Biomedical subjects

Mitsuaki Isobe

Publications and source records attributed to Mitsuaki Isobe.

At least 19 recordsLinked to original sources

PubMed2007

A functional SNP in ITIH3 is associated with susceptibility to myocardial infarction.

Myocardial infarction (MI) results from complex interactions of multiple genetic and environmental factors. To disclose genetic backgrounds of MI, we performed a large-scale, case-control association study using 52,608 gene-based single-nucleotide polymorphism (SNP) markers, and identified a candidate SNP located on chromosome 3p21.2-p21.1. Subsequent linkage-disequilibrium mapping indicated very significant association between MI and a SNP in exon 2 of the inter-alpha (globulin) inhibitor 3 gene (ITIH3; chi(2) = 24.88, P = 6.1 x 10(-7), 3,353 affected individuals versus 3,807 controls). In vitro functional analyses showed that this SNP enhanced the transcriptional level of the ITIH3 gene. Furthermore, we found expression of the ITIH3 protein in the vascular smooth muscle cells and macrophages in the human atherosclerotic lesions, suggesting ITIH3 SNP to be a novel genetic risk factor of MI.

Alpha-Globulins↗

PubMed2006

Tea catechins attenuate chronic ventricular remodeling after myocardial ischemia in rats.

Tea catechins have many biological functions; these effects are induced by the suppression of several inflammatory factors. However, the effects of catechins on ventricular remodeling after myocardial ischemia have not been well investigated. To test the hypothesis that catechins can attenuate chronic ventricular remodeling after myocardial ischemia, we performed oral administration of catechins into rat myocardial ischemia models. We analyzed the mechanisms using physiological, pathological and molecular examinations. Although severe myocardial fibrosis with enhancement of inflammatory factors were observed in the non-treated ischemia group on day 28, catechins attenuated these changes with suppressed NF-kappaB and matrix metalloproteinases without systemic adverse effects. Catechins are potent for the suppression of chronic ventricular remodeling after myocardial ischemia because they are critically involved in the suppression of several inflammatory genes.

Animals↗

PubMed2006

Endothelial E-selectin potentiates neovascularization via endothelial progenitor cell-dependent and -independent mechanisms.

BACKGROUND: Although potential participation of bone marrow-derived circulating endothelial progenitor cells (EPCs) to neoangiogenesis has been proposed, the precise molecular mechanisms of EPC recruitment to vascular endothelium has not been fully elucidated. METHODS AND RESULTS: Peripheral blood mononuclear cells were isolated from healthy volunteers and cultured for 7 days to obtain EPCs. Tumor necrosis factor-alpha-activated human umbilical vein endothelial cells (HUVECs) supported significantly more rolling and adhesion of EPCs compared with inactivated HUVEC monolayer. Pretreatment of activated HUVEC with an adhesion-blocking mAb to E-selectin significantly reduced EPCs adhesion to HUVECs. When HUVECs were transduced with a recombinant adenovirus of E-selectin (AdRSVE-sel) or that of beta-galactosidase (AdRSVLacZ), E-selectin-transduced but not LacZ-transduced HUVECs exhibited significantly more EPC rolling as well as adhesion. Further, effect of AdRSVE-sel or AdRSVLacZ was examined in mouse hind limb ischemic model. AdRSVE-sel-transduced mice showed significantly less limb necrosis and higher laser Doppler ratio when compared with AdRSVLacZ-transduced mice. Interestingly, blood flow recovery of ischemic limb observed in AdRSVE-sel-transduced mice was more prominent when combined with EPC administration compared with that of AdRSVLacZ-transduced mice. CONCLUSIONS: Endothelial E-selectin plays a crucial role in EPC-endothelial interaction in vitro. The importance of E-selectin was also confirmed in vivo even in the absence of exogenous EPC. These data provide molecular background for novel cell-based therapy for ischemic atherosclerosis.

