Effects of Statin Treatments on Coronary Plaques Assessed by Volumetric Virtual Histology Intravascular Ultrasound Analysis
Myeong-Ki Hong, MD*,
Duk-Woo Park, MD ,
Cheol-Whan Lee, MD,
Seung-Whan Lee, MD,
Young-Hak Kim, MD,
Duk-Hyun Kang, MD,
Jae-Kwan Song, MD,
Jae-Joong Kim, MD,
Seong-Wook Park, MD,
Seung-Jung Park, MD,*
* Division of Cardiology, Yonsei Cardiovascular Center, Yonsei University College of Medicine, Seoul, Korea
Department of Medicine, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea
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Abstract
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Objectives: We evaluated the effects of statin treatments for each component of coronary plaques.
Background: Effects of statin treatments on coronary plaques have not been sufficiently evaluated.
Methods: One hundred patients without significant lesion stenosis underwent baseline and 12-month follow-up virtual histology (VH) intravascular ultrasound (IVUS) studies and were treated with statin for 1 year. They were randomized to simvastatin (20 mg/day, n = 50) or rosuvastatin (10 mg/day, n = 50). With VH-IVUS, plaque was characterized as fibrotic, fibrofatty, dense calcium, and necrotic core.
Results: In overall patients, necrotic core volume significantly reduced (15.7 to 13.7 mm3, p = 0.010) and fibrofatty plaque volume increased (4.3 to 5.5 mm3, p = 0.006) after statin treatments for 1 year. There were no significant differences of changes in either plaque component volume between simvastatin- and rosuvastatin-treated subgroups. In serial comparisons during 1-year follow-up, simvastatin treatment did not achieve statistically significant changes in fibrofatty plaque (4.1 to 5.1 mm3, p = 0.131) and necrotic core volume (15.8 to 14.4 mm3, p = 0.216). However, there was a significant decrease in necrotic core volume (15.5 to 13.0 mm3, p = 0.015) and an increase in fibrofatty plaque volume (4.5 to 5.9 mm3, p = 0.017) in the rosuvastatin-treated subgroup.
Conclusions: Serial volumetric VH-IVUS analysis showed that statin treatments might be associated with significant changes in necrotic core and fibrofatty plaque volume in overall patients. The changes in both plaques' component volume were not statistically different between simvastatin- and rosuvastatin-treated subgroup.
Key Words: coronary disease • plaque • ultrasonics
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Abbreviations and Acronyms
| | ACS = acute coronary syndrome | | EEM = external elastic membrane | | HDL = high-density lipoprotein | | IVUS = intravascular ultrasound | | LDL = low-density lipoprotein | | P&M = plaque and media | | VH = virtual histology |
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Statin treatments have been reported to reduce major cardiac events in patients with coronary artery disease in several clinical studies (1–3). Although long-term clinical outcomes have been improved after statin therapy, previous angiographic studies showed only minimal changes in angiographic lumen dimension in target lesions in patients who were treated with statin (4,5). Several intravascular ultrasound (IVUS) studies have demonstrated the benefits of statin therapy to be involved in regression or no progression of coronary plaque size (6–8). However, conventional gray-scale IVUS has significant limitations in accurately assessing atheromatous plaque composition and identifying a vulnerable plaque before rupture of the vulnerable plaque occurs. These limitations of gray-scale IVUS have been partially addressed by virtual histology (VH) IVUS, which characterizes plaques as calcified, fibrotic, fibrofatty, and necrotic core (9–11). Rupture of a vulnerable plaque and subsequent thrombus formation have been reported to be the most important mechanism leading to an acute coronary syndrome (ACS) in pathologic and autopsy studies (12,13). Statin treatments have been regarded as 1 of the most effective methods for stabilization of vulnerable plaque and improvements of long-term clinical outcomes in patients with ACS (2,3,8,14). However, effects of statin treatments on coronary plaques in IVUS studies have not been sufficiently validated. Therefore the primary aims of the present study were to evaluate, with VH-IVUS technology, the effects of statin treatments on each component of coronary plaques. We also evaluated, secondarily, the impacts on each component of plaques according to different types of statin treatment regimen.
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Methods
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Study population.
