Advances in invasive evaluation and treatment of patients with ischemic heart disease

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Advances in invasive evaluation and treatment of patients with ischemic heart disease

Hoeven, B.L. van der

Citation

Hoeven, B. L. van der. (2008, May 8). Advances in invasive evaluation and treatment of patients with ischemic heart disease. Retrieved from https://hdl.handle.net/1887/12862

Version: Corrected Publisher’s Version

License: Licence agreement concerning inclusion of doctoral thesis in the Institutional Repository of the University of Leiden

Downloaded from: https://hdl.handle.net/1887/12862

Note: To cite this publication please use the final published version (if applicable).

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Abstract

Aims

Thin cap fibroatheroma’s (TCFA’s) are considered to be the precursors of plaque rupture and secondary intracoronary thrombosis. Virtual histology intravascular ultrasound imaging (IVUS-VH) enables classification of coronary tissue in vivo. This study sought to determine the IVUS-derived TCFA (IDTCFA) characteristics of culprit lesions in ST-segment elevation myocardial infarction (STEMI) patients.

Methods and results

41 STEMI patients referred for primary Percutaneous Coronary Intervention were studied.

IDTCFA was defined as a lesion fulfilling the following criteria: 1). >40% plaque burden; 2).

necrotic core ≥0.5mm in length occupying >10% of the plaque area; 3). no fibrous tissue above the necrotic core and; 4). remodeling index >1.05. Lesion length was 13.7±6.9mm, maximum plaque burden was 68.8±7.6% and the remodeling index was 1.28±0.28. Positive remodeling was present in 81%; 98% of the lesions showed >40% plaque burden and 95% of the lesions showed a necrotic core, with a necrotic core length of 5.2±4.9mm and maximum percentage necrotic core area of 25.9±11.3%. A necrotic core without overlying fibrous tissue was present in 94%. Of the lesions, 68% fulfilled all IDTCFA criteria.

Conclusion

In conclusion, approximately 70% of culprit lesions in STEMI patients can be described as IDTCFA’s with necrotic core characteristics corresponding to histopathological findings.

Insight in the natural history of IDTCFA’s is needed to determine the clinical implication of these findings.

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Lesions causing ST-segment

elevation myocardial infarction can be characterized by radiofrequency data analysis intravascular

ultrasound as thin cap fibroatheroma

Bas L. van der Hoeven, MD*, Su-San Liem, MD*, J.

Wouter Jukema, MD*, Jouke Dijkstra, PhD^†, Hein Putter, PhD^‡, Douwe E. Atsma, MD*, Katja Zeppenfeld, MD*, Marianne Bootsma, MD*, Martin J. Schalij, MD*

* Department of Cardiology

† Department of Medical Statistics and Bio-Informatics

‡ Department of Radiology, Division of Image Processing Leiden University Medical Center, Leiden, The Netherlands

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Introduction

Acute myocardial infarction is an important cause of morbidity and mortality in the Western world. In the majority of patients, myocardial infarction is caused by intracoronary thrombosis formed on top of a ruptured atherosclerotic plaque(¹). The typical plaque characteristics of these lesions can be described as thin cap fibroatheroma (TCFA’s). TCFA’s have a significant necrotic core and a thin overlying fibrous cap with infiltration of inflammatory cells. TCFA’s are usually located at sites with significant plaque burden and positive remodeling [1,2].

It is not uncommon that within the coronary tree of patients presenting with an acute myocardial infarction, multiple TCFA’s can be identified [1]. Although pharmacological intervention studies demonstrated that treatment of acute myocardial infarction patients, especially with anti-thrombotic and lipid lowering drugs lowers the risk of a second event, these patients are still at risk of plaque progression and recurrent events during the first 12 months after the index event [3,4]. It is currently unknown whether plaque progression and clinical events are related to TCFA instability. As TCFA’s may cause recurrent ischemic events it is of clinical relevance to study the natural course of TCFA’s. However, so far no reliable in vivo technique was available to identify and follow TCFA’s over time.

Recently, a new technique, virtual histology intravascular ultrasound imaging (IVUS-VH), was introduced, which allows determination of plaque characteristics in vivo [5]. IVUS-VH uses radiofrequency backscatter signals to reconstruct intracoronary tissue into four different tissue types: fibrous, fibrofatty, dense calcium and necrotic [6]. IVUS-VH was validated by comparing post-mortem IVUS-VH tissue maps with histological findings [7].

