Plaque Regression In Patients Research Articles

TCT-835 Impact of Early Intervention With Alogliptin on Coronary Plaque Regression in Patients with Acute Coronary Syndromes: A Prospective, Single-Center, Randomized Trial

The clinical significance of pharmacological intervention with dipeptidyl peptidase-4 inhibitors for dysglycemia at early stage remains poorly understood in patients with acute coronary syndromes (ACS). The aim of this study was to investigate the effect of alogliptin on coronary atherosclerosis as

Lifestyle Interventions and Carotid Plaque Burden: A Comparative Analysis of Two Lifestyle Intervention Programs in Patients with Coronary Artery Disease

The cardioprotective effects of intensive lifestyle regimens in primary prevention have been elucidated; however, there is a paucity of data comparing the effects of different lifestyle regimens in patients with established coronary artery disease (CAD) or CAD equivalent, specifically vis-à-vis carotid plaque regression. We performed a randomized, single-center, single-blind study in 120 patients with established CAD. Patients were randomly assigned to either 9 months of the Complete Health Improvement Program (CHIP), an outpatient lifestyle enrichment program that focuses on improving dietary choices, enhancing daily exercise, increasing support systems, and decreasing stress; or to 9 months of an ad hoc, nonsequential combination of various healthy living classes offered separately through a health maintenance organization and referred to as the Healthy Heart program. Baseline and 9-month change in carotid intima-media thickness (CIMT) were measured. Among 120 participants, data were analyzed for 79, of which 68 (86%) completed the study. Both average CIMT and average maximum CIMT increased over 9 months, but the changes between groups were insignificant. There were marked differences in the mean body mass index favoring the CHIP group (-1.9 [standard deviation = 1.9]; p < 0.001) and statistically significant within-group improvements in blood pressure, triglyceride level, 6-minute walk test result, self-assessment well-being score, and Patient Health Questionnaire-9 score that were not observed between groups. Neither the CHIP nor Healthy Heart was effective in inducing plaque regression in patients with established CAD after a 9-month period. However, both were effective in improving several CAD risk factors, which shows that the nonsequential offering of healthy lifestyle programs can lead to similar outcomes as a formal, sequential, established program (CHIP) in many aspects. These results have important implications as to how lifestyle changes will be implemented as tertiary prevention measures in the future.

Low Baseline High-Sensitive C-Reactive Protein is Associated with Coronary Atherosclerosis Regression: Insights from the MILLION Study.

Aim: The prospective, randomized, multicenter Myocardial Ischemia Treated with Percutaneous Coronary Intervention and Plaque Regression by Lipid Lowering & Blood Pressure Controlling assessed by Intravascular Ultrasonography (MILLION) study demonstrated that combined treatment with atorvastatin and amlodipine enhanced coronary artery plaque regression. Although the baseline high-sensitive C-reactive protein (hs-CRP) reportedly plays an important role in atherogenesis, few data exist regarding the relationship between hs-CRP and plaque regression in patients receiving a combined atorvastatin and amlodipine therapy.Methods: A total of 68 patients (male, 55; mean age, 64.2 years) with baseline and follow-up 3-dimensional intravascular ultrasound examinations in the MILLION study were stratified by baseline hs-CRP level quartiles. The serial measurements of lipid, blood pressure, and percentage changes in the plaque volume were compared between the groups, and the factors associated with the percentage change in the plaque volume were assessed.Results: There were no significant between-group differences in the extent of change in low-density lipoprotein cholesterol (LDL-C) or systolic and diastolic blood pressure after 18–24 months of treatment. The percentage change in the plaque volume showed a linear association with the baseline hs-CRP (p for trend < 0.05); however, there was no correlation with changes in LDL-C or systolic and diastolic blood pressure. In the multiple regression analysis, the baseline hs-CRP level was independently associated with the percentage change in the plaque volume (β = 0.29, p = 0.022).Conclusions: Coronary plaque regression was associated with the baseline hs-CRP level in patients treated with a combined lipid- and blood pressure-lowering therapy.