Analysis of Variance↗

PubMed2006

Critical role of inducible costimulator signaling in the development of arteriosclerosis.

OBJECTIVE: Proliferation and migration of smooth muscle cells (SMCs) and migration and accumulation of monocytes and T cells are landmark events in the development of arteriosclerosis. SMC proliferation in the intima induces interruption of blood flow and results in ischemia and graft rejection. Inducible costimulator (ICOS) is a major costimulator of T cell activation. However, the effect of costimulatory molecules on the formation of neointimal hyperplasia has not been fully elucidated. We examined the role of the ICOS pathway in SMC proliferation. METHODS AND RESULTS: ICOS ligand (ICOSL) was detected in SMCs stimulated by interleukin (IL)-1beta, and coculture of stimulated SMCs and activated T cells induced SMC proliferation. Inhibition of the ICOS pathway resulted in inhibition of SMC proliferation. In models of transplantation and vascular injury, ICOSL was induced in SMCs in the neointima. Expression of IL-1beta, a key inducer of ICOSL expression, was significantly reduced in mice treated with anti-ICOS antibody or soluble form of ICOS (ICOSIg) and in ICOS-deficient mice. Inhibition of the ICOS pathway significantly suppressed neointimal thickening. CONCLUSIONS: These results indicate that ICOS on activated T cells contributes to neointimal formation through the regulation of SMC proliferation. These findings provide insights into new therapeutic strategies for arteriosclerosis.

Animals↗

PubMed2006

A new RXR agonist, HX630, suppresses intimal hyperplasia in a mouse blood flow cessation model.

The nuclear receptor retinoid X receptor (RXR) forms heterodimers with other nuclear receptors and exerts anti-inflammatory effects. RXR is implicated in the progression of arteriosclerosis; however, the effects of selective RXR activation on smooth muscle cell (SMC) proliferation are unknown. We synthesized a novel RXR agonist, HX630, and examined its effect on vascular SMC (VSMC) proliferation. Male C57BL/6 mice (n=15) were subjected to ligation of the left carotid artery and fed 5 or 10 mg/kg/day HX630 for 4 weeks. HX630-fed mice showed significantly suppressed intimal hyperplasia progression compared to that in control mice (0.286+/-0.093 vs. 1.022+/-0.134 intima/media ratio, P<0.05). Immunohistochemistry of the carotid artery showed that HX630 suppressed cytokine and adhesion molecule staining in lesions undergoing intimal thickening. Interleukin (IL)-1beta-induced VSMC proliferation was inhibited by HX630 and the expression of IL-6 mRNA and protein in VSMCs was suppressed. The RXR agonist HX630 exerts antiproliferative effects in VSMCs in vivo and in vitro. Thus, the RXR may serve as a therapeutic target for vascular injury and intimal thickening.

Animals↗

PubMed2006

Inhibition of NF-{kappa}B improves left ventricular remodeling and cardiac dysfunction after myocardial infarction.

Several studies have demonstrated that NF-kappaB is substantially involved in the progression of cardiac remodeling; however, it remains uncertain whether the continuous inhibition of NF-kappaB is effective for the prevention of myocardial remodeling. Myocardial infarction (MI) was produced by ligation of the left anterior coronary artery of rats. IMD-0354 (10 mg/kg per day), a novel phosphorylation inhibitor of IkappaB that acts via inhibition of IKK-beta, was injected intraperitoneally starting 24 h after induction of MI for 28 days. After 28 days, the IMD-0354-treated group showed significantly improved survival rate compared with that of the vehicle-treated group (P < 0.05). Although infarct size was similar in both groups, improved left ventricular (LV) remodeling and diastolic dysfunction, as indicated by smaller LV cavity (LV end-diastolic area: vehicle, 74.13 +/- 3.57 mm(2); IMD-0354, 55.00 +/- 3.73 mm(2); P < 0.05), smaller peak velocity of early-to-late filling wave (E/A) ratio (vehicle, 3.87 +/- 0.26; IMD-0354, 2.61 +/- 0.24; P < 0.05), and lower plasma brain natriuretic peptide level (vehicle, 167.63 +/- 14.87 pg/ml; IMD-0354, 110.75 +/- 6.41 pg/ml; P < 0.05), were observed in the IMD-0354-treated group. Moreover, fibrosis, accumulation of macrophages, and expression of several factors (transforming growth factor-beta1, monocyte chemoattractant protein-1, matrix metalloproteinase-9 and -2) in the noninfarcted myocardium was remarkably inhibited by IMD-0354. In conclusion, inhibition of NF-kappaB activation may reduce the proinflammatory reactions and modulate the extracellular matrix and provide an effective approach to prevent adverse cardiac remodeling after MI.

