External Elastic Membrane Volume Research Articles

Possible mechanism of late lumen enlargement after treatment for de novo coronary lesions with drug-coated balloon

BackgroundDrug-coated balloon (DCB) treatment for de novo coronary artery disease has demonstrated late lumen enlargement (LLE) in mid-term follow-up and it was considered as clinical benefit; however, its mechanism and the predictive factor remains unclear. MethodsThis study enrolled 46 consecutive patients (54 lesions) treated with DCB, using intravascular ultrasound (IVUS) at the index procedure and at the 9-month follow-up. We measured IVUS parameters at 1-mm intervals and calculated the mean volume of the external elastic membrane (EEM), lumen, and plaque. We calculated the dissection index (DI) defined as summation of the following points, 2: dissection over EEM, 1: intra-EEM dissection, 0: no dissection at every 1-mm interval, and divided by lesion length. ResultsIVUS showed that there was no flow limiting dissection just after DCB treatment, the mean EEM and lumen volume (LV) had significantly increased while mean plaque volume had significantly decreased at 9 months, and 74.1% lesions exhibited LLE. We divided the patients into three groups according to delta mean LV. Mean EEM volume significantly increased and mean plaque volume significantly decreased in the larger and smaller LLE groups, but not in the non-LLE group. The DI was higher in a descending order in the three groups. The multiple regression analysis demonstrated that the DI was the strongest predictor of the change in mean LV. ConclusionsLLE after DCB treatment may be caused by vessel enlargement and plaque regression. The non-flow limiting larger dissection just after DCB treatment may strongly associate with the intending LLE.

Extent of coronary atherosclerosis and arterial remodelling in women: the NHLBI-sponsored Women's Ischemia Syndrome Evaluation.

Information regarding the pathogenesis of ischemic heart disease (IHD) in women is limited. Sex-specific responses to atherosclerosis and coronary arterial remodelling in women versus men have been hypothesized, but limited study exists. Case-matched study of 174 women with suspected ischemia referred for coronary angiography: 87 with non-obstructive coronary artery disease (CAD) (no luminal diameter stenosis >20% in any coronary artery) and 87 age and ethnicity matched women with obstructive CAD. Groups were compared with regard to atheroma burden and coronary arterial remodelling assessed by coronary artery intravascular ultrasound (IVUS). IVUS revealed more extensive atheroma with obstructive CAD vs. those without obstructive CAD, with greater percent atheroma volume (PAV) (36.1%±9.8% vs. 25.4%±9.1%, P<0.0001), total atheroma volume (TAV) (140.8±58.7 vs. 98.8±46.9 mm3, P<0.0001) and percentage of images containing plaque (70.0%±30.5% vs. 35.7%±32.6%, P<0.0001). Adjusting for risk factors, PAV (35%±1% vs. 28%±1%, P=0.0008), TAV (131±7 vs. 115±7 mm3, P=0.110) and percentage of images containing plaque (66%±4% vs. 45%±5%, P=0.0008) remained greater with obstructive CAD. Obstructive CAD was associated with smaller lumen volumes (251.9±92.8 vs. 289.7±91.8 mm3, P=0.005), but surprisingly, the external elastic membrane (EEM) volume was very similar comparing the groups (392.7±128.1 vs. 388.6±113.7 mm3, P=0.910). Our findings suggest that women referred to angiography for suspected ischemia, have differing patterns of coronary arterial response to injury with regard to accumulation of atherosclerosis and compensatory remodelling related to the presence and absence of obstructive CAD. Preservation and cultivation of compensatory arterial remodelling may be a novel CAD therapeutic target.

Relationship between optical coherence tomography-defined in-stent neoatherosclerosis and out-stent arterial remodeling assessed by serial intravascular ultrasound examinations in late and very late drug-eluting stent failure