Implications of GLAGOV study.

Proprotein convertase subtilisin kexin type 9 (PCSK9) inhibition has emerged as a novel approach to lowering levels of low-density lipoprotein cholesterol (LDL-C). The impact of PCSK9 inhibition in statin-treated patients on coronary atherosclerosis had remained unknown. The GLAGOV trial compared the effect of the PCSK9 inhibitor, evolocumab, and placebo on progression of coronary atherosclerosis in patients treated with at least moderate intensity statin therapy. Predictable lowering of LDL-C with evolocumab (36.6 versus 93.0 mg/dl) associated with significant regression of coronary atherosclerosis. A direct relationship was observed between achieved LDL-C levels and disease progression. Addition of evolocumab to statin therapy produces incremental regression of plaque regression in patients with established coronary artery disease. This finding provides a biological rationale for the reported beneficial effects of evolocumab on cardiovascular events.

Lipid profile associated with coronary plaque regression in patients with acute coronary syndrome: Subanalysis of PRECISE-IVUS trial

Background and aimsAlthough dual low-density lipoprotein cholesterol (LDL-C)-lowering therapy (DLLT) with statin-ezetimibe combination showed clinical benefit in patients with acute coronary syndrome (ACS) confirming “the lower, the better,” the underlying mechanisms of DLLT are still unknown. MethodsPRECISE-IVUS trial evaluated the effects of DLLT on IVUS-derived coronary atherosclerosis and lipid profile, compared with atorvastatin monotherapy, quantifying the coronary plaque response in 100 ACS patients. We explored the potential predictors of plaque regression. ResultsLower total cholesterol, LDL-C, triglyceride, remnant-like particles cholesterol, and stronger reduction of small dense LDL-C and cholesterol absorption markers were observed in patients with plaque regression compared to those with progression. Multivariate analysis revealed that achieved LDL-C was the strongest predictor for coronary plaque regression (95% CI: 0.944–1.000, p = 0.05), followed by age (95% CI: 0.994–1.096, p = 0.09). ConclusionsIncremental LDL-C lowering by DLLT was associated with stronger coronary plaque regression, reconfirming that lowering LDL-C to levels below previous targets provided additional clinical benefit.

Efficacy of Statin Therapy in Inducing Coronary Plaque Regression in Patients with Low Baseline Cholesterol Levels.

Aim: The efficacy of statin therapy in inducing coronary plaque regression may depend on baseline cholesterol levels. We aimed to determine the efficacy of statin therapy in inducing coronary plaque regression in statin-naïve patients with low cholesterol levels using serial intravascular ultrasound (IVUS) data from the treatment with statin on atheroma regression evaluated by virtual histology IVUS (TRUTH) study.Methods: The TRUTH study is a prospective, multicenter trial, comparing the efficacies of pitavastatin and pravastatin in coronary plaque regression in 164 patients. All patients were statin-naïve and received statin therapy only after study enrollment. The primary endpoint was the observation of coronary plaque progression, despite statin therapy.Results: Serial IVUS data, at baseline and after an 8-month follow-up, were available for 119 patients. The patients were divided into three groups based on non-high-density lipoprotein cholesterol (HDL-C) levels—low: ≤ 140 mg/dl, n = 38; moderate: 141–169 mg/dl, n = 42; and high: ≥ 170 mg/dl, n = 39. Coronary plaque progression was noted in the low cholesterol group, whereas plaque regression was noted in the moderate and high cholesterol groups [%Δplaque volume: 2.3 ± 7.4 vs. − 2.7 ± 10.7 vs. − 3.2 ± 7.5, p = 0.004 (analysis of variance)]. After adjusting for all variables, a low non-HDLC level (≤ 140 mg/dl) was identified as an independent predictor of coronary plaque progression [odds ratio, 3.7; 95% confidence interval, 1.5–9.1, p = 0.004].Conclusion: Serial IVUS data analysis indicated that statin therapy was less effective in inducing coronary plaque regression in patients with low cholesterol levels but more effective in those with high cholesterol levels at baseline.University Hospital Medical Information Network (UMIN) (UMIN ID: C000000311).

