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J Am Coll Cardiol Img, 2010; 3:19-28, doi:10.1016/j.jcmg.2009.09.016
© 2010 by the American College of Cardiology Foundation
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The Association Between Plaque Characterization by CT Angiography and Post-Procedural Myocardial Infarction in Patients With Elective Stent Implantation

Tadayuki Uetani, MD, PhD*,*, Tetsuya Amano, MD, PhD*, Ayako Kunimura, MD*, Soichiro Kumagai, MD*, Hirohiko Ando, MD*, Kiminobu Yokoi, MD*, Tomohiro Yoshida, MD*, Bunichi Kato, MD, PhD*, Masataka Kato, MD*, Nobuyuki Marui, MD, PhD*, Michio Nanki, MD, PhD*, Tatsuaki Matsubara, MD, PhD{dagger}, Hideki Ishii, MD, PhD{ddagger}, Hideo Izawa, MD, PhD{ddagger}, Toyoaki Murohara, MD, PhD{ddagger}

* Department of Cardiology, Chubu Rosai Hospital, Nagoya, Japan
{dagger} Department of Internal Medicine Aichi-Gakuin School of Dentistry, Nagoya, Japan
{ddagger} Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan


    Abstract
 Top
 Abstract
 Methods
 Results
 Discussion
 Conclusions
 REFERENCES
 
Objectives: This study sought to evaluate the association between volumetric characterization of target lesions by multidetector computed tomography (MDCT) angiography and the risk of post-procedural myocardial injury after elective stent implantation.

Background: Previous reports have shown that plaque characterization of the target lesion may provide useful information for stratifying the risk of coronary stenting.

Methods: A total of 189 consecutive patients were enrolled; they underwent elective stent implantation after volumetric plaque analysis with 64-slice MDCT. Each plaque component and lumen (filled with dye) was defined as follows: 1) low-attenuation plaque (LAP) (<50 HU); 2) moderate-attenuation plaque (MAP) (50 to 150 HU); 3) lumen (151 to 500 HU); and 4) high-attenuation plaque (HAP) (>500 HU). The volume of each plaque component in the target lesion was calculated using Color Code Plaque. Post-procedural creatine kinase-MB isoform and troponin-T (TnT) at 18 h after percutaneous coronary intervention were also evaluated.

Results: The volumes of LAP (87.9 ± 94.8 mm3 vs. 47.4 ± 43.7 mm3, p < 0.01) and MAP (111.6 ± 77.5 mm3 vs. 89.8 ± 67.1 mm3, p < 0.05) were larger in patients with post-procedural myocardial injury (defined as positive TnT) than in those with negative TnT. The volumes of LAP and MAP and fraction of LAP in total plaque (LAP volume/total plaque volume) correlated with biomarkers; the MAP fraction was inversely correlated with biomarkers. The volume of LAP was an independent predictor of positive TnT after adjusting for patient background, conventional IVUS parameters, and procedural factors.

Conclusions: Post-procedural myocardial injury was associated with the volume and fraction of LAP as detected by MDCT. The volume of LAP was an independent predictor of positive TnT. Plaque analysis by MDCT would be a useful method for predicting post-procedural myocardial injury after percutaneous coronary intervention.

Key Words: coronary stent • computed tomography • coronary plaque

Abbreviations and Acronyms
  CK = creatine kinase
  CSA = cross-sectional area
  CT = computed tomography
  EEM = external elastic membrane
  HAP = high-attenuation plaque
  IVUS = intravascular ultrasound
  LAP = low-attenuation plaque
  MAP = moderate-attenuation plaque
  MDCT = multidetector computed tomography
  PCI = percutaneous coronary intervention
  PMI = post-procedural myocardial injury/infarction
  TnT = troponin-T


