B. CORRELATION BETWEENHS-CRP AND PLAQUE COMPONENTS
V. CONCLUSION
The hs-CRP is an inflammatory marker in the atherosclerosis and is closely related to DC and FF of a 3-vessel VH-IVUS study. This biomarker reflect the burden of plaque and the maturing of atherosclerosis, and not plaque vulnerability. Elevated hs-CRP to predict cardiovascular events can indicate atherosclerosis severity of whole coronary tree but not current plaquevulnerability.
19
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가상조직-혈관내초음파는죽상반의 성분을 fibrous, fibrofatty, necrotic core, dense calicum 으로 4 개의 색을 통해 구별하였고, 죽상반의 양적 분석 결과 및
24
상관관계를 보였다. 그러나 necrotic core 의 각종 양적 수치들과 VH-TCFA 와는 유의한 상관관계를 보이지 못했다. 다변량 분석결과 dense calcium 의 양적 지수가 hs-CPR 를 가장 잘 예측하는 인자로 분석되었다.
(β=3.646, CI=2.036 to 5.255, p<0.001)
결론:이상의 결과를 통해 혈중 hs-CRP 수치는 죽상반의 취약성보다는 동맥경화증의 양적 및 질적 정도와 연관성이 있음을 알 수 있었다. 이를 통해 혈중 hs-CRP 수치를 통해 심혈관 질환의 예후를 예상할 수 있을 것으로 생각된다.
핵심어: high sensitive C-reactive protein, hs-CRP, 관상동맥경화증, 혈관내 초음파, 죽상반 취약성
hs-CRP level represents
the disease burden and the age but not vulnerability of
coronary atherosclerosis
by
Se Jun Park
Major in Medicine
Department of Medical Science
The Graduate School, Ajou University
hs-CRP level representsthe disease burden and the age but not vulnerability of coronary atherosclerosis
: a study of volumetric plaque composition by 3-vessel virtual histology-intravascular ultrasound
by
Se Jun Park
A Dissertation Submitted to The Graduate School of Ajou University in Partial fulfillment of The Requirements for
The Degree of Master of Medicine
Supervised by
SeungJeaTahk, M.D., Ph.D.
Major in Medicine
Department of Medical Science The Graduate School, Ajou University
August, 2013
This certifies that the dissertation of Se Jun Park is approved .
SUPERVISORY COMMITTEE
Seung Jea Tahk Seung Jea Tahk
Joon Han Shin Joon Han Shin
So Yeon Choi So Yeon Choi The Graduate School, Ajou University
June 21st, 2013
i -ABSTRACT -
hs-CRP level represents the disease burden and the age but not vulnerability of coronary atherosclerosis : a study of volumetric plaque composition by 3-vessel virtual histology-intravascular
ultrasound
Background:hs-CRP (high sensitive C-reactive protein) has been known as a systemic inflammatory marker of atherosclerosis and considered as one of the predictors of future cardiac events. Some reports presented hs-CRP level was associated with plaque
vulnerability but most studies were performed by assessing focal target plaque but not whole plaques from a coronary tree.
Methods: To evaluate of the relationship of plasma hs-CRP level and volumetric plaque composition of the coronary arterial tree, we performed ‘whole vessel” virtual histology-intravascular ultrasound (VH-IVUS) in 189 vessels of 63 patients. The
components of atherosclerosis were classified as fibrous (FI), fibrous-fatty (FF), necrotic core (NC) and dense calcium (DC). Quantitative assessment of these plaque components and the presence of VH-IVUS–derived thin-cap fibroatheroma (VH-TCFA) in the coronary arterial trees were compared to hs-CRP levels in individuals. hs-CRP levels were measured before coronary angiogram and IVUS study.
Results: Forty-nine patients (77.8%) were diagnosed with acute coronary syndrome in this population. The mean values of hs-CRP were 0.24±0.52 mg/dl (0~3.27mg/dl). The analyzed vessel length was 56.1±17.4 mm for the left anterior descending coronary artery, 51.9±19.0 mm for the left circumflex coronary artery, and 74.2±18.8 mm for the right coronary artery. The number of VH-TCFAs was 1.0±0.8 for the left anterior descending, 0.6±0.7 for the left circumflex, and 0.8±1.0 for the right coronary arteries.
The hs-CRP levels were positively correlated to mean plaque burden, total plaque
ii
volume index, volume index of FF and DC. But parameters of NC and the number of VH-TCFA were not related with hs-CRP level. In multivariate analysis, the volume index of DC was most reliable factor to hs-CRP (β=3.646, CI=2.036 to 5.255, p<0.001)
Conclusions: This three-vessel VH-IVUS presented that hs-CRP were related to the total atherosclerotic burden and the maturing (coronary calcium) but not vulnerable features (NC or VH-TCFA) of plaques in coronary arterial tree. Increased hs-CRP level as a biomarker to predict cardiovascular events might imply atherosclerosis severity of whole coronary tree but not current plaque vulnerability.