Animals↗

PubMed2006

Tea catechins improve left ventricular dysfunction, suppress myocardial inflammation and fibrosis, and alter cytokine expression in rat autoimmune myocarditis.

BACKGROUND: Myocarditis is a clinically serious disease. Tea catechins have been shown to reduce inflammation; however the effects of catechins on the development of myocarditis have not been well studied. AIMS: To clarify the role of catechins, using an experimental autoimmune myocarditis (EAM) model. METHODS AND RESULTS: Lewis rats were immunized with porcine cardiac myosin to establish EAM. Tea catechins were administered orally from day 0 to day 21 (Group A, n=12), from day 14 to day 21 (Group B, n=8), or saline (Group C, n=9) daily. Rats were killed on day 21. Echocardiograms indicated that Group A showed significantly improved cardiac function compared to Group C. Pathologically, non-treated EAM hearts showed severe myocardial cell infiltration and fibrosis; however Group A showed significantly less area. Immunohistochemistry revealed enhanced expression of NF-kappaB and ICAM-1 in non-treated EAM hearts, which was suppressed by catechin administration in Group A. mRNA levels of TNF-alpha were decreased and Th2 cytokines were markedly enhanced in Group A compared with the control group. Late catechin administration (Group B) showed limited effects on EAM. CONCLUSION: The catechins suppressed ventricular remodelling in EAM; thus catechin treatment might be a promising option for the prevention of EAM myocarditis.

Animals↗

PubMed2006

Pioglitazone prevents acute and chronic cardiac allograft rejection.

BACKGROUND: Peroxisome proliferator-activated receptor-gamma plays an important role in regulating inflammation. Although cardiac transplantation is an established therapy for patients with end-stage heart disease, allograft rejection is a major concern for long-term survival. We investigated the role of pioglitazone in acute and chronic rejection in a murine cardiac transplantation model. METHODS AND RESULTS: We performed heterotopic murine cardiac transplantation in total allomismatch or major histocompatibility complex class II-mismatched combinations. Recipient mice were given standard chow or chow containing pioglitazone (3 mg.kg(-1).d(-1)) beginning 1 day before cardiac transplantation. In acute rejection, animals given pioglitazone showed significantly longer cardiac allograft survival than control mice (mean survival time, 34.6+/-7.8 versus 8.4+/-0.4 days; P<0.003). Treatment with pioglitazone significantly suppressed graft expression of interferon-gamma and monocyte chemoattractant protein-1. In chronic rejection, neointimal hyperplasia was significantly lower in allografts from mice treated with pioglitazone (luminal occlusion, 25.1+/-8.8%) than in those from control mice (65.8+/-7.3%, P<0.001). Pioglitazone-treated allografts showed significantly reduced expression of interferon-gamma, interleukin-10, and monocyte chemoattractant protein-1. We performed mixed lymphocyte reactions and in vitro proliferation assays of smooth muscle cells. Addition of pioglitazone to mixed lymphocyte reactions inhibited proliferation of T cells. Smooth muscle cells showed significant proliferation when cocultured with activated splenocytes. This proliferation was significantly inhibited by the addition of pioglitazone (1 micromol/L). CONCLUSIONS: Pioglitazone prolongs allograft survival and attenuates neointimal hyperplasia through the suppression of proliferation of smooth muscle cells. Pioglitazone may be a novel means to prevent acute and chronic allograft rejection.