Abstract 12156: Greater Regression of Coronary Atherosclerosis With the Pre-Beta High-Density Lipoprotein Mimetic CER-001 in Patients With More Extensive Plaque Burden

Introduction: Infusing high-density lipoprotein (HDL) has been shown to promote plaque regression in patients with acute coronary syndrome (ACS). The factors associated with a greater propensity to regression have not been elucidated. We hypothesized greater plaque regression with HDL infusion would be observed in patients with greater baseline plaque burden. Methods: The CHI-SQUARE study compared the effect of infusing the pre-beta HDL mimetic CER-001 (3 to 12 mg/kg) versus placebo weekly for 5 weeks in patients with a recent ACS on plaque burden using serial intravascular ultrasound. Receiver operating characteristics curve analysis determined that a baseline percent atheroma volume (PAV) ≥30% optimally associated with greater regression. Clinical and imaging characteristics were compared in patients with baseline PAV &lt;30% (n=74) or ≥30% (n=271). Results: There were no differences between the groups apart from greater use of statin in patients with baseline PAV ≥30% (100 v. 90%, p=0.01). Patients with a greater baseline PAV were more likely to demonstrate echolucency (20 v. 9%, p=0.02) and ultrasound attenuation (21 v. 7%, p=0.01), consistent with lipidic and inflammatory material. On serial evaluation, PAV decreased with CER-001 infusion in patients with baseline PAV ≥30% by -0.27% (p=0.01 v. baseline), but not in those with baseline PAV &lt;30% (+0.43%, p=0.15 v. baseline, p=0.01 between plaque burden groups). The greatest PAV regression was observed with infusing CER-001 3 mg/kg in patients with baseline PAV ≥30% by 0.96% (p=0.04 v. baseline, p=0.02 v. placebo) (Table), but not in those patients with baseline PAV &lt;30% (+0.08%, p=0.55 v. baseline, p=0.004 for comparison between plaque burden groups). Conclusions: Greater plaque regression with CER-001 3 mg/kg was observed in ACS patients with greater atheroma burden and more vulnerable features. The findings identify ACS patients with high-risk plaque features most likely to benefit from HDL mimetic therapy.

Impact of Dual Lipid-Lowering Strategy With Ezetimibe and Atorvastatin on Coronary Plaque Regression in Patients With Percutaneous Coronary Intervention: The Multicenter Randomized Controlled PRECISE-IVUS Trial

BackgroundDespite standard statin therapy, a majority of patients retain a high “residual risk” of cardiovascular events. ObjectivesThe aim of this study was to evaluate the effects of ezetimibe plus atorvastatin versus atorvastatin monotherapy on the lipid profile and coronary atherosclerosis in Japanese patients who underwent percutaneous coronary intervention (PCI). MethodsThis trial was a prospective, randomized, controlled, multicenter study. Eligible patients who underwent PCI were randomly assigned to atorvastatin alone or atorvastatin plus ezetimibe (10 mg) daily. Atorvastatin was uptitrated with a treatment goal of low-density lipoprotein cholesterol (LDL-C) <70 mg/dl. Serial volumetric intravascular ultrasound was performed at baseline and again at 9 to 12 months to quantify the coronary plaque response in 202 patients. ResultsThe combination of atorvastatin/ezetimibe resulted in lower levels of LDL-C than atorvastatin monotherapy (63.2 ± 16.3 mg/dl vs. 73.3 ± 20.3 mg/dl; p < 0.001). For the absolute change in percent atheroma volume (PAV), the mean difference between the 2 groups (–1.538%; 95% confidence interval [CI]: –3.079% to 0.003%) did not exceed the pre-defined noninferiority margin of 3%, but the absolute change in PAV did show superiority for the dual lipid-lowering strategy (–1.4%; 95% CI: –3.4% to –0.1% vs. –0.3%; 95% CI: –1.9% to 0.9% with atorvastatin alone; p = 0.001). For PAV, a significantly greater percentage of patients who received atorvastatin/ezetimibe showed coronary plaque regression (78% vs. 58%; p = 0.004). Both strategies had acceptable side effect profiles, with a low incidence of laboratory abnormalities and cardiovascular events. ConclusionsCompared with standard statin monotherapy, the combination of statin plus ezetimibe showed greater coronary plaque regression, which might be attributed to cholesterol absorption inhibition–induced aggressive lipid lowering. (Plaque Regression With Cholesterol Absorption Inhibitor or Synthesis Inhibitor Evaluated by Intravascular Ultrasound [PRECISE-IVUS]; NCT01043380)