According to current European Society of Cardiology/American College of Cardiology guidelines, any myocardial biomarker elevation above the normal upper limits, in a rise-and-fall pattern, on serial blood samples drawn after percutaneous coronary intervention (PCI) allows a diagnosis of post-procedural myocardial injury/infarction (PMI) (1). Previous studies have reported subclinical creatine kinase (CK)-MB isoenzyme elevation of 5% to 26% and post-procedural cardiac troponin-T (TnT) elevation of 5% to 53% in post-PCI patients (2–4). Modest elevation of cardiac enzymes after PCI has been shown to be associated with worse clinical outcomes (5). Contrast-enhanced magnetic resonance imaging studies provide evidence that a post-procedural elevation of cardiac biomarkers is associated with microinfarction of myocardial regions, originating from the target vessel (6). Clinical, lesion, and procedural characteristics related to PMI have been indicated in various analyses (7–9). Recently we reported a correlation between lipid-rich plaque volume, measured by radiofrequency analysis of intravascular ultrasound (IVUS), and the extent of PMI (10).

In recent investigations, multidetector computed tomography (MDCT) with retrospective electrocardiographic gating has permitted high-resolution imaging of coronary arteries and plaques (11–13). Differentiation of coronary lesion morphology and configuration of plaques by MDCT have been reported previously; studies have also shown that soft (lipid-rich), fibrous, calcified plaques show different Hounsfield units and that the distribution of such plaque components corresponds to IVUS findings (14,15). However, few data exist on quantitative or volumetric evaluation of coronary plaque components by MDCT.

It is hypothesized that 64-slice MDCT would provide the volumetric plaque characteristics of the target lesion of a patient who intends to undergo elective stenting. This study aims to evaluate the relationship of quantitative analysis of a target lesion with the extent of PMI, measured as cardiac biomarker elevation after PCI.


    Methods
 Top
 Abstract
 Methods
 Results
 Discussion
 Conclusions
 REFERENCES
 
Study populations.   We carried out a prospectively planned observational study of target lesions in patients with elective coronary stenting. Consecutive patients (n = 331) who planned elective coronary intervention of angiographically significant stenosis were enrolled from November 2005 to September 2007; MDCT angiography was performed on 252 patients who had consented to this study within 2 weeks after initial angiography. We excluded 8 patients who were either suspected to have acute coronary syndrome or had severe symptoms before MDCT. All participants had angina, documented myocardial ischemia, or both, and provided informed consent to this study. The exclusion criteria for this study were as follows: patients with chronic total occlusion (n = 13), elevated pre-procedural cardiac biomarkers (n = 13), angioplasty with debulking device (n = 4), multivessel stenting in a single procedure (n = 22), and inestimable-quality MDCT imaging (n = 11). Thus, the study included 189 patients. This study was approved by the ethics committee of Chubu Rosai Hospital.

Study protocol.   The study protocol was as follows. The computed tomographic (CT) coronary angiography was performed using a 64-slice MDCT within 2 weeks before the PCI procedure. The position and length of the target lesion were defined on the basis of prior conventional angiography by the attending physician, and an analysis of the corresponding site of the MDCT image was performed before the PCI procedure. Coronary stent implantation was performed after pre-procedural IVUS recording. Finally, blood samples collected approximately 18 h after PCI were used to evaluate cardiac biomarkers.

Protocol of 64-slice CT scan.   The CT coronary angiographies were performed using a 64-slice CT scanner (Light Speed VCT, GE Healthcare, Waukesha, Wisconsin). Before CT angiography, a test injection was performed to determine the delay time of the main scanning, and a monitoring scan was acquired at the center of the ascending aorta. To measure the time to maximum enhancement, an enhancement curve was created during the test injection. In the main scan, contrast material (Iopamiron 370, Nihon Schering, Osaka, Japan) and a saline chaser of 20 ml was injected at a rate of 3.2 to 4.0 ml/s; the total volume of the contrast material was 59 ± 19 ml. The main scanning started after a delay time (i.e., the time to maximum enhancement for the test injection plus 3 s). Whole-heart images were acquired within a 7- to 9-s breath-hold. The detector collimation was 64 x 0.625 mm, the gantry rotation speed was 350 ms/rotation, the tube voltage was 120 kV with a current of 350 to 700 mA, and the table feed was 8 mm/rotation.