Animals↗

PubMed2006

A CCR1 antagonist prevents the development of experimental autoimmune myocarditis in association with T cell inactivation.

Chemokines play an important role in induction of chemotaxis of immune cells. CCR1 is a chemokine receptor expressed on neutrophils, monocytes, and T lymphocytes. The role of CCR1 in immunity is not well examined. We demonstrated the role of CCR1 on T lymphocytes and the effect of a CCR1 antagonist, BX471 in myocarditis. Lewis rats were immunized with cardiac myosin on day 0 to establish experimental autoimmune myocarditis. Rats were then administered BX471 subcutaneously every day (group BX0: n = 7) or from day 14 (group BX14: n = 7) and were killed on day 21. We confirmed expression of CCR1 in cells infiltrating the myocardium by immunohistochemistry and FACS analysis. The development of myocarditis was almost completely prevented in group BX0, and myocarditis-affected areas were significantly decreased in size in group BX14. Cardiac function was markedly improved. Ribonuclease protection assay showed that the CCR1 antagonist treatment suppressed mRNA expression for IL-6, IL-1beta, and TNF-alpha in the hearts. An antigen-specific T cell proliferation assay was performed with CD4-positive T cells isolated from control rats immunized with cardiac myosin. T cell proliferation was inhibited by the CCR1 antagonist. Additionally, we showed by Western blot that the CCR1 antagonist suppressed ERK1/2 and JNK activities in T cells stimulated with myosin and that IL-2 reversed this suppression. The CCR1 antagonist reduced the severity of EAM by inhibiting cytokine expression and inducing T cell inactivation. Thus, the CCR1 antagonist may provide a novel therapeutic strategy treatment of myocarditis.

Animals↗

PubMed2006

Serum tenascin-C might be a novel predictor of left ventricular remodeling and prognosis after acute myocardial infarction.

OBJECTIVES: We investigated clinical implications of serum tenascin-C (TN-C) levels in patients with acute myocardial infarction (AMI). BACKGROUND: Tenascin-C, an extracellular matrix glycoprotein, is not normally expressed in the adult heart, but transiently appears during pathological conditions and plays important roles in tissue remodeling. METHODS: Serum TN-C levels were measured by ELISA in 105 AMI patients at various time points, in 10 old myocardial infarction (OMI) patients, and 20 normal controls. RESULTS: The mean serum TN-C level of AMI patients on admission (63.3 +/- 30.1 ng/ml) was significantly higher than that of controls and OMI (30.9 +/- 8.8 ng/ml and 27.4 +/- 11.7 ng/ml, respectively, p < 0.01), and peaked at 5 days (83.2 +/- 43.0 ng/ml). Follow-up examination (mean: 43.9 +/- 19.6 months) revealed that 25 of 105 AMI (23.8%) patients showed left ventricular (LV) remodeling (> or =20% end-diastolic volume increase), and in 15 (14.3%), major adverse cardiac events (MACE) were detected. The peak TN-C level was significantly higher in the remodeling group than the nonremodeling group (112 +/- 37 ng/ml vs. 66 +/- 29 ng/ml; p < 0.0001). By receiver-operating characteristic (ROC) analysis, TN-C levels clearly discriminated prediction of LV remodeling and MACE compared with other variables including plasma B-type natriuretic peptide, creatine kinase-MB, and LV function. Best predictive values of TN-C for remodeling and MACE were 84.8 and 92.8 ng/ml, respectively. Cox proportional hazards model analysis showed that TN-C was an important independent predictor of MACE. CONCLUSIONS: The findings suggest that serum TN-C levels might be useful in predicting LV remodeling and prognosis after AMI.