Using this technique enables identification and quantification of IVUS-derived TCFA’s (IDTCFA’s) along the coronary tree. Recently, it was demonstrated that IDTCFA’s are mainly present within the proximal coronary artery segments [8]. Since these proximal segments are also known predilection sites causing ischemic events, it is tempting to speculate about the relationship between the occurrence of ischemic events and IDTCFA’s [9]. Currently, studies are ongoing to determine the natural history of IDTCFA’s in patients presenting with acute coronary syndromes.

To study the potential benefit of IVUS-VH imaging in the identification of ST-segment elevation myocardial infarction (STEMI) lesions IVUS-VH imaging was performed of culprit lesions in patients presenting with a STEMI.

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Methods

Study population

IVUS-VH imaging of the culprit lesion was performed in 41 out of 135 consecutive patients presenting with a STEMI, referred for primary Percutaneous Coronary Intervention. The protocol was approved by the institutional Ethical Review Board. All patients gave written informed consent before start of the procedure. Patients were eligible if they had a STEMI within 9 hours after the onset of symptoms. Patients with previous myocardial infarction, Coronary Artery Bypass Grafting or Percutaneous Coronary Intervention were excluded.

Patients had to be hemodynamically stable (systolic blood pressure >100mmHg without inotropic support) and the estimated risk of IVUS imaging had to be low as determined by the operator. Before start of the procedure, all patients received a 300mg loading dose of aspirin and 600mg of clopidogrel. Moreover, all patients received an intravenous bolus of abciximab (0.25μg/kg) before the procedure, followed by abciximab infusion of 0.125μg/kg with a maximum of 10μg/min for 6 hours. At start of the procedure, patients received 5000U of heparin. Identification of the culprit lesion was based on a combination of ECG characteristics and angiographic findings.

IVUS imaging

IVUS-VH imaging was performed using a 2.9F 20MHz catheter and a dedicated IVUS-VH console (Eagle Eye, Volcano Corp. Rancho Cordova; California; USA). The ultrasound transducer was advanced beyond the culprit lesion under fluoroscopic guidance, immediately after crossing the stenosis with a guide wire, but before balloon inflation. A motorized pullback at 0.5mm/s was performed starting at least 15mm distal to the culprit lesion up to the coronary ostium after administration of intracoronary nitroglycerin (0.3mg). Sampling of the images was gated to peak R-wave during continuous ECG registration. Data were stored digitally on CD for off-line analysis.

IVUS analysis

Analysis was performed offline by experienced analysts, using customized software (IVUS- lab 4.4, Volcano Corp. Rancho Cordova; California; USA and QCU-CMS 4.14, Medis, Leiden, The Netherlands). The lumen border and external elastic membrane (EEM) were detected on all individual frames. Intra-luminal thrombus was excluded from the plaque and media area. Thrombus was differentiated from the plaque by careful identification of continuing morphological characteristics of the lesion in the different frames, starting from distal and proximal of the lesion (clear sites) and finishing at the site of thrombus. We used the true grayscale IVUS images (non-ECG-gated, frame acquisition rate 10 frames/second) to support the contour detection in the gray scale images accompanying the IVUS-VH color- coded images. The luminal border was drawn after consensus of at least two analysts. For Lesions causing STEMI can be characterized by radiofrequency data analysis IVUS as thin cap fibroatheroma

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every lesion, the lesion length, minimal lumen area and maximum percent plaque burden (%PB) were determined. The %PB was calculated as the EEM area minus the lumen area, divided by the EEM area and multiplied by 100% [10].

Within the culprit lesion, the necrotic core associated with the thrombotic occlusion was identified. This necrotic core was described according to the length, localization, maximum %PB, maximum and mean percentage necrotic area, the arc, the different tissue characteristics and the presence or absence of overlying fibrous tissue. The length of the necrotic core was measured as the distance between the first and final frame of consecutive frames containing the same necrotic core and morphological characteristics.