Rosuvastatin induced carotid plaque regression in patients with inflammatory joint diseases

Objective. Patients with rheumatoid arthritis (RA) and carotid artery plaques have an increased risk of acute coronary syndromes. Statin treatment with the goal of achieving a low-density lipoprotein (LDL) cholesterol level of £1.8 mmoles/liter (£70 mg/dl) is recommended for individuals in the general population who have carotid plaques. The aim of the ROsuvastatin in Rheumatoid Arthritis, Ankylosing Spondylitis and other inflammatory joint diseases (RORA-AS) study was to evaluate the effect of 18 months of intensive lipid-lowering treatment with rosuvastatin with regard to change in carotid plaque height. Methods. Eighty-six patients (60.5% of whom were female) with carotid plaques and inflammatory joint disease (55 with RA, 21 with AS, and 10 with psoriatic arthritis) were treated with rosuvastatin to obtain the LDL cholesterol goal. Carotid plaque height was evaluated by B-mode ultrasonography. Results. The mean6SD age of the patients was 60.86 8.5 years, and the median compliance with rosuvastatin treatment was 97.9% (interquartile range [IQR] 96.0–99.4). At baseline, the median number and height of the carotid plaques were 1.0 (range 1–8) and 1.80 mm (IQR 1.60–2.10), respectively. The mean6SD change in carotid plaque height after 18 months of treatment with rosuvastatin was 20.196 0.35 mm (P < 0.0001). The mean6SD baseline LDL cholesterol level was 4.06 0.9 mmoles/liter (154.76 34.8 mg/dl), and the mean reduction in the LDL cholesterol level was 22.3 mmoles/liter (95% confidence interval [95% CI] 22.48, 22.15) (288.9 mg/dl [95% CI 295.9, 283.1]). The mean 6 SD LDL cholesterol level during the 18 months of rosuvastatin treatment was 1.76 0.4 mmoles/liter (area under the curve). After adjustment for age/sex/blood pressure, no linear relationship between a reduction in carotid plaque height and the level of LDL cholesterol exposure during the study period was observed. Attainment of the LDL cholesterol goal of £1.8 mmoles/liter (£70 mg/dl) or the amount of change in the LDL cholesterol level during the study period did not influence the degree of carotid plaque height reduction. Conclusion. Intensive lipid-lowering treatment with rosuvastatin induced atherosclerotic regression ClinicalTrials.gov identifier: NCT01389388. EudraCT database no. 2008-005551-20. Supported by the South-Eastern Regional Health Authority of Norway. AstraZeneca provided the study drug. S. Rollefstad, MD, PhD, E. Ikdahl, MD, I. C. Olsen, PhD, H. B. Hammer, MD, PhD, T. K. Kvien, MD, A. G. Semb, MD, PhD: Diakonhjemmet Hospital, Oslo, Norway; J. Hisdal, PhD: Oslo University Hospital, Aker, Oslo, Norway; I. Holme, PhD: Oslo University Hospital, Ulleval, Oslo, Norway; K. T. Smerud, MSc: Smerud Medical Research International AS, Oslo, Norway; G. D. Kitas, MD, PhD, FRCP: The Dudley Group NHS Foundation Trust, West Midlands, UK; T. R. Pedersen, MD, PhD: Centre of Preventive Medicine, Oslo University Hospital, Ulleval, and University of Oslo, Oslo, Norway. Dr. Hammer has received consulting fees, speaking fees, and/ or honoraria from Pfizer, Roche, AbbVie, UCB, and Merck Sharp & Dohme (less than $10,000 each). Dr. Pedersen has received speaking fees from Amgen (less than $10,000) and consulting/speaking fees from Merck Sharp & Dohme (more than $10,000). Dr. Semb has received speaking fees, consulting fees, and/or honoraria from Merck Sharp & Dohme, Schering Plough, AbbVie, Bristol-Myers Squibb, UCB, Wyeth/ Pfizer, and Hoffmann-La Roche/Genentech (less than $10,000 each). Address correspondence to S. Rollefstad, MD, PhD, Preventive Cardio-Rheuma Clinic, Department of Rheumatology, Diakonhjemmet Hospital, PO Box 23 Vinderen, NO-0319 Oslo, Norway. E-mail: s-rollef@diakonsyk.no or s.c.h.rollefstad@medisin.uio.no. Submitted for publication October 20, 2014; accepted in revised form March 10, 2015.