BackgroundLittle is known regarding the association between chronological out-stent vessel remodeling and in-stent tissue characteristics of drug-eluting stent (DES) failure. We aimed to evaluate the relationship between serial vessel remodeling after DES implantation and neoatherosclerosis (NA) assessed by optical coherence tomography (OCT) in patients with DES failure. MethodsForty-eight patients with late and very late stent failure after DES implantation, who underwent intravascular ultrasound (IVUS) at both the initial percutaneous coronary intervention and the time of stent failure and OCT imaging at the time of stent failure, were retrospectively investigated. NA on OCT was defined as neointimal formation with the presence of lipids or calcification inside the stents. Lesions were divided into two groups: those with NA and those without NA (NA: n=21; non-NA: n=27). From the serial IVUS examinations, external elastic membrane (EEM) volume and out-stent plaque volume were normalized by stent length and their changes were compared between the two groups. ResultsThe NA group showed older stent age [median, 5.1 years (IQR, 4.8–8.3) vs 1.4 years (IQR, 0.8–4.5); p<0.01] and more prevalent sirolimus-eluting stents (SES; 81.0% vs. 29.6%; p<0.01). IVUS findings of the NA group showed a greater serial increase in both normalized EEM volume and normalized out-stent plaque volume (OSPVI) [1.05 (0.41–1.90) vs. 0.11 (−0.64 to 0.80) mm2; p<0.01; and 0.88 (0.57–1.98) vs. 0.12 (−0.41 to 0.78) mm2; p<0.01]. On multivariate analysis, percentage change in OSPVI (OR, 1.07; 95% CI, 1.01–1.14; p=0.02) and SES (OR, 9.78; 95% CI, 2.20–43.40; p<0.01) remained independent predictors of NA. ConclusionsNA in late and very late DES failure was associated with out-stent positive vessel remodeling. In addition to SES, out-stent progressive positive remodeling may help predict NA in late and very late DES failure.

Lipid-core burden response to stent implantation assessed with near-infrared spectroscopy and intravascular ultrasound evaluation in patients with myocardial infarction.

Near-infrared spectroscopy (NIRS) is a new method to identify lipid core plaque (LCP). The LCP and vascular response were assessed with NIRS to examine whether LCP was compressed or redistributed during percutaneous coronary intervention with stent implantation. In 25 patients with non-ST segment elevation myocardial infarction (NSTEMI) NIRS acquisition was performed after predilation, stent implantation with nominal pressure and high-pressure post-dilation with a non-compliant balloon. The intravascular ultrasound (IVUS) measures included volumes of external elastic membrane (EEM), lumen and plaque+media. The NIRS measures included lipid core burden index (LCBI) and maximum value of LCBI for any of the 4-mm segment (maxLCBI4mm). From predilation to stent implantation and post-dilation EEM volume increased from 337±124mm3 to 369±136mm3 and to 397±144mm3 (p<0.001), while plaque volume decreased from 225±84mm3 to 202±85mm3 and to 192±81mm3 (p<0.001). Plaque shift to the proximal reference segment was found in 40% of the lesions. The maxLCBI4mm decreased significantly from predilation to stent implantation (492±235 to 208±193 (p<0.001), whereas post dilation did not cause any further significant reduction. Also LCBI decreased significantly from predilation to stent implantation (173±103 to 68±67, p<0.001), without any further significant reduction during post-dilation. The LCBI did neither in the proximal nor in the distal reference segments change significantly during stent implantation or post-dilation. Lumen enlargement was caused by vessel expansion, plaque compression and longitudinally plaque redistribution. Lipid-core burden at the stented segment was decreased.

Impact of statin therapy on coronary plaque composition: a systematic review and meta-analysis of virtual histology intravascular ultrasound studies.

BackgroundVirtual histology intravascular ultrasound (VH-IVUS) imaging is an innovative tool for the morphological evaluation of coronary atherosclerosis. Evidence for the effects of statin therapy on VH-IVUS parameters have been inconclusive. Consequently, we performed a systematic review and meta-analysis to investigate the impact of statin therapy on plaque volume and its composition using VH-IVUS.MethodsThe search included PubMed, Cochrane Library, Scopus and Embase (through 30 November 2014) to identify prospective studies investigating the effects of statin therapy on plaque volume and its composition using VH-IVUS.ResultsWe identified nine studies with 16 statin treatment arms and 830 participants. There was a significant effect of statin therapy in reducing plaque volume (standardized mean difference (SMD): −0.137, 95 % confidence interval (CI): −0.255, −0.019; P = 0.023), external elastic membrane volume (SMD: −0.097, 95 % CI: −0.183, −0.011; P = 0.027) but not lumen volume (SMD: −0.025, 95 % CI: −0.110, +0.061; P = 0.574). There was a significant reduction in fibrous plaque volume (SMD: −0.129, 95 % CI: −0.255, −0.003; P = 0.045) and an increase of dense calcium volume (SMD: +0.229, 95 % CI: +0.008, +0.450; P = 0.043), while changes in fibro-fatty (SMD: −0.247, 95 % CI: −0.592, +0.098; P = 0.16) and necrotic core (SMD: +0.011, 95 % CI: −0.144, +0.165; P = 0.892) tissue volumes were not statistically significant.ConclusionsThis meta-analysis indicates a significant effect of statin therapy on plaque and external elastic membrane volumes and fibrous and dense calcium volumes. There was no effect on lumen volume, fibro-fatty and necrotic tissue volumes.