Aged↗

PubMed2006

HMG-CoA reductase inhibitor fluvastatin prevents angiotensin II-induced cardiac hypertrophy via Rho kinase and inhibition of cyclin D1.

HMG-CoA reductase inhibitors, so called statins, decrease cardiac events. Previous studies have shown that HMG-CoA reductase inhibitors inhibit cardiomyocyte hypertrophy in vitro and in vivo by blocking Rho isoprenylation. We have shown that the G1 cell cycle regulatory proteins cyclin D1 and Cdk4 play important roles in cardiomyocyte hypertrophy. However, the relation between Rho and cyclin D1 in cardiomyocyte is unknown. To investigate whether HMG-CoA reductase inhibitors prevent cardiac hypertrophy through attenuation of Rho and cyclin D1, we studied the effect of fluvastatin on angiotensin II-induced cardiomyocyte hypertrophy in vitro and in vivo. Angiotensin II increased the cell surface area and [(3)H]leucine uptake of cultured neonatal rat cardiomyocytes and these changes were suppressed by fluvastatin treatment. Angiotensin II also induced activation of Rho kinase and increased cyclin D1, both of which were also significantly suppressed by fluvastatin. Specific Rho kinase inhibitor, Y-27632 inhibited angiotensin II-induced cardiomyocyte hypertrophy and increased cyclin D1. Overexpression of cyclin D1 by adenoviral gene transfer induced cardiomyocyte hypertrophy, as evidenced by increased cell size and increased protein synthesis; this hypertrophy was not diminished by concomitant treatment with fluvastatin. Infusion of angiotensin II to Wistar rats for 2 weeks induced hypertrophic changes in cardiomyocytes, and this hypertrophy was prevented by oral fluvastatin treatment. These results show that an HMG-CoA reductase inhibitor, fluvastatin, prevents angiotensin II-induced cardiomyocyte hypertrophy in part through inhibition of cyclin D1, which is linked to Rho kinase. This novel mechanism discovered for fluvastatin could be revealed how HMG-CoA reductase inhibitors are preventing cardiac hypertrophy.

Adenoviridae Infections↗

PubMed2006

T cell costimulation in the development of cardiac allograft vasculopathy: potential targets for therapeutic interventions.

Cardiac allograft vasculopathy (CAV) is a form of coronary arterial stenosis and a leading cause of death in patients who survive beyond the first year after heart transplantation. Histopathologically, this lesion is concentric diffuse intimal hyperplasia of the arterial wall that is accompanied by extensive infiltration of inflammatory cells, including T cells. Many studies have explored the potential risk factors related to this arterial lesion and its pathogenesis. Continuous minor endothelial cell damage evokes inflammatory processes including T cell activation. Costimulatory molecules play crucial roles in this T cell activation. Many costimulatory pathways have been described, and some are involved in the pathogenesis of CAV, atherogenesis, and subsequent plaque formation. In this review, we summarize the present knowledge of the role of these pathways in CAV development and the possibility of manipulating these pathways as a means to treat heart allograft vascular disease and atherosclerosis.

Coronary Stenosis↗

PubMed2006

Utility of gallium-67 scintigraphy for evaluation of cardiac sarcoidosis with ventricular tachycardia.