FRI0050 Rosuvastatin Induced Carotid Plaque Regression in Patients with Inflammatory Joint Diseases

BackgroundPatients with rheumatoid arthritis (RA) and carotid artery plaques (CP) have increased risk of acute coronary syndrome. Statin treatment with low density lipoprotein cholesterol (LDL-c) goal ≤1.8 mmol/L is recommended...

Effect of combination of ezetimibe and a statin on coronary plaque regression in patients with acute coronary syndrome: ZEUS trial (eZEtimibe Ultrasound Study)

BackgroundMany trials have shown that statins can reduce plaque volume (PV) associated with the degree of LDL-C reduction.The goal of this study is to determine whether the combination of ezetimibe and a statin produces greater reductions in coronary plaque volume compared to statin monotherapy in patients with acute coronary syndrome (ACS). MethodsProspective serial intravascular ultrasound (IVUS) of non-culprit lesions of the target vessel was performed in 95 patients with ACS. Of these, 50 patients were administered combination of atorvastatin 20mg/day and ezetimibe 10mg/day. 45 subjects treated by atorvastatin 20mg/day alone were the control group. At the beginning and 24weeks after PCI, quantitative PV was accessed by IVUS. The primary end point was the percentage change in non-culprit coronary PV. ResultsLDL-C was significantly decreased by 49.8% in the ezetimibe/atorvastatin group compared with 34.6% in the atorvastatin group. Significant regression of plaque volume was observed from baseline to follow-up in both groups. The percentage changes in PV were greater in the ezetimibe/atorvastatin group than in the atorvastatin alone group (12.5% versus 7.6%, p=0.06), but statistically not significant. In 34 diabetic patients, regression of PV was significantly greater in the ezetimibe/atorvastatin group than in the statin alone group (13.9% versus 5.1%, p=0.04) and % change of PV significantly correlated with LDL-C reduction. ConclusionsAdditional LDL-C reduction with combination therapy tended to reduce more plaque regression compared to a statin alone in patients with ACS. In diabetic patients, further reduction of LDL-C was associated with a significantly greater reduction in PV.