Age-Related Effects of Smoking on Coronary Artery Disease Assessed by Gray Scale and Virtual Histology Intravascular Ultrasound

Although smoking is a risk factor for coronary atherosclerosis, the age-related impact on lesion morphology has not been studied. The aim of this study was to assess the age-related impact of smoking on the extent of atherosclerosis and arterial remodeling. In Providing Regional Observations to Study Predictors of Events in the Coronary Tree, 687 patients with acute coronary syndrome underwent 3-vessel gray scale and virtual histology intravascular ultrasound imaging of 3,185 nonculprit lesions. In 207 patients ≤65 years, current (smoking within 1 month) and former (no smoking for >1 month) smokers showed significantly smaller normalized volumes of external elastic membrane (EEM), lumen, and P + M (plaque + media) compared with nonsmokers. At the minimal lumen area site, current and former smokers had significantly smaller EEM, lumen, and P + M areas than nonsmokers. Conversely, in 480 patients >65 years, current smokers had greater normalized P + M volumes than nonsmokers with no difference in normalized EEM or lumen volumes. Finally, in patients >65 years (but not in patients ≤65 years), current smokers showed more plaque ruptures (4.7% vs 1.8%, p = 0.05) and echolucent plaques (8.3% vs 3.9%, p = 0.05) compared with nonsmokers. On multivariable analysis, a history of smoking (combining current and former smoking) predicted smaller normalized EEM volumes compared with nonsmokers ≤65 years. In conclusion, in patients ≤65 years, but not in patients >65 years, smoking had a vascular constrictive effect that contributed to severe luminal stenosis. Conversely, smokers >65 years had more plaque with greater plaque instability.

Effect of statins on the serum soluble form of receptor for advanced glycation end-products and its association with coronary atherosclerosis in patients with angina pectoris

BackgroundAdvanced glycation end-products (AGEs) and their receptor (RAGE) play an important role in the pathogenesis of diabetic vascular complications. Recently, soluble form of RAGE (sRAGE) has been identified in mice and humans. Statins have been reported to increase serum sRAGE levels. However, whether modulation of circulating sRAGE levels has a beneficial effect on the progression of atherosclerosis is unknown. MethodsWe reviewed 91 patients who had undergone percutaneous coronary intervention for angina pectoris. Coronary atherosclerosis in non-culprit lesions in the target vessel was evaluated, using virtual histology intravascular ultrasound, and serum levels of AGEs and sRAGE were measured, at baseline and after 8months of statin therapy. ResultsStatins had no effects on serum AGEs levels; however, serum levels of sRAGE were significantly higher at the 8-month follow-up. A significant decrease in external elastic membrane (EEM) volume (−1.6%, p=0.005) was observed, whereas a decrease in plaque volume did not reach statistical significance (−1.9%, p=0.16). Univariate regression analyses showed that the percentage changes in serum sRAGE were negatively correlated with those in EEM volume (r=−0.198, p=0.06) and plaque volume (r=−0.247, p=0.02). Multivariate regression analysis showed that an increase in serum sRAGE level was an independent predictor of atheroma regression after statin therapy (β=−0.290, p=0.006). ConclusionsStatin therapy increased serum sRAGE levels, and this increase was associated with negative vessel remodeling and atheroma regression in the coronary artery.

Correlations between serum uric acid and coronary atherosclerosis before and during statin therapy

The role of serum uric acid (UA) in the pathophysiology of atherosclerosis is ambiguous and remains controversial. The purpose of the present study was to evaluate the relationship between serum UA and coronary atherosclerosis. Coronary atherosclerosis in the nonculprit lesions was evaluated using virtual histology intravascular ultrasound in 119 patients with angina pectoris at the time of percutaneous coronary intervention and 8 months after statin therapy. Serum UA levels showed weak but significant positive correlations with external elastic membrane volume (baseline: r=0.236, P=0.02; 8-month follow-up: r=0.307, P=0.0009) and with plaque volume (baseline: r=0.263, P=0.007; 8-month follow-up: r=0.349, P=0.0001). Significant decreases in the fibrofatty and fibrous components and increases in the necrotic core and dense calcium components were observed during statin therapy. Serum UA (r=0.257, P=0.009) and unstable angina pectoris (r=0.208, P=0.02) correlated significantly with change in the calcified plaque volume, whereas the estimated glomerular filtration rate trended (r=-0.166, P=0.07). Multivariate regression analyses showed that UA was a significant independent predictor associated with an increase in the dense calcium plaque volume during statin therapy (β=0.244, P=0.03). In this preliminary study, serum UA levels correlated with coronary atherosclerosis before and during statin therapy. It remains unknown whether these correlations are a direct effect of UA itself or a marker of increased risk.

