regression of an atherosclerotic coronary artery plaque demonstrated by multislice spiral computed...

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GRAPHIC REPORT Heart Vessels (2003) 18:224–226 © Springer-Verlag 2003 DOI 10.1007/s00380-003-0712-1 Yuichi Sato · Fumio Inoue · Akihiro Yoshimura Takahiro Fukui · Takako Imazeki · Masahiko Kato Hideki Ono · Shunichi Yoda · Masayasu Mitsui Naoya Matsumoto · Satoru Furuhashi Motoichiro Takahashi · Katsuo Kanmatsuse Regression of an atherosclerotic coronary artery plaque demonstrated by multislice spiral computed tomography in a patient with stable angina pectoris Received: January 17, 2003 / Accepted: April 19, 2003 Y. Sato (*) · F. Inoue · A. Yoshimura · T. Fukui · T. Imazeki · M. Kato · H. Ono · S. Yoda · M. Mitsui · N. Matsumoto · K. Kanmatsuse Department of Cardiology, Nihon University Surugadai Hospital, 1-8-13 Kanda-Surugadai, Chiyoda-ku, Tokyo 101-8309, Japan Tel. 81-3-3293-1711; Fax 81-3-3295-1859 e-mail: [email protected] S. Furuhashi · M. Takahashi Department of Radiology, Nihon University Surugadai Hospital, Tokyo, Japan Abstract Multislice spiral computed tomography (MSCT) permits direct visualization of not only coronary artery stenosis but also atherosclerotic plaques in patients with coronary artery disease. In this report, we describe a patient with stable angina in whom the regression of the plaque was documented by serial MSCT examinations. In the patient, a 46-year-old man with stable angina, MSCT revealed a stenotic lesion at the proximal portion of the left anterior descending artery. Axial, curved multiplanar reconstruction and cross-sectional images consistently depicted a protrud- ing computed tomography low-signal mass suggesting an atherosclerotic plaque. Intracoronary ultrasound (ICUS) also documented an eccentric soft plaque with an echo- lucent mass suggesting a lipid core. Lipid-lowering therapy with pravastatin was started. Follow-up MSCT performed 7 months later documented an increase in the luminal area while the external vessel area remained unchanged. The regression of the plaque was also confirmed by a follow-up ICUS study. MSCT was thought to be feasible for serial evaluation of the plaque size and texture. Key words Multislice spiral computed tomography · Intracoronary ultrasound · Coronary artery plaque Introduction Multislice spiral computed tomography (MSCT) is capable of detecting not only significant coronary artery stenoses and occlusions, 1–3 but also coronary artery plaques 4 non- invasively. However, serial changes in the plaque size have not yet been documented by MSCT. In this report, we describe a patient in whom MSCT showed regression of the plaque after lipid-lowering therapy. Case report A 46-year-old man was referred to our hospital because of anterior chest pain upon exercise. He had a history of hypercholesterolemia, but had remained untreated. His initial laboratory examinations showed that the total cho- lesterol level was 256 mg/dl, low-density lipoprotein (LDL)- cholesterol level 176 mg/dl, and triglyceride level 184 mg/dl. MSCT was performed using a Somatom Volume Zoom (Siemens, Munich, Germany) which provided a 4-detector- row gantry and up to 250 ms temporal resolution. Our scan protocol and the retrospectively ECG-gated reconstruction method have been described previously. 5 In brief, metoprolol (40 mg) was given orally 2 h prior to the scan to lower the heart rate in order to apply the single-phase algo- rithm. 1 After measuring the contrast transit time from the intravenous injection to the maximum contrast enhance- ment of the ascending aorta, a nonionic contrast medium (Iomeron 350, 100 ml syringe, Eisai, Tokyo, Japan) was in- jected at a rate of 3.0 ml/s. The scan was performed with a collimation 1.0 mm, gantry rotation 0.5/s, and a pitch of 1.5 (table feed 1.5 mm/rotation). ECG-gated image reconstruc- tion was made under the ECG guidance. Our scan protocol and retrospectively ECG-gated image reconstruction method have been described previously. 5 In brief, the end of the reconstruction window (250 ms) was positioned at the peak of the P waves to avoid cardiac motion artifacts occurring during the ventricular rapid filling and atrial con- traction periods. The scan data were transferred to a work- station (3D Virtuoso, Siemens) and volume-rendering images, axial images, curved multiplanar reconstruction (MPR), and cross-sectional MPR images of the coronary artery were obtained. All the axial and MPR images were

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GRAPHIC REPORT

Heart Vessels (2003) 18:224–226 © Springer-Verlag 2003DOI 10.1007/s00380-003-0712-1

Yuichi Sato · Fumio Inoue · Akihiro YoshimuraTakahiro Fukui · Takako Imazeki · Masahiko KatoHideki Ono · Shunichi Yoda · Masayasu MitsuiNaoya Matsumoto · Satoru FuruhashiMotoichiro Takahashi · Katsuo Kanmatsuse

Regression of an atherosclerotic coronary artery plaque demonstratedby multislice spiral computed tomography in a patient withstable angina pectoris