Impact of Cilostazol on the Progression of Carotid Atherosclerosis in Patients with Retinal Vascular Occlusion

Cilostazol, a selective phosphodiesterase three inhibitor, has been proposed to have beneficial effects in the prevention of atherosclerosis. We aimed to investigate the effects of cilostazol on carotid intima-media thickening (IMT) and total plaque area (TPA) in patients with retinal vascular occlusion. A total of 63 consecutive vascular occlusive retinopathy patients with carotid atherosclerosis were enrolled. We examined changes in the carotid IMT/TPA and visual acuity/macular thickness before and after 1-year treatment with cilostazol (200mg/day). The mean IMT of both common carotid arteries (CCAs) and internal carotid arteries (ICAs) were significantly reduced after cilostazol treatment. There was no significant difference in the TPA of both CCAs before and after the treatment (before; 0.61±0.94 vs. after; 0.45±0.79cm(2) , P=0.291); however, significant plaque regression (before; 0.14±0.15 vs. after; 0.25±0.14 cm(2) , P=0.004) was observed in selected patients (n=30) with a TPA <0.5cm(2) . The improvement in macular thickness was significantly associated with an improvement in carotid IMT (r=0.42, P=0.001) and TPA (r=0.23, P=0.04). Cilostazol potently inhibited the progression of carotid IMT and may play a role in the early carotid plaque regression in patients with retinal vascular occlusion.

High HbA1c levels correlate with reduced plaque regression during statin treatment in patients with stable coronary artery disease: Results of the coronary atherosclerosis study measuring effects of rosuvastatin using intravascular ultrasound in Japanese subjects (COSMOS)

BackgroundThe incidence of cardiac events is higher in patients with diabetes than in people without diabetes. The Coronary Atherosclerosis Study Measuring Effects of Rosuvastatin Using Intravascular Ultrasound in Japanese Subjects (COSMOS) demonstrated significant plaque regression in Japanese patients with chronic coronary disease after 76 weeks of rosuvastatin (2.5 mg once daily, up-titrated to a maximum of 20 mg/day to achieve LDL cholesterol <80 mg/dl).MethodsIn this subanalysis of COSMOS, we examined the association between HbA1c and plaque regression in 40 patients with HbA1c ≥6.5% (high group) and 86 patients with HbA1c <6.5% (low group).ResultsIn multivariate analyses, HbA1c and plaque volume at baseline were major determinants of plaque regression. LDL cholesterol decreased by 37% and 39% in the high and low groups, respectively, while HDL cholesterol increased by 16% and 22%, respectively. The reduction in plaque volume was significantly (p = 0.04) greater in the low group (from 71.0 ± 39.9 to 64.7 ± 34.7 mm3) than in the high group (from 74.3 ± 34.2 to 71.4 ± 32.3 mm3). Vessel volume increased in the high group but not in the low group (change from baseline: +4.2% vs −0.8%, p = 0.02). Change in plaque volume was significantly correlated with baseline HbA1c.ConclusionsDespite similar improvements in lipid levels, plaque regression was less pronounced in patients with high HbA1c levels compared with those with low levels. Tight glucose control during statin therapy may enhance plaque regression in patients with stable coronary disease.Trial registrationClinicalTrials.gov, Identifier NCT00329160