Intimal hyperplasia and vascular remodeling after everolimus‐eluting and sirolimus‐eluting stent implantation in diabetic patients: The randomized diabetes and drug‐eluting stent (DiabeDES) IV intravascular ultrasound trial

To evaluate the effects of the everolimus-eluting Xience™/Promus™ stent (EES) and the sirolimus-eluting Cypher™ stent (SES) on intimal hyperplasia (IH) in diabetic patients. Patients with diabetes mellitus have increased risk of in-stent restenosis after coronary stent implantation due to intimal hyperplasia (IH). In a sub study of the Randomized Comparison of Everolimus-Eluting and Sirolimus-Eluting Stents in Patients Treated with Percutaneous Coronary Intervention (SORT OUT IV trial), serial intravascular ultrasound (IVUS) 10-month follow-up data were available in 88 patients, including 48 EES and 40 SES treated patients. IVUS endpoints included IH volume, in-stent % volume obstruction and changes in external elastic membrane (EEM) volume. Compared with the SES group, IH volume was increased in the EES group [median (interquartile range): 2.8 mm(3) (0.0-12.6) vs. 0.0 mm(3) (0.0-1.1), P = 0.001]. In-stent % volume obstruction was increased in EES compared to SES [median (interquartile range): 1.6% (0.0-8.2) vs. 0.0% (0.0-1.0), P = 0.001]. Peri-stent external elastic membrane (EEM) volume: (post procedure vs. follow-up EES [300 mm(3) (219-491) vs. 307 mm(3) (223-482), P = 0.73] and SES [316 mm(3) (235-399) vs. 323 mm(3) (246-404), P = 0.05]) and peri-stent plaque volume: EES [163 mm(3) (103-273) vs. 184 mm(3) (115-291), P = 0.18] and SES [186 mm(3) (139-248) vs. 175 mm(3) (153-243), P = 0.26]) were unchanged in both groups. In the proximal reference segment a significant increase in plaque area was seen in the EES group only, without vascular remodeling. In diabetic patients, EES stent implantation was associated with increased IH volume obstruction without involvement of vascular remodeling.

Time course of statin-induced changes in coronary atherosclerosis using intravascular ultrasound with virtual histology

Recent trials using intravascular ultrasound (IVUS) have shown that statins induce regression and stabilization of coronary artery plaques. However, there are no reports on whether regression and stabilization in coronary artery plaques associated with statin therapy continue or not. The purpose of the present study was to examine the time course of statin-induced changes in coronary atherosclerosis. Coronary atherosclerosis was evaluated using virtual histology-IVUS in 39 patients at the time of a percutaneous coronary intervention, 8 months after statin therapy (mid-term), and at 48-month (long-term) follow-up. IVUS images qualified for evaluation obtained from 30 of these patients at three time points. Significant decreases in low-density lipoprotein cholesterol and high-sensitivity C-reactive protein were observed at 8 months and these decreases continued for 48 months. A decrease in external elastic membrane volume was observed at 8 months (-1.1%) and reached significance at 48 months (-5.9%, P=0.0001). Plaque volume tended to decrease over time, but this was not statistically significant (-1.6% at 8 months and -3.8% at 48 months). An increase in the calcified plaque component was observed at 8 months (0.09±0.34 mm/mm) and reached significance at 48 months (0.21±0.33 mm/mm, P=0.002). Change in the calcified component and change in the external elastic membrane volume showed a significant negative correlation at the long-term follow-up (r=-0.598, P=0.0005). Continued negative vessel remodeling associated with an increase in the calcified plaque component was observed following prolonged statin therapy by serial virtual histology-IVUS analysis.

Impact of Kissing Balloon Inflation on the Main Vessel Stent Volume, Area, and Symmetry After Side-Branch Dilation in Patients With Coronary Bifurcation Lesions: A Serial Volumetric Intravascular Ultrasound Study