One hundred patients with de novo nonculprit/nontarget lesions were included in this randomized study at Asan Medical Center. These patients who were randomized to simvastatin (20 mg/day, n = 50) or rosuvastatin (10 mg/day, n = 50) treatment for 1 year underwent baseline and 12-month follow-up VH-IVUS study. The inclusion criteria of this study were lesions without significant stenosis by coronary angiogram (diameter stenosis <50%), lesions with a plaque burden <0.75 by gray-scale IVUS, and lesions located in 1 of 3 major epicardial arteries in which stent implantation was not performed. The exclusion criteria were severely calcific lesions, hemodynamically unstable patients, cardiogenic shock, recommended coronary artery bypass graft surgery, and previous history of administration of lipid-lowering agents including statin. During the 1-year follow-up, the occurrence of major adverse cardiac events including death of any causes, acute myocardial infarction (elevation of the creatine kinase-myocardial band fraction to a value 3 times the upper limit of normal), and target lesion revascularization (percutaneous or surgical intervention of these nonstenotic lesions) was evaluated. This study was performed with the patient's written informed consent and approval of the institutional review board. Changes ( ) in lipid profiles, C-reactive protein, and VH-IVUS variables were calculated as follow-up minus baseline values.
IVUS imaging and analysis.
Baseline and 1-year follow-up VH-IVUS examinations were performed before any intervention and after intracoronary administration of 0.2 mg nitroglycerin with motorized transducer pullback system (0.5 mm/s). The 2.9-F IVUS imaging catheter (Eagle Eye, Volcano Corp., Rancho Cordova, California) incorporated a 20-MHz phased-array transducer.
Conventional gray-scale quantitative IVUS analyses were performed according to criteria of the clinical expert consensus document on IVUS to include external elastic membrane (EEM), lumen, and plaque & media (P&M) (P&M = EEM – lumen) areas (15). Plaque burden was defined as P&M divided by EEM area.
Volumetric VH-IVUS analysis was performed along a 10-mm segment with 1-mm interval centered on the minimal lumen area and was calculated with Simpson's rule. The VH-IVUS analysis classified color-coded tissue as green (fibrotic), yellow-green (fibrofatty), white (dense calcium), and red (necrotic core) (9,10). The VH-IVUS analyses were reported in absolute amounts and as a percentage (relative amounts) of plaque volume. The study populations were also arbitrarily divided into 2 subgroups: the subgroup with a decrease in necrotic core volume by serial analysis in group 1 (Fig. 1), and the subgroup without a decrease in necrotic core volume in group 2.
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Figure 1 A Decrease in Necrotic Core Volume After Statin Treatment
Typical example of a decrease in necrotic core volume by serial volumetric virtual histology (VH) intravascular ultrasound (IVUS) analysis is shown. (A) Baseline and (B) 12-month follow-up gray-scale IVUS images. (C) Baseline and (D) 12-month follow-up VH-IVUS images. The amounts of necrotic core components decreased from 2.3 mm2 (47%) baseline to 1.1 mm2 (24%) 12-month follow-up.
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Statistical analysis.
Statistical analysis was performed with SPSS (SPSS Inc., Chicago, Illinois). Data are presented as frequencies or mean ± SD. Comparison was performed with chi-square statistics or Fisher exact test and paired or unpaired Student t test or Mann-Whitney U test. Nonparametric analysis with Wilcoxon signed rank test was also done. Multiple stepwise logistic regression analysis was performed to assess independent clinical predictors for decrease in necrotic core volume by serial analysis. A p value <0.05 was considered statistically significant.
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Results
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Baseline clinical characteristics are shown in Table 1. There were no significant differences of baseline clinical characteristics between simvastatin- and rosuvastatin-treated patients. Compared with simvastatin-treated patients, 12-month follow-up total and low-density lipoprotein (LDL) cholesterol levels were significantly lower in rosuvastatin-treated patients. No major adverse cardiac events occurred in either group for 12-month follow-up. Baseline and 12-month follow-up and changes during 1-year follow-up gray-scale and VH-IVUS analysis are shown in Table 2. There were no significant differences of baseline and 12-month follow-up gray-scale and VH-IVUS variables in volumetric analysis between simvastatin- and rosuvastatin-treated patients. There were also no statistically significant differences of changes in each plaque component between simvastatin- and rosuvastatin-treated subgroups.