Pitavastatin: An overview

Compared to other statins, pitavastatin is a highly potent 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase inhibitor and an efficient hepatocyte low-density lipoprotein-cholesterol (LDL-C) receptor inducer. Its characteristic structure (heptenoate as the basic structure, a core quinoline ring and side chains that include fluorophenyl and cyclopropyl moieties) provides improved pharmacokinetics and significant LDL-C-lowering efficacy at low doses. Unlike other statins, the cyclopropyl group on the pitavastatin molecule appears to divert the drug away from metabolism by cytochrome P450 (CYP) 3 A4 and allows only a small degree of clinically insignificant metabolism by CYP2C9. As a result, pitavastatin is minimally metabolized; most of the bioavailable fraction of an oral dose is excreted unchanged in the bile and is reabsorbed by the small intestine ready for enterohepatic recirculation. This process probably accounts for pitavastatin's increased bioavailability relative to most other statins and contributes to its prolonged duration of action. In addition to its potent LDL-C-lowering efficacy, a number of pleiotropic benefits that might lead to a reduction in residual risk have been suggested in vitro. These include beneficial effects on endothelial function, stabilisation of the coronary plaque, anti-inflammatory effects and anti-oxidation. With regard to the clinical safety and efficacy of pitavastatin, the Phase IV Collaborative study of Hypercholesterolemia drug Intervention and their Benefits for Atherosclerosis prevention (CHIBA study) showed similar changes in lipid profile with pitavastatin and atorvastatin in Japanese patients with hypercholesterolemia. However, a subgroup analysis of the CHIBA study showed that pitavastatin produced more significant changes from baseline in LDL-C, TG, and HDL-C in patients with hypercholesterolemia and metabolic syndrome. The clinical usefulness of pitavastatin has been further demonstrated in a number of Japanese patient groups with hypercholesterolemia, including those with insulin resistance, low levels of high-density lipoprotein-cholesterol (HDL-C), high levels of C-reactive protein, and chronic kidney disease. Finally, the Japan Assessment of Pitavastatin and AtorvastatiN in Acute Coronary Syndrome (JAPAN-ACS) study showed that pitavastatin induces plaque regression in patients with ACS, which suggests potential benefits for pitavastatin in reducing CV risk.

Decreased circulating lipoprotein-associated phospholipase A2 levels are associated with coronary plaque regression in patients with acute coronary syndrome

ObjectiveLipoprotein-associated phospholipase A2 (Lp-PLA2) is a vascular-specific inflammatory enzyme, of which increases are associated with cardiovascular events. However, the relationship between circulating Lp-PLA2 levels and coronary plaque volume has not been clarified in patients with acute coronary syndrome (ACS). MethodsWe studied 40 patients with ACS (age, 61.4±8.0 years; male, 87.5%; statin use, 45.0%) who had undergone successful percutaneous coronary intervention (PCI). Plaque volume (PV) in non-culprit sites of PCI lesions was precisely determined using grayscale intravascular ultrasound (IVUS) at onset and at six months later. We then analyzed associations among PV, lipid profiles and Lp-PLA2 levels. ResultsCirculating Lp-PLA2 levels and PV significantly decreased between baseline and six months of follow-up (458.6±166.7IU/L vs. 378.4±158.5IU/L, p<0.001 and 82.2±34.8mm3 vs. 77.3±33.1mm3, p<0.001, respectively). The % change in PV positively and significantly correlated with % change in LDL-C and in the LDL-C/HDL-C ratio (r=0.444, p=0.004 and r=0.462, p=0.003, respectively). Furthermore, % changes in Lp-PLA2 and in PV correlated even more closely (r=0.496, p=0.001). The absolute change in PV also significantly correlated with the change in Lp-PLA2 levels (r=0.404, p=0.009). ConclusionsCirculating Lp-PLA2 levels are associated with changes in coronary plaque determined by IVUS in patients with ACS.

Comparison of Effects of Rosuvastatin and Atorvastatin on Plaque Regression in Korean Patients With Untreated Intermediate Coronary Stenosis

Serial intravascular ultrasound (IVUS) was used to compare the effects of moderate doses of rosuvastatin and atorvastatin on plaque regression in patients with intermediate coronary stenosis. This was a prospective, randomized, and comparative study for lipid-lowering therapy with rosuvastatin 20mg (n=65) and atorvastatin 40mg (n=63) using serial IVUS (baseline and 11-month follow-up). Efficacy parameters included changes in total atheroma volume (TAV) and percent atheroma volume (PAV) from baseline to follow-up. Changes of TAV (-4.4±7.3 vs. -3.6±6.8mm(3), P=0.5) and PAV (-0.73±2.05 vs. -0.19±2.00%, P=0.14) from baseline to follow-up were not significantly different between the 2 groups. Plaque was increased in 15% in the rosuvastatin group and in 30% in the atorvastatin group at follow-up (P=0.064). The plaque increase group had higher baseline high-sensitivity C-reactive protein (hs-CRP; 1.28±2.70mg/dl vs. 0.54±1.16mg/dl, P=0.034) and higher follow-up low-density lipoprotein cholesterol (LDL-C) (78±24mg/dl vs. 63±21mg/dl, P=0.002) compared with the plaque non-increase group. Follow-up LDL-C (odds ratio [OR]=1.038, 95% confidence interval [CI]=1.003-1.060, P=0.036) and baseline hs-CRP (OR=1.025, 95%CI=1.001-1.059, P=0.046), not the type of statin, were the independent predictors of plaque increase at follow-up. Moderate doses of rosuvastatin and atorvastatin could contribute to effective plaque regression. Follow-up LDL-C and baseline hs-CRP are associated with plaque progression in patients with intermediate coronary stenosis.