Image reconstruction and analysis of the coronary artery.   Axial CT images were automatically sent to a workstation (Advantage Workstation 4.2, GE Healthcare), where they were reconstructed and analyzed by 2 independent human readers who were not involved in either the PCI procedure or the biomarker analysis, using the CardIQ Analysis Pro software package (GE Healthcare). Serial multiplanar reconstruction images were created. A cylindrical-shaped, 3-dimensional region of interest was defined in the target lesion along the visually estimated centerline of the target vessel in the multiplanar reconstruction image. The region of interest diameter was defined on the basis of the outer vessel contour identified by visual estimation. The target lesion was divided into 1 to 8 regions of interest as the vessel diameter varied along the longitudinal axis of the multiplanar reconstruction image. The volume of each component within the region of interest was measured automatically, using Color Code Plaque analysis (GE Healthcare) (16), based on the stratified CT density, as described later.

Komatsu et al. (17) has reported plaque characterization based on CT density, which shows good agreement between IVUS and angioscopic findings. On the basis of this analysis, each instance of low-attenuation plaque (LAP), moderate-attenuation plaque (MAP), high-attenuation plaque (HAP), and lumen (filled with contrast medium) was defined as having a CT density of <50 HU, 50 to 150 HU, >500 HU, and 151 to 500 HU, respectively. The fraction of each plaque component, defined as the volume of each component divided by the total plaque volume, was also estimated (Fig. 1).


Figure 1
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Figure 1 Representative Plaque Images

The multidetector computed tomography images of target lesions in patients with post-procedural myocardial injury (I) and without myocardial injury (II). Color-coded maps show low-attenuation plaque (LAP) (blue), moderate-attenuation plaque (MAP) (yellow), and high-attenuation plaque (HAP) (red) areas. (I) Multiplanar reconstruction images (A, axial view; C, cross-sectional view), color-coded plaque images that represent computed tomography density (B, axial view; D, cross-sectional view), and intravascular ultrasound image (E) of a patient with elevated post-procedural cardiac biomarkers (troponin-T, 0.44 ng/ml). LAP, MAP, and HAP volumes were 252.8 mm3, 210.8 mm3, and 0 mm3, respectively. (II) Corresponding images of a patient without thrombotic complication during percutaneous coronary intervention or elevation of post-procedural cardiac biomarkers. LAP, MAP, and HAP volumes were 93.8 mm3, 207.7 mm3, and 7.0 mm3, respectively.

 
PCI procedure.   All patients enrolled in this study underwent elective coronary stent implantation, with or without balloon pre-dilation. All patients received antiplatelet agents for at least 24 h before the procedure. Furthermore, 10,000 IU of heparin was administered before the procedure, and an additional bolus of 1,000 IU was given every hour if the procedure lasted for more than 1 h. The glycoprotein IIb/IIIa receptor inhibitor has not been approved in Japan, and none of the patients received it. All procedures were performed using 6- to 8-F guiding catheters, with either a radial or a femoral approach. A successful PCI, which was defined as <50% residual stenosis and final Thrombolysis In Myocardial Infarction (TIMI) flow grade 3, was realized in each of the enrolled patients. We started the administration of clopidogrel (loading dose 75 to 300 mg and daily maintenance dose 75 mg) in each patient to prevent stent thrombosis after stent implantation.

Angiography and IVUS.   Angiography and IVUS results were evaluated by an independent investigator who was not involved in the procedures but was aware of the final outcomes. A computerized quantitative analysis system (QCA-CMS system, version 3.32, MEDIS, Leiden, the Netherlands) was used with a guiding catheter for calibration. Angiographic measurements included reference diameter, minimum lumen diameter, percentage of diameter stenosis, and lesion length.

