Rationale and Objectives
To quantitatively assess coronary atherosclerotic plaque composition in patients with acute non–ST elevation myocardial infarction (NSTEMI) and patients with stable coronary artery disease (CAD) by coronary computed tomography angiography (cCTA) correlated with virtual histology intravascular ultrasound (VH-IVUS).
Materials and Methods
Sixty patients (35 with NSTEMI) were included. Corresponding plaques were assessed by dual-source cCTA and VH-IVUS regarding volumes and percentages of fatty, fibrous, and calcified component; overall plaque burden; and maximal percent area stenosis. Possible differences between patient groups were investigated. Concordance between cCTA and VH-IVUS measurements was validated by Bland–Altman analysis.
Results
Forty corresponding plaques (22 of patients with NSTEMI) were finally analyzed by cCTA and VH-IVUS. cCTA plaque analysis revealed no significant differences between plaques of patients with NSTEMI and stable CAD regarding absolute and relative amounts of any plaque component (fatty: 20 mm³/13% versus 17 mm³/14%; fibrous: 81 mm³/63% versus 80 mm³/53%; calcified: 16 mm³/14% versus 26 mm³/26%; all P > .05) or overall plaque burden (153 mm³ versus 165 mm³; P > .05), nor did VH-IVUS plaque analysis. VH-IVUS measured a higher area stenosis in patients with NSTEMI compared to patients with stable CAD (76% versus 68%, P = .01; in cCTA 69% versus 65%, P = .2). Volumes of fatty component were measured systematically lower in cCTA, whereas calcified and fibrous volumes were higher. No significant bias was observed comparing volumes of overall noncalcified component and overall plaque burden.
Conclusion
Plaques of patients with acute NSTEMI and of patients with stable CAD cannot be differentiated by quantification of plaque components. cCTA and VH-IVUS differ in plaque component analysis.
Coronary CT angiography (cCTA) has been proved to reliably exclude presence of coronary artery disease (CAD) and is increasingly used to assess CAD and further characterize atherosclerotic lesions as well . Histopathology studies have assessed characteristics of stable and instable plaques . The likeliness of a plaque to rupture—its vulnerability—and to subsequently cause vessel obstruction and myocardial infarction is known to be largely dependent on its composition, and strong efforts are made to reliably risk-stratify plaques and patients. The invasive reference standard for plaque composition imaging is intravascular ultrasound (IVUS) . The search for accurate noninvasive plaque imaging modalities is ongoing. With further improvement of temporal and spatial resolution, cCTA continues to emerge as a promising technique in the quest for a noninvasive plaque imaging reference standard .
Plaque analysis with cCTA was previously evaluated in mostly select plaque and patient samples concerning, for example, proximal lesion localization, nonobstructive CAD, absence of arrhythmias, or low Agatston score with the goal of achieving optimal CT image quality . The parameters most frequently studied were stenosis grading, overall plaque burden, and classification into calcified and noncalcified plaques and plaque components. Data about the performance of cCTA with regard to further differentiation and quantification of plaque components in correlation to virtual histology IVUS (VH-IVUS) are limited. To our knowledge, Brodoefel et al were the first to differentiate and quantitatively assess fatty, fibrous, and calcified components using dual-source CT in plaques of patients with stable CAD .
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Materials and methods
Ethics Statement
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Study Population
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cCTA
Image acquisition
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cCTA image reconstruction
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CT plaque analysis
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ICA and IVUS
Image acquisition
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VH-IVUS image reconstruction and plaque analysis
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Statistical Analysis
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Results
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Table 1
Patient Characteristics
Patient Group_P_ Value NSTEMI Stable CAD Total No. 15 13 Men/women 13/2 10/3 .64 Age (yr) 72.6 ± 8.9 71.4 ± 8.3 .71 Cardiovascular risk factors Hypertension 13/15 (87%) 9/13 (69%) 1.00 Dyslipidemia 8/15 (53%) 11/13 (85%) .38 Diabetes mellitus 3/15 (20%) 1/13 (8%) .63 Smoking history 7/15 (47%) 3/13 (23%) .68 BMI (kg/m²) 26.3 ± 3.8 30.0 ± 4.1 .04 ∗ Laboratory findings Triglycerides (mg/dL) 118.0 ± 40.2 116.0 ± 52.7 .91 Total cholesterol (mg/dL) 176.1 ± 37.9 156.6 ± 26.2 .13 LDL (mg/dL) 111.1 ± 37.0 98.6 ± 22.1 .30 HDL (mg/dL) 47.7 ± 17.4 42.1 ± 11.2 .32 CRP (mg/L) 4.4 (2.9–14.6) 2.9 (2.9–5.7) .20 Agatston score 252 (78–878.4) 507.3 (237.4–918.0) .70
BMI, body mass index; CRP, C-reactive protein; HDL, high-density lipoprotein; LDL, low-density lipoprotein; NSTEMI, non–ST elevation myocardial infarction; CAD, coronary artery disease. Values are expressed as counts (percentages), median (25th to 75th percentile), or mean ± standard deviation. Statistical independence of the groups is expressed by P value on the basis of Fisher exact test statistics for categorical variables, Wilcoxon rank sum test for non-normally distributed data, or Student t test for normally distributed data.
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Table 2
Plaque Localization
Localization in Coronary Tree AHA Segments Patients with NSTEMI Patients with Stable CAD Counts Percentage (%) Distal 3, 4, 8, 10, 14, 15 7 2 9 22.5 Mid 2, 7, 9, 12, 13 (16) ∗ 10 8 18 45.0 Proximal 1, 5, 6, 11 5 8 13 32.5 Sum 22 18 40 100.0
AHA, American Heart Association; CAD, coronary artery disease; NSTEMI, non–ST elevation myocardial infarction. Segmentation of coronary tree is based on the 1976 AHA 15-segment model by .