TCT-396: Comparison of Effects of Moderate Doses of Rosuvastatin and Atorvastatin on Plaque Regression in Patients with Non-intervened Intermediate Coronary Stenosis

TCT-396: Comparison of Effects of Moderate Doses of Rosuvastatin and Atorvastatin on Plaque Regression in Patients with Non-intervened Intermediate Coronary Stenosis

P-266 Effectiveness of Early EPA Treatment in Plaque Regression in Patients with Acute Coronary Syndrome

P-266 Effectiveness of Early EPA Treatment in Plaque Regression in Patients with Acute Coronary Syndrome

The Effects of Rosuvastatin on Plaque Regression in Patients Who Have a Mild to Moderate Degree of Coronary Stenosis With Vulnerable Plaque

Background and Objectives: Intensive lipid-lowering therapy with statins improves the clinical outcomes and patient survival and it reduces the progression of atherosclerosis. Intravascular ultrasound (IVUS) has been used for calculating the plaque volumes to evaluate the mechanisms that may be involved in the progression or regression of coronary artery disease. We used serial IVUS exams to assess the efficacy of rosuvastatin on plaque regression in angina patients who had a mild to moderate degree of vulnerable plaque burden. Subjects and Methods: This study was a prospective, randomized, comparative study for lipid lowering therapy with using rosuvastatin 20 mg or atorvastatin 40 mg. IVUS was performed during the baseline coronary angiography and it was repeated after 12 months of treatment. The efficacy parameters included the changes in the atheroma volume and the lipid pool size as determined by IVUS. A total of 45 lesions in 30 patients were analyzed (rosuvastatin: 24 lesions in 16 patients vs. atorvastatin: 21 lesions in 14 patients). Results: The low density lipoprotein (LDL)-cholesterol level was reduced from 121±45 mg/dL to 65±25 mg/dL in the rosuvastatin group (a 46% decrease, p<0.001), and from 127±37 mg/dL to 72±26 mg/dL in the atorvastatin group (a 43% decrease, p<0.001). The total atheroma and vessel volumes were significantly decreased, whereas the lumen volume was significantly increased from baseline to follow-up in both groups (for the rosuvastatin group: the total atheroma volume, 252±80 to 246±79 mm 3 , p<0.001; the vessel volume, 555±158 to 553±130 mm 3 , p<0.001; the lumen volume, 303±91 to 307±92 mm 3 , p<0.001, and for the atorvastatin group: the total atheroma volume, 288±98 to 283±98 mm 3 , p<0.001; the vessel volume, 607±165 to 604±166 mm 3 , p<0.001; the lumen volume, 319±71 to 321±73 mm 3 , p<0.001). The follow-up LDL-cholesterol level was correlated with the change in the total atheroma volume (r=0.577, p< 0.001), the change in the percent atheroma volume (r=0.558, p<0.001) and the change in the lipid pool size (r=0.470, p=0.001). Conclusion: Both rosuvastatin 20 mg and atorvastatin 40 mg could contribute to the regression of lipid-rich plaque. The follow-up LDL-cholesterol level is related to the regression and stabilization of vulnerable coronary plaque. (Korean Circ J 2008;38:366-373)