The remodeling index (RI) was calculated by dividing the lesion EEM area by the reference EEM area. RI and %PB were calculated at the site of the necrotic core. If no necrotic core

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Age – yrs 57±12

Male sex - % 71

Weight – kg 82±14

Height – cm 176±10

Body Mass Index - kg/m² 27±3.5

Diabetes mellitus - % 2

Hypertension - % 17

Hyperlipidemia - % 17

Current smoker - % 51

Previous smoker - % 15

Family history of CAD - % 39

Medication at entry - % Aspirin

Statin B-blockers

ACE-inhibitors / ATII-antagonists

7 10 12 5 Cholesterol spectrum at entry – mmol/l

Total cholesterol LDL cholesterol HDL cholesterol

Total cholesterol - HDL ratio

5.7±0.9 4.1±0.8 1.3±0.4 4.8±1.4 Culprit vessel - %

LAD RCA LCX

44 41 15 CAD = coronary artery disease; LAD = left anterior descending artery; RCA = right coronary artery; LCX: left circumflex artery

Table 1. Clinical characteristics (n=41)

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could be identified, these parameters were derived from the site of the maximum plaque area within the culprit lesion. The reference area was defined as the segment with the least amount of %PB within 10mm proximal to the lesion, without intervening side branches. If no proximal reference was available, the reference area was taken within 10mm distal to the lesion without intervening side branches.

IDTCFA definition

An IVUS-derived thin cap fibroatheroma (IDTCFA) was defined as an atherosclerotic site fulfilling all of the following four criteria [11]: 1). percentage plaque burden of more than 40%; 2). necrotic core without evidence of overlying fibrous tissue (no fibrous cap detectable); 3). percentage necrotic area of at least 10% over a length of at least 0.5mm, and 4). positive remodeling, defined as a remodeling index of 1.05 or more. Finally, the percentage of lesions, fulfilling all IDTCFA criteria was calculated. Figure 1 explains and summarizes the IVUS-VH characteristics of two culprit lesions fulfilling all necessary IDTCFA criteria.

Statistical analysis

Categorical variables were expressed as numbers and percentages and continuous variables as mean±standard deviation and range. Comparison of continuous variables between groups was performed with an unpaired t-test or 1-way-Anova. Correlation of sets of continuous variables was calculated by Pearson's method. Values of p <0.05 were considered statistically significant. SPSS version 12.0.1 was used as statistical analysis program.

Results

Patient characteristics are summarized in Table 1. Mean age was 57±12 years and approximately 30% were female. More than 50% were current smokers and only 2 (5%) had diabetes mellitus. At first injection of contrast in the infarct related artery 35 (86%) showed TIMI 0/1 flow and 6 (15%) had TIMI 2/3 flow. The culprit vessel was the LAD in 44%, the RCA in 41 %, and the LCX in 15%, 35 lesions (86%) were located in the proximal or mid RCA, proximal or mid LAD or proximal LCX. The general lesion and necrotic core characteristics of the culprit lesions are summarized in Table 2. Average lesion length, as determined by IVUS, was 13.7±6.9mm. Both RI and %PB were highly variable between the different IDTCFA’s, although the average RI was positive (1.28±0.28) and the average %PB was higher than 40% (58±8%). A necrotic core was present in 95% of the patients, with a length of 5.2±4.9mm and a maximum percentage necrotic core area of 25.9±11.3%.

Table 3 summarizes the different tissue characteristics of the IDTCFA’s. The mean percentage fibrous tissue within the IDTCFA’s was approximately 60% and the percentage

Lesions causing STEMI can be characterized by radiofrequency data analysis IVUS as thin cap fibroatheroma

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necrotic tissue was 16.7±6.5%. There were no statistically significant differences between the different coronary arteries for the amount of the different tissue types. The necrotic core length was positively correlated with the maximum necrotic core area (R=0.60;

p<0.01). The maximum necrotic core area was positively correlated with the RI (R=0.33;

p<0.05).

IDTCFA criteria and their prevalence within the culprit lesions of STEMI patients are given in Table 4. Based on the definition of IDTCFA, 68% of the culprit lesions fulfilled all IDTCFA criteria. Of interest, as shown in Figure 1, the plaque composition of STEMI patients was highly variable. In Figure 1, panel A, the lesion (male patient, 52 years of age) had a large necrotic core covering 180 degrees of the vessel circumference containing some calcium.