The IVUS studies were performed after intracoronary injections of 1,000 µg isosorbide dinitrate with a mechanical sector scanner (Atlantis SR Pro, Boston Scientific Corporation, Natick, Massachusetts) and a motorized transducer pullback system (0.5 mm/s). Image slices of minimum lumen, proximal reference, and distal reference sites were analyzed according to previously described methods (18). The cross-sectional area (CSA) of the external elastic membrane (EEM), lumen CSA, plaque plus media CSA (EEM CSA minus lumen CSA), and plaque burden (plaque plus media CSA/EEM CSA) of these slices were measured. The remodeling index was defined as follows: target lesion EEM CSA divided by the average of the proximal and distal reference EEM CSA. To compare plaque volume measured by MDCT and IVUS, the total plaque volume by IVUS was calculated in 60 randomly selected lesions. The total plaque volume was calculated as the sum of plaque plus media in each CSA, at 1-mm axial intervals, from the IVUS images of the target lesion.

Evaluation of cardiac biomarkers.   Blood was sampled before the procedure and 18 h after the procedure. Serum TnT was measured with an enzyme immunoassay kit (Roche Diagnostics, Tokyo, Japan), the detection limit of which was 0.03 ng/ml; linearity was achieved between 0.1 and 2 ng/ml. A TnT level of <0.03 ng/ml was considered as 0 ng/ml (negative), and 0.03 to 0.1 ng/ml was considered as 0.1 ng/ml; a TnT level of >2 ng/ml was considered as 2 ng/ml. The PMI was defined as a post-procedural TnT level of ≥0.1 ng/ml on the basis of the manufacturer's statement regarding the clinical cutoff value for TnT. The CK-MB activity was measured using an immunoinhibition assay kit (Sysmex, Kobe, Japan).

Statistics.   All data are expressed as mean ± SD values. A comparison of continuous variables was achieved with an unpaired Student t test or a Mann-Whitney U test, and categorical variables were derived by a chi-square analysis or Fisher exact probability test. We used Bland-Altman and linear regression analyses for comparison of plaque volume measured by MDCT and IVUS. Linear regression analysis was performed to assess the association of quantitative plaque characterization by MDCT with an increase in cardiac biomarkers. To identify predictors of PMI, we performed univariate and multivariate analyses using the logistic regression method. Variables with a significance level of <0.2 in the univariate analysis were considered candidate variables for inclusion in the multivariable analysis. A receiver-operator characteristic curve analysis was performed to examine the possibility of using LAP volume to diagnose patients with post-procedural TnT elevation (≥0.1, ≥0.2, and ≥0.3 ng/ml, respectively). Differences were considered significant at p < 0.05.


    Results
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 Abstract
 Methods
 Results
 Discussion
 Conclusions
 REFERENCES
 
Baseline patient, lesion, and procedural characteristics.   Post-procedural TnT elevation of ≥0.10 ng/ml occurred in 59 (31.2%) patients. The clinical characteristics of the entire study population are listed in Table 1. No significant differences were found between patients with and without PMI. Lesion and procedural characteristics are listed in Table 2. In terms of angiographic measurements, lesion length was significantly greater in patients with positive TnT. No difference was found in terms of IVUS measurements or procedural characteristics.


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Table 1 Baseline Characteristics
 

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Table 2 Lesion and Procedural Characteristics
 
Volumetric plaque measurements using MDCT.   Forty randomly selected lesions were measured by 2 observers. Their measurements showed good correlation vis-à-vis total plaque volume (r2 = 0.76, p < 0.01), LAP volume (r2 = 0.78, p < 0.01), MAP volume (r2 = 0.76, p < 0.01), and HAP volume (r2 = 0.74, p < 0.01). To validate plaque volume measurements by MDCT, we compared plaque volume measurements by MDCT and IVUS on 60 randomly selected lesions (Fig. 2). Plaque volumes measured by MDCT and IVUS showed a significant correlation (r2 = 0.63, p < 0.01). In Bland-Altman plots, mean differences in volume were 3.77 ± 53.5 mm3. The upper and lower limits for plaque volume agreement were between –101.1 mm3 (95% confidence interval [CI]: –124.8 to –108.6) and 108.6 mm3 (95% CI: 84.9 to 132.4).