Intravascular ultrasound (IVUS) was performed to investigate the impact of kissing balloon inflation (KBI) on the main vessel (MV) stent volume, area, and symmetry after side-branch (SB) dilation in patients with coronary bifurcation lesions (CBL). It remains controversial whether KBI would restore the MV stent area and symmetry loss after SB dilation. A total of 88 serial IVUS examinations of the MV were performed after MV angioplasty, MV stenting, SB dilation, and KBI in 22 patients with CBL. The MV stent was divided into proximal, bifurcation, and distal segments; the stent volume index (SVI), minimal stent area (MSA), stent symmetry index (SSI), and external elastic membrane (EEM) volume index were measured in 198 stent segments and compared after MV stenting, SB dilation, and KBI. In the bifurcation segment, SVI, MSA, and SSI were significantly smaller after SB dilation than after MV stenting and KBI (SVI was 6.10 ± 1.50 mm(3)/mm vs. 6.68 ± 1.60 mm(3)/mm and 6.57 ± 1.60 mm(3)/mm, respectively, p < 0.05; MSA was 5.15 ± 1.30 mm(2) vs. 6.08 ± 1.40 mm(2) and 5.86 ± 1.50 mm(2), respectively, p < 0.05; and SSI was 0.78 ± 0.02 mm(2) vs. 0.87 ± 0.03 mm(2) and 0.84 ± 0.03 mm(2), respectively, p < 0.05). KBI restored the MV SVI, MSA, and SSI after SB dilation. In the proximal segment, SVI, MSA, and EEM volume index were significantly larger, but SSI was smaller after KBI than after MV stenting and SB dilation. In the distal segment, neither SB dilation nor KBI had a significant impact on the MV stent volume or symmetry. This is the first comprehensive volumetric IVUS analysis of CBL, to our knowledge, demonstrating that KBI restores the MV stent volume, area, and symmetry loss after SB dilation in the bifurcation segment, and induces asymmetric stent expansion in the proximal segment.

Impacts of age on coronary atherosclerosis and vascular response to statin therapy

Age is a well-established risk factor for cardiovascular disease. Recent trials using intravascular ultrasound (IVUS) have shown that lipid-lowering therapy with statins halts the progression or induces the regression of coronary artery plaques. However, impacts of age on coronary atherosclerosis and vascular response to statin therapy have not been fully evaluated. The effects of 8-month statin therapy on coronary atherosclerosis were evaluated using virtual histology-IVUS. IVUS data were analyzed from 119 patients who were divided into two groups according to age: elderly patients (≥65 years, n = 72) and non-elderly patients (<65 years, n = 47). No patients were taking statins or other lipid-lowering therapies at baseline. At baseline, external elastic membrane (EEM) volume (17.27 vs. 14.95 mm(3)/mm, p = 0.02) and plaque volume (9.49 vs. 8.11 mm(3)/mm, p = 0.03) in the elderly patients were significantly greater than in the non-elderly patients. The EEM volume (-2.4 %, p = 0.007) and plaque volume (-3.1 %, p = 0.007) after 8-month of statin therapy had significantly decreased in the non-elderly patients but not in the elderly patients. A significant positive correlation was observed between age and percentage change in plaque volume (r = 0.265, p = 0.004). A multivariate regression analysis showed that age was a significant predictor of the percentage change in plaque volume during statin therapy (β = 0.223, p = 0.02). Coronary atherosclerosis was more advanced and vascular responses to statin therapy were attenuated in the elderly patients compared to the non-elderly patients.

Three‐dimensional intravascular ultrasound evaluation of carina and plaque shift at the distal left main coronary artery bifurcation after treatment with a one‐stent cross‐over technique

To assess the geometrical changes in the distal left main coronary artery (LMCA), left anterior descending (LAD), and left circumflex (LCX) that occur after a distal LMCA lesion is treated using a one-stent cross-over strategy. Morphological changes after stent implantation into distal LMCA lesions are not fully understood. We used pre- and postintervention three-dimensional intravascular ultrasound of both the LAD and LCX as well as of the LMCA to evaluate distal LMCA lesions after a 1-stent cross-over strategy. In 38 distal LMCA bifurcation lesions, cross-sectional measurements were performed every 1 mm over a 5-mm segment in the LAD and LCX distal to the carina and over the entire LMCA proximal to the carina. The increase in lumen volume correlated with the increase in external elastic membrane volumes: R = 0.917, P < 0.001, in the LMCA and R = 0.785, P < 0.001, in the LAD with no decrease in plaque volume except at the distal end of the LMCA (P = 0.081) and at the LAD carina (P = 0.11). The LCX lumen area decreased significantly at the LCX carina from 5.9 ± 2.0 mm(2) to 5.3 ± 1.9 mm(2) (P < 0.01); however, the response was variable from a 4.0 mm(2) decrease to a 1.8 mm(2) increase in lumen area. While the change in LCX lumen area at the carina correlated with the change in vessel area (R = 0.791, P < 0.001), there was also a small increase in plaque area at the LCX carina from 6.4 ± 2.9 mm(2) to 6.8 ± 2.9 mm(2) (P < 0.01). LMCA bifurcation lumen changes after cross-over single-stent implantation were determined primarily by conformational changes in vessel geometry.