Lesion

Lesion length – mm (range) Minimum lumen area - mm² (range) Maximum plaque burden - % (range)

13.7±6.9 (3.5–30.4) 4.93±2.04 (2.63–11.92)

68.8±7.6 (42.5–80.0) Necrotic core

Necrotic core present - No. (%) Length - mm (range)

Superficial localization - No. (%) Maximum necrotic core area - % (range)

Mean plaque burden - % (range) Mean arc - º (range)

39 (95) 5.2±4.9 (0.7–21.0)

38 (97) 25.9±11.3 (5.1–57.1) 57.7±8.4 (37.6–75.5) 139±80 (32–337) Remodeling

Reference vessel area - mm² (range) Lesion EEM area - mm² (range) Remodeling index (range)

14.7±4.4 (6.7–25.1) 19.2±5.4 (7.5–33.8) 1.28±0.28 (0.80–2.02) IDTCFA = IVUS-derived thin cap fibroatheroma; EEM = external elastic membrane

Table 2. Lesion, necrotic core and remodeling characteristics of culprit sites (n=41)

Table 3. IDTCFA tissue characteristics (n=39)

Total Fibrous

tissue

Fibrofatty tissue

Dense calcium

Necrotic core Volume - mm³

(range)

84±88 (6.3–322.5)

19.2±19.7 (0.7–95.8)

5.1±5.2 (0.1–24.3)

2.3±3.3 (0.0–14.8)

6.5±8.4 (0.2–39.9) Percentage volume - %

(range)

100 60.9±7.4

(44.0–74.4)

16.9±18.6 (3.8–43.6)

5.2±4.2 (0.2–16.1)

17.1±6.6 (4.0–31.5) Mean area - mm²

(range)

9.47±3.04 (3.12–16.10)

3.82±1.57 (0.74 ±8.10)

1.17±0.82 (0.05–2.94)

0.28±0.23 (0.02–0.89)

1.00±0.50 (0.21–2.50) Mean percentage area - %

(range) 100 61.1±7.2

(45.6–75.0)

17.1±8.6 (3.8±43.7)

5.0±4.2 (0.3-17.5)

16.7±6.5 (4.0–30.1) IDTCFA = IVUS-derived thin-cap fibroatheroma

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IDTCFA criteria

Percentage plaque burden >40% - No. (%) Necrotic core present - No. (%)

Superficial localization of the necrotic core - No. (%) Necrotic core ≥0.5mm length - No. (%)

Average necrotic core >10% plaque area - No. (%) Positive remodeling - No. (%)

40 (98) 39 (95) 38 (93) 37 (88) 33 (81) 33 (81) Fulfilling all IDTCFA criteria - No. (%) 28 (68) IDTCFA = IVUS-derived thin cap fibroatheroma, STEMI = ST-segment elevation myocardial infarction

Table 4. IDTCFA criteria of STEMI culprit lesions (n=41)

Furthermore, the lesion contained a significant amount of plaque, was asymmetrical and located just distally to a side branch (SB). Figure 1, panel B (female patient, 47 years of age), shows a lesion with minimal plaque burden and focal necrotic spots. Only a small necrotic core can be identified with a necrotic core length of only 3.3mm.

Typical examples of culprit lesions and their necrotic core characteristics are shown in Figure 2. Patient A is a 61 years old male, known with hypertension. He presented with an occlusion of the proximal RCA. The lesion contains a large necrotic core with a moderate degree of calcification. However, mainly the calcium and not the necrotic tissue is in direct contact with the lumen, suggesting that the underlying mechanism of intracoronary thrombosis in this patient is a calcified nodule which, after perforating a thin fibrous cap, provoked the thrombotic process, although a plaque rupture as underlying mechanism cannot be ruled out. Patient B is a 42 years old male without any cardiac risk factors, who presented with an occlusion of the mid-segment of the LAD. In this case a highly fibrotic lesion without a necrotic core was found, suggesting that plaque erosion caused the intracoronary thrombosis. Patient C is a 52 years old male, with a history of hypertension and a positive family history of coronary artery disease, presented with an occlusion of the proximal part of the LAD. There is a plaque rupture (arrow) visible with a (residual) necrotic core at the bottom of the lesion and shoulders of the plaque.