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Table 3
Comparison of Plaques of the Two Patient Groups with cCTA and VH-IVUS
cCTA VH-IVUS NSTEMI Stable CAD_P_ Value NSTEMI Stable CAD_P_ Value Area stenosis (%) 68.9 ± 10.6 64.6 ± 10.1 .20 76.2 ± 8.7 68.3 ± 8.2 ∗ Overall plaque burden (mm³) 141.5 (89.6–210.8) 150.8 (98.3–253.6) .65 121.3 (90.3–239.1) 89.9 (61.7–154) .08 Noncalcified plaque component (%) 85.9 (68.5–94.9) 73.8 (48.7–87.8) .21 87.7 (83.9–95.5) 86.4 (80.0–89.6) .28 Fatty plaque component (%) 12.9 (7.5–28.3) 13.6 (6.8–30.2) .89 35.7 (33.6–39.0) 35.4 (33.2–38.5) .68 Fibrous plaque component (%) 67.1 (41.3–77.2) 55.9 (34.1–72.0) .14 51.2 (44.6–60.9) 49.3 (41.8–58.7) .42 Calcified plaque component (%) 14.1 (5.1–31.5) 26.2 (12.2–51.3) .21 12.3 (4.5–16.1) 13.6 (10.4–20.0) .28 Noncalcified plaque component (mm³) 110.9 (61.9–157.9) 96.5 (46.0–142.3) .87 70.6 (51.6–149.3) 52.7 (28.0–82.1) .08 Fatty plaque component (mm³) 19.4 (11.1–29.2) 16.5 (5.0–33.2) .86 25.9 (20.8–57.7) 21.8 (10.1–35.9) .10 Fibrous plaque component (mm³) 81.0 (51.1–116.2) 80.2 (36.5–119.9) .67 45.1 (27.3–91.4) 31.3 (16.6–43.8) .07 Calcified plaque component (mm³) 16.3 (9.2–40.9) 26.3 (5.3–97.4) .44 9.6 (4.9–13.8) 8.5 (3.3–15.0) .76
CAD, coronary artery disease; cCTA, coronary computed tomography angiography; NSTEMI, non–ST elevation myocardial infarction; VH-IVUS, virtual histology intravascular ultrasound.
For intermodality correlation of fatty component, VH-IVUS necrotic core and VH-IVUS fatty-fibrous tissue are summed. Noncalcified plaque component = fatty component plus fibrous component. Values are expressed as median (25th to 75th percentile) or mean ± standard deviation. Differences between the patient groups are expressed by P value on the basis of Wilcoxon rank sum test for non-normally distributed data or Student t test for normally distributed data.
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Table 4
Intermodality Correlation of Quantitative Plaque Analysis Assessed with cCTA and VH-IVUS
cCTA VH-IVUS Correlation Bias Overall plaque burden (mm³) 141.5 (91.9–220.5) 113.7 (73.2–192.4) 0.11; P = .49 13.8; −26.2 to 53.8; P = .31 Area stenosis (%) 67.0 ± 10.5 72.7 ± 9.2 0.63; P < .0001 ∗ −5.7; −8.4 to −3.0; P = .0001 ∗ Fibrous plaque component (mm³) 80.2 (48.0–117.5) 36.0 (21.2–65.2) 0.20; P = .21 33.9; 8.9 to 58.9; P = .004 ∗ Fatty plaque component (mm³) 17.5 (7.5–30.6) 25.1 (19.4–46.5) 0.12; P = .45 −14.6; −24.5 to −4.8; P = .008 ∗ Noncalcified plaque component (mm³) 98.0 (59.2–148.3) 66.1 (39.7–103.9) 0.23; P = .16 19.2; −13.0 to 51.5; P = .08 Calcified plaque component (mm³) 17.7 (8.5–59.0) 9.4 (4.5–14.5) 0.18; P = .27 29.5; 13.6 to 45.4; P < .0001 ∗ Fibrous plaque component (%) 62.5 (39.2–73.8) 43.8 (49.7–60.3) 0.38; P = .02 ∗ 7.0; 13.0 to 1.1; P = .06 Fatty plaque component (%) 13.4 (7.6–29.1) 35.6 (33.6–38.5) −0.35; P = .03 ∗ −18.8; −23.0 to −14.5; P < .0001 ∗ Noncalcified plaque component (%) 79.1 (61.9–93.6) 87.4 (83.5–94.2) 0.39; P = .01 ∗ −11.7; −18.1 to −5.3; P = .0008 ∗ Calcified plaque component (%) 20.9 (6.4–38.1) 12.6 (5.8–16.5) 0.39; P = .01 ∗ 11.7; 5.3 to 18.1; P = .0008 ∗
CAD, coronary artery disease; VH-IVUS, virtual histology intravascular ultrasound.
For intermodality correlation of fatty component, VH-IVUS necrotic core and VH-IVUS fatty-fibrous tissue are summed. Noncalcified plaque component = fatty component plus fibrous component. Values are expressed as median (25th to 75th percentile) or mean ± standard deviation. Correlation between cCTA and VH-IVUS measurements is expressed by Spearman’s rho or by Pearson correlation coefficient r according to the normal or non-normal distribution of the data and P value. Bland–Altman bias analysis to determine possible systematic differences between VH-IVUS and cCTA measurements is expressed by mean difference, confidence interval values, and P value.
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Discussion
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Conclusion
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Appendix
Supplementary material
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Supplementary Information
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