIONS: Negative arterial remodeling occurs in early atherosclerosis. Higher HDL cholesterol may favor positive remodeling.

Adolescent↗