Figure 2
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Figure 2 Bland-Altman Plot for Total Plaque Volumes of the Target Lesion Measured by MDCT and IVUS

To validate plaque volume measurements by MDCT, a comparison of plaque volume between MDCT and IVUS was carried out on 60 randomly selected lesions. The correlation coefficient for plaque volumes measured by MDCT and IVUS was r2 = 0.63 (p < 0.01). In Bland-Altman plots, the mean differences in volume were 3.77 ± 53.5 mm3. The limits of agreement for plaque volume were between –101.1 mm3 (95% CI: –124.8 to –108.6) and 108.6 mm3 (95% CI: 84.9 to 132.4). CI = confidence interval; IVUS = intravascular ultrasound; MDCT = multidetector computed tomography.

 
Figure 3 shows measurements of each plaque component obtained by MDCT. Total plaque volumes (223.8 ± 165.5 mm3 vs. 150.9 ± 113.3 mm3, p < 0.01), LAP volumes (87.9 ± 94.8 mm3 vs. 47.4 ± 43.7 mm3, p < 0.01), and MAP volumes (111.6 ± 77.5 mm3 vs. 89.8 ± 67.1 mm3, p < 0.05) were significantly larger in patients with PMI; the fractions (i.e., volume of each component/total plaque volume) of LAP (32.9 ± 15.0% vs. 29.0 ± 10.5%, p < 0.05) and HAP (12.9 ± 16.5% vs. 8.4 ± 13.4%, p < 0.05) in plaque were higher in patients with PMI. In contrast, the fraction of MAP in plaque was lower in patients with PMI (54.2 ± 13.9% vs. 62.6 ± 14.0%).


Figure 3
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Figure 3 The Volume and Fraction of Each Plaque Component (LAP, MAP, and HAP) of Target Lesion in Patients With or Without Myocardial Injury

Total plaque (223.8 ± 165.5 mm3 vs. 150.9 ± 113.3 mm3, p < 0.01), LAP (87.9 ± 94.8 mm3 vs. 47.4 ± 43.7 mm3, p < 0.01), and MAP (111.6 ± 77.5 mm3 vs. 89.8 ± 67.1 mm3, p < 0.05) volumes were significantly larger in patients with PMI (A); the fractions of LAP (32.9% vs. 29.0%, p < 0.01) and HAP (12.9% vs. 8.4%, p < 0.05) in plaque were higher in patients with PMI (B). The fraction of MAP was lower in patients with PMI (54.2% vs. 62.6%, p < 0.01). HAP = high-attenuation plaque; LAP = low-attenuation plaque; MAP = moderate-attenuation plaque; PMI = post-procedural myocardial injury/infarction.

 
Post-procedural increase in cardiac biomarkers.   Simple and multiple regression analyses with post-procedural TnT (log transformed) were performed; the results are listed in Table 3. The LAP (Fig. 4A), MAP, and HAP volumes significantly correlated with post-procedural TnT (log transformed) and CK-MB values. However, although the fraction of LAP in plaque correlated positively with TnT and CK-MB (Fig. 4B), that of MAP correlated inversely with each of the 2 biomarkers.


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Table 3 Linear Regression Analysis Between Each Plaque Component and Post-Procedural TnT and CK-MB
 

Figure 4
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Figure 4 Scatter Plots of Post-Procedural TnT and CK-MB Versus Volume or Fraction of LAP

Scatter plots of post-procedural troponin-T (A) and CK-MB (B) versus volume or fraction of LAP. The LAP, MAP, and HAP volumes significantly correlated with post-procedural TnT (log-transformed) and CK-MB. However, although the fraction of LAP in plaque correlated positively with TnT (log-transformed) and CK-MB, that of MAP was found to be inversely correlated with each of the 2 biomarkers. CK = creatine kinase; TnT = troponin-T; other abbreviations as in Figure 3.