Keyword: high sensitive C-reactive protein, hs-CRP, coronary atherosclerosis, virtual histology, intravascular ultrasound, vulnerable plaque, vulnerability
iii
TABLE OF CONTENTS
ABSTRACT ··· i TABLE OF CONTENTS ··· iii LIST OF FIGURES ···iv LIST OF TABLES···vi INTRODUCTION ··· 1 II. MATERIAL AND METHODS ··· 2 A. PATIENTS··· 2 B. LABORATORY ASSESSMENT··· 2 C. IVUS IMAGING AND ANALYSIS··· 2 D. STATISTICAL ANALYSIS··· 3 III. RESULTS··· 4 A. BASELINE CLINCAL AND VH-IVUS DATA···4 B. CORRELATION BETWEENHS-CRP AND PLAQUE COMPONENTS··· 9 IV. DISCUSSION··· 15 V. CONCLUSION··· 18 REFERENCES···19 국문요약··· 23
iv
LIST OF FIGURE
Fig 1. The correlation of hs-CRP with mean plaque burden and plaque volume index
··· 10
Fig 2. The correlation of hs-CRP with mean burdens of each plaque
components.··· 11
Fig 3.The correlation of hs-CRP with volume indices of each plaque components.
··· 12
Fig 4. The correlation of hs-CRP with the number of VH-TCFA
··· 13
v
LIST OF TABLES
Table 1. Baseline clinical data··· 5
Table 2. Baseline lesion characteristics in the VH-IVUS analysis··· 6
Table 3. Volumetric data of VH-IVUS according to interquartile range of
hs-CRP··· 8
Table 4. Multivariate analysis for predictors of hs-CRP··· 14
1
I. INTRODUCTION
Coronary artery disease has have high mortality and incidence, although the technology of the medicine has been developed. The atherosclerosis is most important cause for coronary artery disease, so it’s important to know the pathogenesis of that. It has known the fate of atherosclerosis is related to the characteristic and composition of the plaque according to autopsy data(David MJ, 1993).The concept of ‘Vulnerable plaque’originated from aforementioned cause, composed of large lipd core, thin fibrous cap, positive remodeling, abundant inflammatory cells and scant smooth muscle cells(Yamagishi et al., 2000). The inflammatory reaction is also key factors in determining plaque vulnerability. Inflammatory cell is considered to have a role in the loss of fibrous cap, that is related to plaque rupture and thrombosis (Shah, 2009).
During the past decade, there were remarkable developments of the evaluation for intra-coronary imaging in ex-vivo. The gray scaled intravascular ultrasound (IVUS) can show the anatomical characteristics of the plaque. But there are some limitations of IVUS in detecting vulnerable plaque and one of those is not to distinguish the elements of plaque composition exactly. The virtual histology-intravascular ultrasound (VH-IVUS)come over this one;
description of the composition of the plaque as 4 color codes (Rodriguez-Granillo et al., 2005).
It is known the inflammatory reaction and the vulnerable plaque are intercorrelated by some VH studies, but that were set limits to culprit lesion, not whole coronary trees (Otake et al., 2008; Ko et al., 2012). Therefore, the purpose of this study was to find out the relationship between the plaque vulnerability and inflammation by the analaysis of 3-vessel VH-IVUS and inflammatory biomarker; high-sensitive C-reactive protein (hs-CRP).
2
II. Material and Method
A. Patients
A total of 63 patients diagnosed with ischemic heart disease (history of angina and ≥ 30%
luminal narrowing on coronary angiogram by visual estimation) were enrolled into this study from September 2006 and August 2008, at a single medical center. They were performed preinterventional 3-vessel VH-IVUS. Patients with any totally occlusive vessel, severely tortuous vessel, extensively calcified lesions, severe left main coronary artery disease (diameter stenosis ≥ 50%), and hemodynamic instability were excluded. Written informed consent was obtained from all patients.
B. Laboratory assessment
Blood samples were obtained within 24 hours before coronary angiography and VH-IVUS, and then were centrifuged immediately, aliquoted and stored at -80℃ for subsequent analysis. Serum hs-CRP was measured by a latex-enhanced turbidmetry immunoassay, using a chemistry autoanalyzer (TBA 200FR, TOSHIBA Co., Tokyo, Japan).