BACKGROUND: The outcome of cardiac sarcoidosis is sometimes very poor. Ventricular tachycardia (VT) associated with cardiac sarcoidosis is the most common cause of sudden death among most patients. However, there is no established method for potential VT in patients with cardiac sarcoidosis. Thus, we investigated the utility of evaluation of gallium-67 scintigraphy for potential VT in patients with cardiac sarcoidosis. METHODS AND RESULTS: Cardiac sarcoidosis was diagnosed in 25 patients at ours or collaborating hospitals during the period 1982 through 2004. Twenty-one of these patients were treated with corticosteroid, and these patients were divided into two groups, depending on whether VT was present: a non-VT group (n=7) and a VT group (n=14). Laboratory and gallium-67 scintigraphy findings were examined in both groups. During the follow-up period, initial and maintenance dosages of corticosteroid did not differ significantly between the groups. Accumulation of gallium-67 in the heart at the time of diagnosis was detected more frequently in the VT group than in the non-VT group (14.3 vs. 71.4%, p<0.05). Six of the seven VT patients who underwent follow-up examination showed improvement on the scintigram obtained after treatment. Five of the six showed no VT recurrence in terms of Holter electrocardiogram, electrophysiologic study, or delivery of implantable cardioverter defibrillator shock. Serum angiotensin-converting enzyme and lysozyme concentrations were within normal limits in most patients in both groups. CONCLUSIONS: Activity of sarcoid granulomas may be associated with the occurrence of VT. Gallium-67 scintigraphy reflects the activity of sarcoid granulomas and thus is useful for evaluation of cardiac sarcoidosis in patients with potential VT.

Adrenal Cortex Hormones↗

PubMed2006

A cyclooxygenase-2 inhibitor alters Th1/Th2 cytokine balance and suppresses autoimmune myocarditis in rats.

Acute myocarditis is a clinically serious disease; however, no effective treatment has been elucidated. Cyclooxygenase (COX)-2 is a key factor for progression of inflammation. Although inflammation is an essential pathological feature of acute myocarditis, the role of COX-2 in this process remains unclear. Thus, the purpose of this study was to clarify the role of COX-2 in acute myocarditis. We used a rat experimental autoimmune myocarditis (EAM) model and a specific COX-2 inhibitor in this study. Lewis rats were immunized on day 0 with porcine cardiac myosin to establish EAM. We administered the COX-2 inhibitor (meloxicam, 0.1 mg/kg per day) daily; the rats were killed on day 21. Echocardiograms, body and heart weight, heart rate, blood pressure, and histological and molecular examinations were performed. Cytokine expression in the hearts and cell proliferation against cardiac myosin were also analyzed. The COX-2 inhibition during the immune response (late) phase attenuated EAM development; however, the inhibition during the antigen priming (early) phase did not attenuate EAM. The COX-2 inhibitor altered Th1/Th2 cytokine balance and inhibited cell proliferation in vitro. The COX-2 inhibitor suppresses the development of EAM. COX-2 regulation is promising for treating acute myocarditis.

Animals↗

PubMed2006

Hepatocyte growth factor: Effects on immune-mediated heart diseases.

There is growing evidence of the potential role of hepatocyte growth factor (HGF) in various cardiovascular diseases. In addition to the beneficial effects of HGF in myocardial infarction, heart failure, and occlusive peripheral arterial disease, administration of HGF effectively suppresses acute and chronic cardiac allograft rejection and autoimmune myocarditis. The present review summarizes recent advances in the utility of HGF for heart diseases, especially immune-mediated heart diseases. Possible mechanisms of action in the suppression of T-cell-mediated immunity are also discussed.

Animals↗

PubMed2006

Oxygen therapy prevents ventricular arrhythmias in patients with congestive heart failure and sleep apnea.

BACKGROUND: Although ventricular arrhythmia is critical for the prognosis of patients with severe congestive heart failure (CHF), it is difficult to control the arrhythmia using conservative therapies. However, many CHF patients also have sleep apnea syndrome (SAS) and oxygen supply improves their prognosis. The beneficial effects of oxygen treatment for ventricular arrhythmia have not yet been clarified, so the present study was designed to evaluate the effects of oxygen treatment for premature ventricular contraction (PVC). METHODS AND RESULTS: Patients with CHF and SAS were divided into 3 groups: (1) the "PVC declined" group that included patients who had frequent PVCs and oxygen treatment that suppressed the number of PVC; (2) the "PVC not affected" group that included patients who had frequent PVCs and oxygen treatment did not affect the number of PVC; and (3) the "few PVC" group that included patients who had no or few PVCs. The group 1 patients showed higher apnea-hypopnea index, standard deviation of all R-R intervals, left ventricular ejection fraction, and brain natriuretic peptide levels than the patients in group 2. Oxygen treatment in group 3 did not affect the PVC frequency. CONCLUSIONS: Oxygen treatment may be useful for preventing ventricular arrhythmia in selected patients with CHF and SAS.