 
Multivariable linear regression analysis showed that LAP volume was independently associated with post-procedural TnT (Table 4). We also found that the fraction of LAP in plaque was significantly associated with post-procedural TnT, even after adjusting for significant confounding factors (p < 0.2 in a simple regression analysis).


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Table 4 Simple- and Multiple-Regression Analysis With Periprocedural Troponin-T (Log Transformed)
 
Predictor of PMI.   In this study population, PMI was observed in 59 patients (31.2%). Multivariate logistical regression analysis showed that larger volumes of LAP were independently associated with PMI, even after adjusting for significant confounding factors (Table 5). Although a higher LAP fraction was independently associated with PMI, a lower MAP fraction was associated with PMI. Neither the volume of HAP nor its fraction in plaque was associated with PMI. A receiver-operator characteristic analysis of LAP volume to identify post-procedural TnT elevation (≥0.1 ng/ml, ≥0.2 ng/ml, and ≥0.3 ng/ml) is shown in Table 6.


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Table 5 Multiple Logistic Regression Models for Prediction of PMI
 

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Table 6 Receiver-Operator Characteristic Analysis for the Volume of LAP to Identify Post-Procedural TnT Elevation
 

    Discussion
 Top
 Abstract
 Methods
 Results
 Discussion
 Conclusions
 REFERENCES
 
Volumetric plaque characterization and PMI.   This study showed that LAP and MAP volumes were larger in patients who had incurred myocardial injury after stent implantation. The MAP volume correlated positively and MAP fraction in plaque correlated inversely with biomarkers. On the other hand, both the volume of LAP and its fraction correlated positively with biomarkers. These findings suggest that MAP volume does not essentially contribute to a post-procedural elevation of cardiac biomarkers. Therefore, in multivariate analysis, a larger LAP volume, higher LAP fraction, and lower MAP fraction were each identified as independent predictors of post-procedural cardiac biomarker elevation.

Distal embolism after stent expansion may play an important role in the development of a PMI. Recent studies on distal protection devices confirm mobilization of plaque material after coronary stenting in patients with stable or unstable angina (19). When the stent was expanded in the lesion, the stent strut grated up the plaque and broke up and loosened the microembolic debris, releasing it into the bloodstream (thus demonstrating the so-called cheese-grater effect) (20). Therefore, plaque that contains larger lipid-rich or soft components may be prone to being broken down into larger numbers of atherosclerotic particles after stent expansion. These hypotheses are strongly supported by the following findings: a reduction of plaque volume after stenting is significantly related to a mass of post-procedural myonecrosis being detected by enhanced magnetic resonance imaging (21), and baseline plaque characteristics evaluated by ultrasound radiofrequency data (i.e., virtual histology) are associated with procedure-related distal embolism (22,23).

Quantitative analysis of coronary plaques using MDCT.   In addition to evaluating luminal narrowing, noncalcified coronary atherosclerotic plaque can frequently be visualized by MDCT. Investigations into the quantitative measurements of plaque areas, remodeling index, and plaque volume measurement by MDCT have been reported (14,24,25). On the assumption that lipid-rich plaque has lower CT density than fibrous plaque, investigators have attempted to use measurements with CT attenuation values to differentiate plaque types. A plaque profile as determined by MDCT may represent different stages of atherosclerosis as assessed by histopathological findings (26), gray-scale IVUS (15,17), and virtual histology analysis (27).

There seems to be a large overlap of plaque characteristics between patients with and without PMI. Previous reports comparing IVUS and MDCT show a wide overlap of density values measured within hyperechoic and hypoechoic plaques (28). This finding results from the natural course of atherosclerotic plaque evolution and technical factors that affect density measurements, such as slice width and contrast medium concentration (25,28–30). These findings raise concerns about the accuracy of distinguishing lipid-rich plaque from fibrous plaque and detecting vulnerable plaque solely on the basis of measurements of CT density. However, recent studies have shown that LAP detected by MDCT is associated with acute coronary syndrome (31,32) and a no-reflow phenomenon during elective PCI (33). These reports, as well as the present study, suggest that plaque with a larger LAP volume may be a high-risk finding, even if it does not closely correspond to a lipid-rich or necrotic histological pattern.