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Table 2 Gray-Scale and Virtual Histology Intravascular Ultrasound Analysis Between Simvastatin- and Rosuvastatin-Treated Patients
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Serial changes of gray-scale and VH-IVUS variables in overall patients are shown in Table 3. Overall, there were significant changes in gray-scale IVUS plaque volumes: EEM volume (176.2 ± 42.0 mm3 at baseline and 172.3 ± 41.6 mm3 at follow-up, p < 0.001), P&M volume (89.8 ± 27.1 mm3 at baseline and 87.1 ± 27.2 mm3 at follow-up, p < 0.001), and lumen volume (86.4 ± 23.4 mm3 at baseline and 85.2 ± 22.8 mm3 at follow-up, p = 0.041). The VH-IVUS analysis showed that necrotic core volume significantly reduced (15.7 ± 9.9 mm3 at baseline and 13.7 ± 9.9 mm3 at follow-up, p = 0.010) and fibrofatty plaque volume significantly increased (4.3 ± 3.5 mm3 at baseline and 5.5 ± 4.0 mm3 at follow-up, p = 0.006) after statin treatments for 1 year. In the simvastatin-treated subgroup, the changes in fibrofatty plaque (4.1 ± 2.9 mm3 at baseline and 5.1 ± 4.4 mm3 at follow-up, p = 0.131) and necrotic core volume (15.8 ± 11.3 mm3 at baseline and 14.4 ± 10.5 mm3 at follow-up, p = 0.216) did not achieve statistical significance (Table 2). However, there was a significant decrease in necrotic core volume (15.5 ± 8.4 mm3 at baseline and 13.0 ± 9.4 mm3 at follow-up, p = 0.015) and an increase in fibrofatty plaque volume (4.5 ± 4.0 mm3 at baseline and 5.9 ± 3.5 mm3 at follow-up, p = 0.017) in the rosuvastatin-treated subgroup (Table 2).
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Table 3 Gray-Scale and Virtual Histology Intravascular Ultrasound Analysis Between Baseline and 1-Yr Follow-Up in Overall Patients
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Baseline clinical characteristics between group 1 and group 2 are shown in Table 4. A decrease in necrotic core volume by serial analysis was observed in 27 (54%) simvastatin-treated and 35 (70%) rosuvastatin-treated patients (p = 0.099). Compared with the patients in group 2, the patients in group 1 were significantly older and had higher level of baseline high-density lipoprotein (HDL)-cholesterol. There were more male patients and rosuvastatin treatments and higher level of 12-month follow-up HDL cholesterol in the patients in group 1. All clinical univariate predictors for a decrease in necrotic core volume at a p < 0.2 level were entered into the multiple logistic regression model; sex, age, types of statin treatment, and baseline and 12-month follow-up HDL-cholesterol level. The only independent clinical predictor for a decrease in necrotic core volume was baseline HDL-cholesterol level (p = 0.040, odds ratio: 1.044, 95% confidence interval (CI): 1.002 to 1.089) by multiple stepwise logistic regression analysis. There was a significant linear correlation between baseline HDL-cholesterol level and change in necrotic core volume (p = 0.030, r = 0.217, 95% CI: –0.293 to –0.015) (Fig. 2).
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Figure 2 Baseline HDL-Cholesterol Level Versus Necrotic Core Volume
The correlation between baseline high-density lipoprotein (HDL) cholesterol level and change in necrotic core volume is shown (p = 0.030, r = 0.217, 95% confidence interval: –0.293 to –0.015).
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In overall patients, compared with the patients in group 2, fibrotic and fibrofatty plaque volume were significantly smaller and necrotic core volume was significantly greater in the patients in group 1 in baseline VH-IVUS study. In 12-month follow-up study, however, fibrofatty plaque volume was significantly greater and necrotic core volume was significantly smaller in the patients in group 1 (Table 5).