Left Main Coronary Atherosclerosis Progression, Constrictive Remodeling, and Clinical Events

The aim of this study was to evaluate the progression of atherosclerosis within the left main coronary artery (LMCA) in association with risk factor modifying therapies. Despite studies demonstrating slowing of disease progression within epicardial coronaries with risk factor modification, little is known about the natural history and clinical sequelae of atherosclerosis progression within the LMCA. In 340 patients with angiographic coronary artery disease who underwent serial intravascular ultrasound imaging to evaluate the effects of anti atherosclerotic therapies across 7 clinical trials, LMCA and epicardial disease progression was characterized. Relationships between changes in plaque burden with remodeling parameters and the incidence of major adverse cardiovascular events (MACE) (death, myocardial infarction, hospital stay for unstable angina, and coronary revascularization) were investigated. Plaque regression was observed in the LMCA segment, and progression was observed in adjacent epicardial segments (percent atheroma volume [PAV] -0.39 ± 0.1% vs. +0.37 ± 0.1%, p < 0.001). Changes in LMCA lumen volume correlated strongly with changes in external elastic membrane (beta coefficient 0.91, p < 0.001) and negatively with the change in PAV (beta coefficient -0.55, p < 0.001). Patients who experienced a MACE had smaller baseline LMCA minimum lumen area (11.6 vs. 12.2 mm(2), p = 0.05) and greater progression of PAV in the LMCA (+0.51 ± 0.3% vs. -0.35 ± 0.2%, p = 0.02) compared with those who were MACE-free. Significant reductions from baseline in both external elastic membrane (-4.7 ± 1.7 mm(3), p < 0.01) and lumen volumes (-4.0 ± 1 mm(3), p < 0.01) were also observed in those having an event. Left main coronary atherosclerosis responds to systemic risk factor modification. Patients experiencing a MACE were more likely to demonstrate progressive disease and constrictive arterial remodeling within the LMCA segment.

TCT-278 Two year Clinical Impact of Postprocedural Incomplete Stent Apposition and Late Acquired Incomplete Stent Apposition After Deployment of Zotarolimus Eluting Stent or Everolimus Eluting Stent

Background: We already reported the preliminary data for the one year clinical impact of post-procedural incomplete stent apposition (PISA) and late incomplete stent apposition (LISA) in the newer generation of drug eluting stent. The aim of this study was to investigate the clinical impact of LISA and PISA during 24-month clinical follow up. Methods: We prospectively enrolled 178 patients who underwent percutaneous coronary intervention (PCI) in de novo coronary lesions; stable angina (n 41), unstable angina (n 91), and non-ST segment elevation myocardial infarction (n 46) (63.7 9.4 years, 125 male, 187 lesions). The group was randomly assigned (proportion of 1:2) to everolimus eluting stent (group I, n 65, Xience V, Abbott Vascular, Illinois) or zotarolimmus eluting stent (group II, n 122, Endeavor Resolute, Medtronic, MN). Post-PCI and follow up intravascular ultrasound (IVUS, mean 10.2 2.9 months) were performed in all patients. We analyzed 24-month major adverse cardiac events including death, myocardial infarction (MI) and target lesion failure (TLR). Results: The Post-PCI external elastic membrane (EEM) volume vs follow up EEM volume (group I: 368.0 169.6 mm vs 373.6 167.2 mm, p NS, group II: 431.0 167.5 vs 440.1 172.0 mm, p NS), and post-PCI lumen volume vs follow up lumen volume (group I: 203.0 86.8 vs 201.7 86.0 mm, p NS, group II: 239.2 92.7 vs 239.5 92.5 mm, p NS) by IVUS were not different. There were three LISAs [1.6%, group I (n 1) vs group II (n 2)] and sixty four PISAs [34.2%, group I (n 24 vs group II (n 40)] that were resolved [12.5%, group I (n 2) vs group II (n 6)]. Post-PCI and follow up volume of PISA was not significantly different in both group I (6.4 4.3 vs 6.3 3.9 mm, p NS) and group II (6.4 5.3 vs 6.2 4.3 mm, p NS). Both PISA and LISA were not related with cardiac death or MI during 24-month clinical follow up. However, there were four TLRs in PISA subgroup [6.3%, group I (n 0) vs group II (n 4)]. Conclusions: The incidence of LISA was low in both groups. Both PISA and LISA were not related with cardiac death or MI during 24-month clinical follow up. Future long-term follow up study to clarify the clinical course of LISA and PISA would be needed to confirm our results.