Comparative results of plaque volume measured by MDCT and IVUS in our study (r2 = 0.63, p < 0.001) are similar to those reported by Leber et al. (24) (r2 = 0.69, p < 0.001). Because the coronary artery is surrounded by tissue with a density that appears in scans and the resolution of MDCT is relatively low compared with that of IVUS, it is difficult to define its outer edges accurately. However, in the current study, the interobserver agreement of MDCT measurements was relatively good.

Thrombus and noncalcified plaque had similar CT densities, and it was difficult to differentiate between these tissue components by MDCT (31). In this study population, the noncalcified plaque detected by MDCT may contain a certain amount of thrombus, thus it may be difficult to differentiate thrombus from noncalcified plaque, although no emergency PCI for acute coronary syndrome was included in this study.

Study limitations.   We stratified coronary plaque according to a previous report by Komatsu et al. (17), although the MDCT device, contrast medium, and scan protocols used by them were different from those used in this study. In our investigation, plaque stratification was not validated by comparison with other modalities.

We obtained post-procedural blood samples only once, at 18 h after PCI. It may not be practicable for investigators in daily practice to collect multiple blood samples from a patient and at the same time to avoid apparent complications or confounding factors. However, 100% of peak TnT elevations and 92% of the peak CK-MB values were observed within 12 to 20 h (mean 17.9 ± 0.46 h) after the procedure in patients who had undergone elective PCI and had no pre-procedural elevations in cardiac biomarkers (34). Therefore, we evaluated only cardiac biomarkers obtained from single blood samples obtained 18 h after PCI.

A relatively low incidence of statin pre-treatment was observed in this study, although the beneficial effect of statin therapy on patients who have undergone PCI has been established (7,35). A relatively small sample size, single-center analysis, and arbitrary definition of PMI were also limitations of the current study. To avoid such arbitrariness, we performed multivariable analyses using TnT as a continuous variable.


    Conclusions
 Top
 Abstract
 Methods
 Results
 Discussion
 Conclusions
 REFERENCES
 
We have shown a significant correlation between LAP volume within target lesions, as measured by MDCT, and post-procedural elevation of cardiac biomarker levels. The LAP volume was found to be an independent predictor of PMI after elective stenting.

Although successful dilatation of coronary stenosis might improve myocardial perfusion and can be expected to reduce cardiovascular events, other benefits of PCI to stable patients with optimal medical therapy are controversial (36). The procedure-related myocardial infarction is a major roadblock to improving clinical outcomes in patients who undergo PCI. Plaque evaluation by MDCT may provide useful information to identify high-risk patients who are expected to have a better outcome with aggressive medical treatment or bypass surgery. Evaluation of coronary plaque by MDCT involves significantly greater exposure to radiation as well as to the contrast medium. Therefore, further evaluation of the clinical benefits of this technique is required.


    Acknowledgments
 
The authors thank Ms. Shiho Okamoto, Mr. Hiromitsu Ukai, Mr. Mitsutomo Arakawa, Mr. Hideki Shibayama, Mr. Kenichi Yoshida, and Mr. Tetsuo Nakai for their technical support in CT scanning and image reconstruction.

* Reprint requests and correspondence: Dr. Tadayuki Uetani, Department of Cardiology, Chubu Rosai Hospital, 1-10-6, Komei, Minato-ku, Nagoya, Japan (Email: london.electricity{at}gmail.com).

Manuscript received April 1, 2009; revised manuscript received August 28, 2009, accepted September 8, 2009.


    REFERENCES
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 Abstract
 Methods
 Results
 Discussion
 Conclusions
 REFERENCES
 

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