Discussion

Key finding of this study is that IDTCFA’s can be found in approximately 70% of the patients without previous cardiac history, presenting with a STEMI. As far as we know, this is the first study which describes the tissue characteristics of lesions causing a STEMI in vivo, with special attention to the extent and localization of the necrotic core. Thus far, tissue characteristics of STEMI patients could only be studied post-mortem. IVUS-VH has the potential to assess the coronary tissue characteristics in vivo. From post-mortem

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Figure 1, Panel A.

0 0,5 1 1,5 2 2,5 3 3,5 4 4,5 5

0,0 0,4 0,8 1,2 1,7 2,1 2,5 3,0 3,4 3,8 4,1 4,5 4,9 5,4 5,8 6,2 6,5 6,9 7,3 7,6 Proximal Distance (mm) Distal

Cross-sectional area (mm2)

Necrotic core Dense calcium Fibrofatty Fibrous Necrotic core characteristics:

Superficial localization: yes

Length: 4.5 mm

Average percentage: 25.0 % Maximum percentage: 44.7 % General characteristics:

Lesion length: 8.0 mm Minimum lumen area: 3.2 mm² Maximum obstruction area: 69.7 % Remodeling index: 1.7

SB REF

L

M EEM PROX A

DIST

Example of a culprit lesions fulfilling IDTCFA criteria: grayscale IVUS and corresponding IVUS-VH images. See text for explanation.

The plaque area is given by the colors. These colors indicate atherosclerotic issue types: green = fibrous tissue;

green-yellow = fibro-fatty tissue; white = dense calcium; red = necrotic tissue. The distribution of the different tissue types within the culprit lesion is summarized in the corresponding bar-graph. A: adventitia. DIST: distal.

EEM: external elastic membrane (the interface between the media and adventitia). L: lumen. M: media (grey zone). PROX: proximal. REF: site of the reference EEM area. SB: side-branch. T: thrombus (speckling blood clot within the lumen)

(The interval between the different bars (corresponding to different images) as indicated on the X-axis is not linear, since this distance is depending on the RR-interval which is variable)

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Figure 1, Panel B.

0 0.5 1 1.5 2 2.5 3 3.5 4 4.5 5 5.5 6

0.0 0.9 1.7 2.6 3.6 4.5 5.4 6.4 7.2 8.0 8.9 9.8 10.7 11.6 12.4 13.3 14.2 Proximal Distance (mm) Distal

Cross-sectional area (mm2)

Necrotic core Dense calcium Fibrofatty Fibrous

Necrotic core length

DIST

T

A EEM

General characteristics:

Lesion length: 14.6 mm Minimum lumen area: 11.9 mm² Maximum obstruction area: 42.5 % Remodeling index: 1.6

PROX SB

M REF L

REF

Necrotic core characteristics:

Superficial localization: yes

Length: 3.3 mm

Average percentage: 14.1 % Maximum percentage: 17.7 % Lesions causing STEMI can be characterized by radiofrequency data analysis IVUS as thin cap fibroatheroma

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pathological studies in patients who died after an acute myocardial infarction, it is known that ruptured plaques can be found in about 60-70% of the patients [11]. These plaques were characterized by a plaque burden of at least 40% of the EEM area, an average necrotic core area of 34%, an average necrotic core length of 8 mm and a thin fibrous cap of less than 65µm. Other mechanisms of acute coronary thrombosis are plaque erosion and the calcified nodule which occur in respectively 30-40% and 5-7% of the patients. Plaque erosion is characterized by de-endothelialization of a proteoglycan and smooth muscle cell rich lesion. The calcified nodule refers to a lesion with fibrous cap disruption and thrombi associated with eruptive, dense, calcified nodules. However, lesions may show several morphological substrates of intracoronary thrombosis.

The results of this study are in line with the pathological findings of previous studies.

Nearly all patients had >40% percent plaque burden at the culprit lesion site. In 95% of the patients a necrotic core without overlying fibrous tissue could be identified. The average maximum necrotic core area was 25.9% and the average necrotic core length was 5.2mm.