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Table 5 Gray-Scale and Virtual Histology Intravascular Ultrasound Analysis in Patients With Versus Without a Decrease in Necrotic Core Volume
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Serial changes of gray-scale and VH-IVUS variables in groups 1 and 2 are also shown in Table 5. In group 2, there were no significant changes of P&M volume; reduction of EEM volume resulted in subsequent reduction of lumen volume in serial gray-scale IVUS analysis. Fibrotic and fibrofatty plaque volume significantly reduced (30.5 ± 14.4 mm3 to 25.6 ± 11.4 mm3, p < 0.001 and 6.1 ± 4.0 mm3 to 4.3 ± 2.6 mm3, p < 0.01, respectively); dense calcium and necrotic core volume significantly increased (5.6 ± 6.2 mm3 to 7.5 ± 6.4 mm3, p < 0.05, and 12.7 ± 9.4 mm3 to 17.9 ± 11.8 mm3, p < 0.001, respectively). In group 1, there were no significant changes of lumen volume; reduction of P&M volume was associated with subsequent reduction of EEM volume in serial gray-scale IVUS analysis. Fibrotic and fibrofatty plaque volume significantly increased (24.7 ± 12.6 mm3 to 26.9 ± 12.6 mm3, p < 0.05, and 3.2 ± 2.5 mm3 to 6.3 ± 4.4 mm3, p < 0.001, respectively); there were no significant changes of dense calcium; necrotic core volume significantly decreased (17.5 ± 9.8 mm3 to 11.2 ± 7.6 mm3, p < 0.001). There was a significant linear correlation between the change in necrotic core volume and the change in P&M volume (p = 0.001, r = 0.329, 95% CI: 0.162 to 0.600) (Fig. 3) and the change in lumen volume (p < 0.001, r = 0.412, 95% CI: –0.787 to –0.304). However, the changes in necrotic core volume did not correlate with the changes in EEM volume (p = 0.9, r = 0.010, 95% CI: –0.253 to 0.229).
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Figure 3 Necrotic Core Volume Versus P&M Volume
The correlation between the change in necrotic core volume and the change in plaque & media (P&M) volume is shown (p = 0.001, r = 0.329, 95% confidence interval: 0.162 to 0.600).
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Discussion
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In this randomized study of 100 patients who were treated with statin, statin treatments might be involved in significant changes of plaques component volume. The changes in plaques component volume were not different between simvastatin- and rosuvastatin-treated subgroups. Baseline HDL-cholesterol level was the only independent clinical predictor for a decrease in necrotic core volume and was significantly correlated with the change in necrotic core volume. Although there were no significant changes of P&M volume in the patients without a decrease in necrotic core volume, there was a significant reduction in P&M volume in the patients with a decrease in necrotic core volume in serial gray-scale IVUS analysis. Serial volumetric VH-IVUS analysis showed that there was a significant decrease in fibrotic and fibrofatty plaque volume and an increase in dense calcium and necrotic core volume in the patients without a decrease in necrotic core volume. However, fibrotic and fibrofatty plaque volume significantly increased and necrotic core volume significantly decreased in the patients with a decrease in necrotic core volume.
The MIRACL (Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering) study in 3,086 patients with ACS showed that lipid-lowering therapy with atorvastatin, 80 mg/day, reduces early, recurrent ischemic events (2). The PROVE IT–TIMI 22 (PRavastatin Or atorVastatin Evaluation and Infection Therapy–Thrombolysis in Myocardial Infarction 22) study in 4,162 patients with ACS reported that an intensive lipid-lowering statin regimen (atorvastatin, 80 mg/day) provides greater protection against death or major cardiovascular events than a standard regimen (pravastatin, 40 mg/day) (3). These clinical benefits of statin might be partially related to the result of a benefit in stabilizing vulnerable plaques with the early and intensive treatment after the acute event in patients with ACS, who have a culprit lesion and frequently additional multiple vulnerable plaques as well (3).
The ASTEROID trial (A Study To Evaluate the Effect of Rosuvastatin on IVUS-Derived Coronary Atheroma Burden), in 349 patients who had serial IVUS examinations, showed that very high-intensity statin therapy with rosuvastatin 40 mg/day achieved an average LDL-cholesterol of 60.8 mg/dl and increased HDL-cholesterol by 14.7%, resulting in significant regression of coronary atherosclerosis (6). The REVERSAL (Reversal of Atherosclerosis with Aggressive Lipid Lowering) trial, in 502 patients who had serial IVUS examinations, reported that compared with baseline values, patients treated with atorvastatin (80 mg/day) had no change in atheroma burden, whereas patients treated with pravastatin (40 mg/day) showed progression of coronary atherosclerosis (7). Because the previous IVUS studies (6,7) were performed with gray-scale IVUS technology, detection of change of each plaque composition was very difficult. However, the present study showed that statin treatment might result in changes of plaque composition (significant reduction in necrotic core volume and increase in fibrofatty plaque volume) by VH-IVUS analysis as well as reduction of P&M volume by gray-scale IVUS analysis. In viewpoints of achievement of Adult Treatment Panel III guideline LDL-cholesterol goals, efficacy of 10 mg of rosuvastatin was comparable to that of 20 mg of atorvastatin and 40 mg of simvastatin (16). The changes in plaques component volume were not different between simvastatin- and rosuvastatin-treated subgroups in this serial VH-IVUS study. Rosuvastatin, 10 mg, and simvastatin, 20 mg, were prescribed and compared in this study because both statin doses are initially recommended for treatment of patients with coronary artery disease in Korea. The LDL-cholesterol level decreased from 119 to 78 mg/dl in the simvastatin-treated subgroup and 116 to 64 mg/dl in the rosuvastatin-treated subgroup. Follow-up LDL-cholesterol reached approximately 70 mg/dl in both statin groups of this study, which are recommended level in patients with ACS by recent Adult Treatment Panel III guideline (17). Without need for statin dose adjustments, LDL-cholesterol level was well-controlled in all patients during 1-year follow-up in this study.