Impacts of estimated glomerular filtration rate on coronary atherosclerosis and plaque composition before and during statin therapy in patients with normal to mild renal dysfunction: Subanalysis of the TRUTH study

Renal dysfunction is an independent risk factor for cardiovascular events. However, little is known regarding the impacts of renal dysfunction on coronary atherosclerosis. The effects of 8-month statin therapy on coronary atherosclerosis were evaluated in the TRUTH study using virtual histology intravascular ultrasound in 164 patients with angina pectoris. We analyzed correlations between the estimated glomerular filtration rate (eGFR) and coronary atherosclerosis before and during statin therapy. Baseline eGFR was 64.5 mL/min per 1.73 m(2) . Serum low-density lipoprotein cholesterol level decreased significantly from 132 to 85 mg/dL (-35%, P < 0.0001) after 8 months. Weak, but significant, negative correlations were observed between eGFR and external elastic membrane volume (r = -0.228, P = 0.01) and atheroma volume (r = -0.232, P = 0.01) at baseline. The eGFR was also negatively correlated with fibro-fatty volume (r = -0.254, P = 0.005) and fibrous volume (r = -0.241, P = 0.008) at baseline. Multivariate regression analyses showed that eGFR was a significant independent predictor associated with statin pre-treatment volume in fibro-fatty (β = -0.23, P = 0.01) and fibrous (β = -0.203, P = 0.02) components. Furthermore, eGFR was positively correlated with volume change in the fibro-fatty component during statin therapy (r = 0.215, P = 0.02). Decreased eGFR is associated with expanding remodelling and a greater atheroma volume, particularly the fibro-fatty and fibrous volume before statin therapy in patients with normal to mild renal dysfunction. Reduction of fibro-fatty volume during statin therapy gradually accelerated with decreasing renal function.

Relationship among coronary plaque compliance, coronary risk factors and tissue characteristics evaluated by integrated backscatter intravascular ultrasound

BackgroundThe purpose of the present study was to evaluate the mechanical properties of coronary plaques and plaque behavior, and to elucidate the relationship among tissue characteristics of coronary plaques, mechanical properties and coronary risk factors using integrated backscatter intravascular ultrasound (IB-IVUS).MethodsNon-targeted plaques with moderate stenosis (plaque burden at the minimal lumen site: 50-70%) located proximal to the site of the percutaneous coronary intervention target lesions were evaluated by IB-IVUS. Thirty-six plaques (less calcified group: an arc of calcification ≤10°) in 36 patients and 22 plaques (moderately calcified group: 10° < an arc of calcification ≤60°) in 22 patients were evaluated. External elastic membrane volume (EEMV) compliance, lumen volume (LV) compliance, plaque volume (PV) response (difference between PV in systole and diastole), EEM area stiffness index were measured at the minimal lumen site. Relative lipid volume (lipid volume/internal elastic membrane volume) was calculated by IB-IVUS.ResultsIn the less calcified group, there was a significant correlation between EEMV compliance and the relative lipid volume (r = 0.456, p = 0.005). There was a significant inverse correlation between EEM area stiffness index and the relative lipid volume (p = 0.032, r = −0.358). The LV compliance and EEM area stiffness index were significantly different in the diabetes mellitus (DM) group than in the non-DM group (1.32 ± 1.49 vs. 2.47 ± 1.79%/10 mmHg, p =0.014 and 28.3 ± 26.0 vs. 15.7 ± 17.2, p =0.020). The EEMV compliance and EEM area stiffness index were significantly different in the hypertension (HTN) group than in the non-HTN group (0.77 ± 0.68 vs. 1.57 ± 0.95%/10 mmHg, p =0.012 and 26.5 ± 24.3 vs. 13.0 ± 16.7, p =0.020). These relationships were not seen in the moderately calcified group.ConclusionThe present study provided new findings that there was a significant correlation between mechanical properties and tissue characteristics of coronary arteries. In addition, our results suggested that the EEMV compliance and the LV compliance were independent and the compliance was significantly impaired in the patients with DM and/or HTN. Assessment of coronary mechanical properties during PCI may provide us with useful information regarding the risk stratification of patients with coronary heart disease.

AS-096 Late Clinical Impact of Postprocedural Incomplete Stent Apposition and Late Acquired Incomplete Stent Apposition After Deployment of Zotarolimus Eluting Stent or Everolimus Eluting Stent