The fact that the maximum necrotic core area was smaller and the necrotic core length was shorter than observed in post-mortem studies can be explained by taken into account the inherent limitations of the IVUS-VH technique. For example in the presence of thrombus material exact assessment of the necrotic core area (and length) is hampered.

Another potential explanation for the differences between the IVUS-VH measurements and the results of post-mortem studies could be that survivors of STEMI may have less necrotic area compared to patients who died during STEMI.

To approach the ruptured plaque characteristics of lesions as observed in autopsy studies and to asses how many STEMI lesions do fulfill these characteristics, IDTCFA criteria were determined. Since it is unknown whether lesions of STEMI survivors are comparable to non-survivors, a relatively short necrotic core length was chosen of 0.5mm as compared to the minimum necrotic core length of 2mm found in post-mortem studies [11]. The necrotic core area in direct contact with the endovascular lumen has to be at least 10%, which is comparable to other studies [8]. We did not use a specific number of frames fulfilling the required necrotic core criteria as done in other studies, since the distance between the frames can be different, dependent on the heart rate.

To prevent intracoronary thrombosis it may be necessary to distinguish the different mechanisms leading to intracoronary thrombosis, based on morphological characteristics [1]. Thus far, IVUS-VH imaging allows identification of a limited number of plaque characteristics, for example the extent and localization of the necrotic core. In some patients, the IVUS-VH images suggested a more fibrotic plaque composition with plaque erosion as a possible cause of intracoronary thrombosis. However, with the current IVUS- VH technique it is not possible to discriminate between these different types of plaque, except for very clear cases. Ideally, in the future, it will be possible to identify other

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vulnerable plaque characteristics, like de-endothelialization or the thickness of the fibrous cap.

Study limitations

This study has some limitations. The luminal border detection in STEMI patients is less accurate due to the presence of thrombus, especially within ulcerations of the plaque.

Thrombus may result in an overestimation of the fibrous and fibrolipidic content of the plaque and underestimation of other plaque components. Moreover, it may influence the accuracy to distinguish a fibrous cap from intracoronary thrombus, precluding definite conclusions whether there is a necrotic core in contact with the lumen or not. However, currently no other techniques are available to study the morphology of STEMI lesions in vivo. Moreover, the available analysis program is limited in it's ability to differentiate between the major necrotic core and other necrotic parts within the culprit lesion, which may result in an overestimation of the size of the major necrotic core [12]. Another limitation is that IVUS-VH seems to be limited in its ability to discriminate between necrotic tissue and calcium [7]. Whether, this has major consequences for the interpretation of the results of this study, is unknown. Therefore, histopathological conformation of IVUS-VH findings is still needed to improve the technique. Moreover, IVUS-VH can only identify some characteristics of ruptured plaques or TCFA’s. Other imaging modalities or biochemical markers are needed to increase the sensitivity to detect vulnerable lesions within the coronary tree. Finally, due to plaque rupture, plaque composition may change, which may influence the created tissue maps. However, this may also be a limitation for pathology studies.

Conclusion

IVUS-VH can be used to detect TCFA’s in vivo. Approximately 70% of the culprit lesions in STEMI patients can be described as IDTCFA’s with necrotic core characteristics corresponding to histopathological findings. IVUS-VH may be a useful technique to identify IDTCFA’s to avoid STEMI. However, insight in the natural history of IDTCFA’s is needed to determine the clinical implication of these findings.

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Circulation 2002;105:297-303.

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Figure 2. Examples of IVUS-VH characteristics of culprit lesions causing STEMI

The plaque area is given by the colors. These colors indicate atherosclerotic tissue types: green = fibrous tissue; green-yellow = fibro-fatty tissue; white = dense calcium; red = necrotic tissue, grey = media.

Patient A. Lesion with severe plaque burden and large necrotic core with calcification in direct contact with the lumen

Patient B. Lesion with high fibrous content, without evidence of necrotic core or calcified tissue, highly suggestive of plaque erosion

Patient C. Lesion showing plaque rupture (arrow) at the site of a large necrotic core

Lumen area: 6.8 mm² Area obstruction: 65.7 % Fibrous (green): 43.3 % Fibrofatty (yellow): 12.0 % Calcified (white): 11.9 % Necrotic (red): 32.7 %

A

B

C

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