Aged↗

PubMed2006

P-selectin expression, but not GPIIb/IIIa activation, is enhanced in the inflammatory stage of Takayasu's arteritis.

BACKGROUND: Inflammation and thrombosis are closely related processes, but the association between disease activity and thrombogenicity in Takayasu's arteritis (TA) is poorly understood. To investigate the link between platelet activation and disease activity, flow cytometric analyses of platelet P-selectin and activated GPIIb/IIIa expression were performed in patients with TA. METHODS AND RESULTS: Twenty-two patients with TA, classified into active (Group A, n = 9) and inactive (Group I, n = 13) according to blood-derived inflammatory markers, and 14 healthy age- and gender-matched controls (Group C) were studied. Compared with Group C, the mean fluorescence intensity of P-selectin in response to 0.1-10 micromol/L of ADP was significantly upregulated in Group A, but not in Group I. No differences in platelet GPIIb/IIIa expression in stimulated platelets were seen among the 3 groups. Standard platelet aggregation studies revealed that disease activity did not influence platelet aggregation by ADP. CONCLUSIONS: P-selectin expression, but not activated GPIIb/IIIa, is enhanced in ADP-activated platelets from patients in the inflammatory stage of TA. P-selectin may play a significant role in the inflammatory and thrombotic responses associated with intractable TA, presumably by inducing platelet-leukocyte interactions.

Adenosine Diphosphate↗

PubMed2006

Poststenting axial redistribution of atherosclerotic plaque into the reference segments and lumen reduction at the stent edge: a volumetric intravascular ultrasound study.

Lumen enlargement during coronary stenting results from vessel expansion and axial redistribution of atheromatous plaque along the stented segment and proximal and distal reference segments. Plaque burden predicts stenosis at the stent edge. The aim of this study was to investigate the fate of shifted plaque with special reference to whether or not plaque shift (PSh) correlates with late lumen reduction. This is a prospective study conducted on 54 consecutive patients who underwent bare metal stenting. In all stent edges (108 edges), PSh volume was measured as postintervention plaque-media volume (PMV) minus preintervention PMV. Changes in lumen volume (DeltaLV), vessel volume (DeltaVV), and PMV (DeltaPMV) were measured by serial intravascular ultrasound (IVUS) examination. After stenting, PSh was detected in 81.5% of proximal edges versus 72.2% of distal edges (P = 0.36). It correlated significantly with DeltaVV (r = 0.34, P = 0.002), and inversely with DeltaLV (r = 0.32, P = 0.003). However, at 6-month follow-up, it did not correlate with DeltaLV (r = -0.03, P = 0.8), DeltaVV (r = 0.1, P = 0.6), or DeltaPMV (r = 0.1, P = 0.4). Furthermore, DeltaLV correlated more strongly with DeltaVV (r = 0.62, P < 0.00001) than with DeltaPMV (r = -0.39, P = 0.001). By multivariate analysis, PSh area was an independent predictor of the postintervention change in lumen area (partial eta squared 0.21, P = 0.01), but not the follow-up change. Two patients (3.7%) developed proximal edge stenosis with no evident PSh after stenting. Thus, axial redistribution of atheromatous plaque into the reference segments was frequently encountered after stenting. Although PSh correlated with the immediate reduction in stent edge lumen volume, it did not correlate with the late lumen reduction.

Aged↗