Background: We already reported the preliminary data for the one year clinical impact of post-procedural incomplete stent apposition (PISA) and late incomplete stent apposition (LISA) in the newer generation of drug eluting stent. The aim of this study was to investigate the clinical impact of LISA and PISA during 24-month clinical follow up. Methods: We prospectively enrolled 178 patients who underwent percutaneous coronary intervention (PCI) in de novo coronary lesions; stable angina (n 41), unstable angina (n 91), and non-ST segment elevation myocardial infarction (n 46) (63.7 9.4 years, 125 male, 187 lesions). The group was randomly assigned (proportion of 1:2) to everolimus eluting stent (group I, n 65, Xience V, Abbott Vascular, Illinois) or zotarolimmus eluting stent (group II, n 122, Endeavor Resolute, Medtronic, MN). Post-PCI and follow up intravascular ultrasound (IVUS, mean 10.2 2.9 months) were performed in all patients. We analyzed 24-month major adverse cardiac events including death, myocardial infarction (MI) and target lesion failure (TLR). Results: The Post-PCI external elastic membrane (EEM) volume vs follow up EEM volume (group I: 368.0 169.6 mm vs 373.6 167.2 mm, p NS, group II: 431.0 167.5 vs 440.1 172.0 mm, p NS), and post-PCI lumen volume vs follow up lumen volume (group I: 203.0 86.8 vs 201.7 86.0 mm, p NS, group II: 239.2 92.7 vs 239.5 92.5 mm, p NS) by IVUS were not different. There were three LISAs [1.6%, group I (n 1) vs group II (n 2)] and sixty four PISAs [34.2%, group I (n 24 vs group II (n 40)] that were resolved [12.5%, group I (n 2) vs group II (n 6)]. Post-PCI and follow up volume of PISA was not significantly different in both group I (6.4 4.3 vs 6.3 3.9 mm, p NS) and group II (6.4 5.3 vs 6.2 4.3 mm, p NS). Both PISA and LISA were not related with cardiac death or MI during 24-month clinical follow up. However, there were four TLRs in PISA subgroup [6.3%, group I (n 0) vs group II (n 4)]. Conclusions: The incidence of LISA was low in both groups. Both PISA and LISA were not related with cardiac death or MI during 24-month clinical follow up. Future long-term follow up study to clarify the clinical course of LISA and PISA would be needed to confirm our results.

Comparison of Arterial Remodeling and Changes in Plaque Composition Between Patients With Progression Versus Regression of Coronary Atherosclerosis During Statin Therapy (from the TRUTH Study)

Statin therapy produces regression of coronary artery plaques and reduces the incidence of coronary artery disease. However, not all patients show regression of coronary atherosclerosis after statin therapy. The purpose of the present study was to identify differences in clinical characteristics, serum lipid profiles, arterial remodeling, and plaque composition between patients with progression and those with regression of coronary atherosclerosis during statin therapy. The effects of 8-month statin therapy on coronary atherosclerosis were evaluated in the Treatment With Statin on Atheroma Regression Evaluated by Intravascular Ultrasound With Virtual Histology (TRUTH) study using intravascular ultrasound-virtual histology. One hundred nineteen patients were divided into 2 groups according to atheroma volume increase (progressors) or decrease (regressors) during an 8-month follow-up period. Fifty-one patients (43%) were categorized as progressors and the remaining 68 (57%) as regressors. External elastic membrane volume increased, although not significantly (0.8%, p = 0.34), and luminal volume decreased significantly (-5.3%, p = 0.0003) in progressors, while external elastic membrane volume decreased significantly (-3.2%, p <0.0001) and luminal volume increased (2.2%, p = 0.13) in regressors. The fibrous component increased significantly in progressors, while this component decreased in regressors. A strong positive correlation was observed between change in atheroma volume and change in fibrous volume (r = 0.812, p <0.0001). In conclusion, coronary arteries showed negative remodeling during statin-induced plaque regression. The difference in plaque composition between patients with progression and those with regression of coronary atherosclerosis during statin therapy arose from the difference in the change in fibrous component.

Impact of Diabetes Mellitus on Coronary Atherosclerosis and Plaque Composition Under Statin Therapy

Patients with diabetes mellitus (DM) have a markedly increased incidence of adverse cardiovascular events, but the mechanisms have not been well-characterized. The TRUTH study evaluated the effects of 8-month statin therapy on coronary artery plaque composition using virtual histology intravascular ultrasound (IVUS). Analyzable IVUS data were obtained from 119 patients, including 50 DM patients. The pattern of arterial remodeling, extent of coronary atherosclerosis, and plaque composition were compared in subjects with and without DM. Significant decreases in atheroma volume (-2.3%, P=0.02) and external elastic membrane volume (-1.7%, P=0.02) were observed only in the non-DM group. Although statin therapy significantly decreased the fibro-fatty component in both groups, this component at follow-up was significantly greater in the DM group (0.99 mm(3)/mm vs. 0.70 mm(3)/mm, P=0.03). Multivariate regression analysis showed that the presence of DM was associated with greater atheroma volume (β=0.203, P=0.02), particularly fibro-fatty plaque volume at follow-up (β=0.215, P=0.01). DM attenuated the degree of regression of coronary atherosclerosis under statin therapy. A large amount of fibro-fatty plaque volume under statin therapy may affect the development of coronary events in patients with DM.