C. IVUS imaging and analysis
VH-IVUS studies were implemented with a phased-array, 20-MHz, 2.9-F IVUS catheter (Eagle eye, Volcano Corporation, Racho Cordova, California). After intracoronary
administration of nitroglycerin (100~200 µg), the transducer was introduced as far distal as possible into each major epicardial artery, paying particular attention to identify any evident atherosclerosis. Using motorized pullback (0.5 mm/s), imaging was performed back to aorto-ostial junction. While on pulling back, the gray-scale IVUS was recorded; and the raw radiofrequency data were captured at the top of the R waves for the reconstruction of color-coded map by VH data recorder (Volcano Corporation).
An experienced analystwho was unaware of the patient’s clinical data, measured the parameters of the lumen and the media-adventitia interface by manual contour tracing.
Volumetric VH-IVUS analysis was done from the most distal part where VH-IVUS plaque components were detected to the respective ostium, and volumetric data were generated with
3
using pcVH software (version 2.1, Volcano Corporation). Total plaque volume was obtained by analyzing 3 vessels in each patient (including all lesions and reference segments), and a volumetric index was calculated as total plaque volume divided by total vessel length. Mean plaque plus media (P+M) burden was calculated as the total plaque volume divided by total vessel volume Ｘ100. VH-IVUS analysis was described as 4 different color-coded tissue;
green (fibous, FI), yellow-green (fibro-fatty, FF), red (necrotic core, NC), and white (dense calcium, DC). Each plaque component was measured in every recorded frame and expressed as the volume index (absolute measure) and percentages of total plaque volume.Virtual histology–intravascular ultrasound–derived thin-cap fibroatheroma (VH-TCFA) was defined as a lesion that fulfilledthe following criteria in at least 3 consecutive frames: 1) NCs ≥ 10%
directly attaching to the lumen; and 2) ≥ 40%P+M burden (Rodriguez-Granillo et al., 2005).
Identifying 2 separate lesions in the sameartery required a ≥ 5-mm reference segment
between them.If there was a <5-mm reference segment, they wereconsidered part of one long lesion(Garcia-Garcia et al., 2009). Similarly, identifying 2 separate VH-TCFAs required a non–VH-TCFA–containing reference segment ≥ 5 mm between them. Two experienced observers who were unaware of the patients’ clinical histories evaluated the VH-TCFA in consensus.
D.Statistical analysis
All analyses were performed using SPSS version 18.0 statistical software (SPSS Inc, Chicago, IL, USA). Categorical variables were expressed as numbers or frequencies of occurrence with comparisons using chi-square statistics or Fisher exact probability test. All continuous variables were tested by Kolmogorov-Smirnov Z test for normality analysis.
Continuous data were reported as mean ± SD with comparisons using unpaired Student ttest and Pearson’s correlation analysis. If normality tests failed, the continuous values were presented as median and interquartile range and were compared by Mann-Whitney U test and Kruskal-Wallis test. Multiple linear regression analysis was performed to assess independent predictors for hs-CRP. A p value < 0.05 was considered statistically significant in this study.
4
III. Results
A. Baseline clinical and VH-IVUS data
It was shown baseline clinical characteristics on Table 1.Patients had a mean age of 59 years; 31.7% of them were ≥ 65 years of age; 65.1% were men. The study cases were composed of diabetes mellitus (DM, 27.0%), hypertension (58.7%), smoking (44.4%), dyslipidemia (20.6%) and familyhistory of premature coronary artery disease(7.9%). Clinical presentation in patients were consisted of stable angina (22.2%), unstable angina (54.0%) and acute myocardial infarction (11.1%; 3 cases: ST segment elevation myocardial
infarction, 4 cases: Non-ST segement elevation myocardial infarction).The level of hs-CRP was not different among groups seperated by clinical presentation. The value of hs-CRP was 0.24 ± 0.52 mg/dl (range: 0~3.72 mg/dl).The number of diseased vessel defined ≥ 60% of plaque burden by IVUS was 94 of whole coronary tree; left anterior descending coronary artery (LAD): 40(42.6%), left cicumflex coronary artery (LCX): 29(30.9%), right coronary artery (RCA): 25(26.6%). The analyzed vessel length was 56.1 ± 17.4 mm of LAD, 51.9 ± 19.0 mm of LCX, and 7.42 ± 18.8 mm for RCA. The number of VH-TCFA was 1.0 ± 0.8 for the left anterior descending, 0.6 ± 0.7 for the left circumflex and 0.8 ± 1.0 for the right coronary arteries (Table 2). The volume data of the total plaque was 596.7 ± 421.7 mm3; 361.8 ± 323.4 mm3 of FI, 76.0 ± 71.0 mm3 of FF, 80.3 ± 76.0 mm3 of NC and 51.6 ± 67.7 mm3 of DC. The volume index of total plaque was 3.0 ± 2.0 mm3/mm; 1.9 ± 1.6 mm3/mm of FI, 0.4 ± 0.4 mm3/mm of FF, 0.4 ± 0.3 mm3/mm of NC and 0.3 ± 0.3 mm3/mm of DC.