With gray-scale IVUS, recent meta-analysis of the studies assessing temporal changes in coronary plaque volume showed that statin therapy, particularly when achieving the target LDL level (100 mg/dl), seems to promote a significant regression of IVUS-measured coronary plaque volume (18). We also reported similar results: 1) follow-up LDL cholesterol level was the only independent predictor for mean P&M area; and 2) the cutoff value for no change or a plaque regression was follow-up LDL-cholesterol <100 mg/dl (19). However, because of the intrinsic limitations of gray-scale IVUS, the previous studies can find only the predictors for changes in overall plaque size (plaques regression or progression), not the predictors for changes in specific plaque composition. The published IVUS data about the predictors for changes in necrotic core size are very limited. In this study, baseline HDL-cholesterol level was the only independent clinical predictor for a decrease in necrotic core volume by multiple stepwise logistic regression analysis. However, its power of positive correlation as an independent predictor (p = 0.040, odds ratio: 1.044, 95% CI: 1.002 to 1.089) was very weak. There was a tendency that a decrease in necrotic core volume was more frequently observed in the rosuvastatin-treated subgroup than in the simvastatin-treated subgroup (70% vs. 54%, p = 0.099); however, statistical significance was not achieved. There were no significant differences of baseline and follow-up LDL-cholesterol level in the subgroup with versus the subgroup without a decrease in necrotic core volume. These findings might suppose that, whereas the LDL-cholesterol level is more significantly involved in changes in gross plaque size, the HDL-cholesterol level has a more specific role in changes in particular plaque components size (i.e., reduction of necrotic core). Although there are no available data that reduction in necrotic core size means plaques stabilization or improved long-term clinical outcomes, reduction in necrotic core size might be 1 of several requirements for plaques stabilization. Therefore, we divided the study populations into 2 subgroups: the patients with versus without a decrease in necrotic core volume by serial analysis. Although significant changes in P&M volume did not occur in the subgroup without a decrease in necrotic core volume, there were significant reductions of P&M volume in the subgroup with a decrease in necrotic core volume. Significant linear correlation between the change in necrotic core volume and the change in P&M volume (p = 0.001, r = 0.329) suggested that plaque regression might result partly from decrease in necrotic core. However, the relations between a decrease in necrotic core size and plaques stabilization or improved long-term clinical outcomes will be further evaluated in more studies with larger study populations and longer follow-up durations.
Study limitations.
This was an open-label trial without masking without nonblinded IVUS analysis. This study has the characteristics of an exploratory nature to analyze the amounts of changes in each plaques component volume after statin treatment. The data in this study will be useful to generate hypotheses in randomized clinical outcomes studies using VH-IVUS.
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Conclusions
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Serial volumetric VH-IVUS analysis showed that statin treatments might have significant impacts on coronary plaques components in overall patients. The changes in plaques component volume were not statistically different between simvastatin- and rosuvastatin-treated subgroups.
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Footnotes
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This study was partly supported by Cardiovascular Research Foundation, Seoul, Korea and a grant of the Korea Health 21 R&D Project, Ministry of Health & Welfare, Korea (0412-CR02-0704-0001)
* Reprint requests and correspondence: Dr. Seung-Jung Park, Departments of Medicine, University of Ulsan College of Medicine, Asan Medical Center, 388-1 Poongnap-dong, Songpa-gu, Seoul 138-736, Korea (Email: sjpark{at}amc.seoul.kr).
Manuscript received March 23, 2009;
accepted March 24, 2009.
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Abstract
Methods