However volume indices of plaque components in three coronary arteries did not demonstrate any distinctive findings except for that of NC (p=0.031).
5 Table 1. Baseline clinical data (n=63)
Age (yrs) 59.6 ± 9.0
≥ 65 yrs of age 21 (31.7%)
Men 41 (65.1%)
DM 17 (27.0%)
Hypertension 37 (58.7%)
Dyslipidemia 13 (20.6%)
Smoking 28 (44.4%)
Family history of premature coronary artery disease 5 (7.9%)
SBP / DBP (mmHg) 137.4 ± 17.2/ 82.9 ± 11.7
hs-CRP (mg/dl) 0.24 ± 0.52 [range: 0~3.72]
Lipid profile (mg/dl)
Total cholesterol 167.0 ± 36.0
Triglyceride 145.6 ± 102.2
LDL 95.8 ± 33.4
HDL 44.0 ± 9.4
Values are mean ± SD or n (%)
DM, diabetes mellitus; SBP, systolic blood pressure; DBP, diastolic blood pressure; hs-CRP, high sensitive C reactive protein; LDL, low density lipoprotein; HDL, high density lipoprotein
6
Table 2. Baseline lesion characteristics in the VH-IVUS analysis (n=63)
Total length of the analyzed vessel per patient (mm) 182.6 ± 45.4
LAD 56.1 ± 17.4
LCX 51.9 ± 19.0
RCA 74.2 ± 18.8
VH-TCFA (n)
Total number per patient 2.5 ± 1.9
LAD 1.0 ± 0.8
LCX 0.6 ± 0.7
RCA 0.8 ± 1.0
Values are mean ± SD
LAD, Left anterior descending artery; LCX, Left circumflex artery; RCA, Right coronary artery; VH-TCFA, virtual histology-thin cap fibroatheroma
7
Patients were divided to 4 groups by the quartile value of hs-CRP; first quartile group: 0 ~ 0.05 mg/dl, second quartile group: 0.05 ~ 0.12 mg/dl, third quartile group: 0.12 ~ 0.22 mg/dl and fourth quartile group: ≥ 0.22 mg/dl. The base data were described in Table 3. Except for the volume and volume index of DC, there were no significant difference of volumetric data among quartile groups.
8
Table 3. Volumetric data of VH-IVUS according tointerquartile range of hs-CRP
First quartile
Plaque volume 560.97±495.90 536.92±319.25 676.06±465.80 507.53±349.55 0.648
FI 393.85±467.61 340.02±205.19 399.42±244.32 293.86±195.92 0.686
FF 79±56.84 69.85±86.55 63.94±39.91 88.58±99.55 0.701
NC 59.12±62.21 79±39.22 128.73±120.0 65.87±43.95 0.096
DC 28.56±34.18 47.37±26.79 83.96±101.01 59.22±83.65 0.038*
Volume Indices, mm3/mm
Plaque volume index 3.11±2.57 2.86±1.34 3.33±1.74 2.83±1.68 0.808
FI volume index 2.17±2.44 1.81±0.89 1.99±0.91 1.65±0.92 0.850
FF volume index 0.46±0.33 0.35±0.34 0.35±0.05 0.50±0.52 0.626
NCvolume index 0.32±0.32 0.44±0.04 0.61±0.48 0.37±0.19 0.072
DC volume index 0.15±0.18 0.27±0.16 0.39±0.40 0.32±0.46 0.020*
Mean Percentages of Plaque Burden and VH-IVUS Components
Mean% plaque burden (%) 19.46±12.36 18.60±6.05 21.14±9.34 19.53±9.11 0.812
Mean %FI (%) 65.33±5.90 62.37±7.50 60.46±8.80 61.49±6.67 0.269
Values were mean±SD. p<0.05 were expressed as ‘*’
The quartile group were divided by hs-CRP; First quartile < 0.05 mg/dl, 0.05 mg/dl ≤Second quartile < 0.12 mg/dl, 0.12 mg/dl
≤ Third quartile < 0.22 mg/dl, Fourth quartile ≥ 0.22 mg/dl
FI, fibrous; FF, fibro-fatty; NC, necrotic core; DC, dense calcium, Mean%, mean percentage of burden
9
B.Corrleation between hs-CRP and plaque components
B.Corrleation between hs-CRP and plaque components