Received: January 17, 2003 / Accepted: April 19, 2003

Y. Sato (*) · F. Inoue · A. Yoshimura · T. Fukui · T. Imazeki ·M. Kato · H. Ono · S. Yoda · M. Mitsui · N. Matsumoto ·K. KanmatsuseDepartment of Cardiology, Nihon University Surugadai Hospital,1-8-13 Kanda-Surugadai, Chiyoda-ku, Tokyo 101-8309, JapanTel. �81-3-3293-1711; Fax �81-3-3295-1859e-mail: [email protected]

S. Furuhashi · M. TakahashiDepartment of Radiology, Nihon University Surugadai Hospital,Tokyo, Japan

Abstract Multislice spiral computed tomography (MSCT)permits direct visualization of not only coronary arterystenosis but also atherosclerotic plaques in patients withcoronary artery disease. In this report, we describe a patientwith stable angina in whom the regression of the plaque wasdocumented by serial MSCT examinations. In the patient, a46-year-old man with stable angina, MSCT revealed astenotic lesion at the proximal portion of the left anteriordescending artery. Axial, curved multiplanar reconstructionand cross-sectional images consistently depicted a protrud-ing computed tomography low-signal mass suggesting anatherosclerotic plaque. Intracoronary ultrasound (ICUS)also documented an eccentric soft plaque with an echo-lucent mass suggesting a lipid core. Lipid-lowering therapywith pravastatin was started. Follow-up MSCT performed 7months later documented an increase in the luminal areawhile the external vessel area remained unchanged. Theregression of the plaque was also confirmed by a follow-upICUS study. MSCT was thought to be feasible for serialevaluation of the plaque size and texture.

Key words Multislice spiral computed tomography ·Intracoronary ultrasound · Coronary artery plaque

Introduction

Multislice spiral computed tomography (MSCT) is capableof detecting not only significant coronary artery stenoses

and occlusions,1–3 but also coronary artery plaques4 non-invasively. However, serial changes in the plaque size havenot yet been documented by MSCT. In this report, wedescribe a patient in whom MSCT showed regression of theplaque after lipid-lowering therapy.

Case report

A 46-year-old man was referred to our hospital becauseof anterior chest pain upon exercise. He had a history ofhypercholesterolemia, but had remained untreated. Hisinitial laboratory examinations showed that the total cho-lesterol level was 256mg/dl, low-density lipoprotein (LDL)-cholesterol level 176mg/dl, and triglyceride level 184mg/dl.MSCT was performed using a Somatom Volume Zoom(Siemens, Munich, Germany) which provided a 4-detector-row gantry and up to 250 ms temporal resolution. Our scanprotocol and the retrospectively ECG-gated reconstructionmethod have been described previously.5 In brief,metoprolol (40mg) was given orally 2h prior to the scan tolower the heart rate in order to apply the single-phase algo-rithm.1 After measuring the contrast transit time from theintravenous injection to the maximum contrast enhance-ment of the ascending aorta, a nonionic contrast medium(Iomeron 350, 100ml syringe, Eisai, Tokyo, Japan) was in-jected at a rate of 3.0ml/s. The scan was performed with acollimation 1.0mm, gantry rotation 0.5/s, and a pitch of 1.5(table feed 1.5 mm/rotation). ECG-gated image reconstruc-tion was made under the ECG guidance. Our scan protocoland retrospectively ECG-gated image reconstructionmethod have been described previously.5 In brief, the end ofthe reconstruction window (250ms) was positioned atthe peak of the P waves to avoid cardiac motion artifactsoccurring during the ventricular rapid filling and atrial con-traction periods. The scan data were transferred to a work-station (3D Virtuoso, Siemens) and volume-renderingimages, axial images, curved multiplanar reconstruction(MPR), and cross-sectional MPR images of the coronaryartery were obtained. All the axial and MPR images were

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stored in the computer for further analysis. We evaluatedall the images with the window level 77 and the width 214.The volume-rendering image showed a significant luminalnarrowing at the proximal portion of the left anterior de-scending artery (LAD, Fig. 1A). A computed tomography(CT) low-dense mass was detected on the curved MPR(Fig. 1B) and axial (Fig. 1C) images. The signal intensity ofthe mass was 20 � 8 Hounsfield Units (HU). Coronaryangiography (CAG) revealed a significant stenosis at seg-ment #7 (Fig. 2A). The intracoronary ultrasound (ICUS)finding at the site of the stenosis was consistent with that ofa soft plaque with an echo-lucent mass suggesting a lipidcore (Fig. 2B). Since stress myocardial perfusion single-photon computed tomography did not reveal severe is-chemia, the patient underwent lipid-lowering therapywith pravastatin (10mg/day). His total cholesterol, LDL-cholesterol, and triglyceride levels decreased to 194, 100,and 99 mg/dl, respectively. MSCT was repeated 7 monthsafter the initial study. To ensure that the same lesion wasassessed by angiography, ICUS, and MSCT, landmarkssuch as the origin of side branches and the distance from theleft coronary artery ostium or bifurcation of the LAD andthe circumflex coronary artery were used. The volume ren-dering (Fig. 1D), curved MPR (Fig. 1E), and axial images

(Fig. 1F) consistently demonstrated a decrement in the se-verity of stenosis and a decrease in the size of the CT-low-signal mass. The CT signal of the mass was increased to 81� 8 HU. A follow-up CAG demonstrated a decrement inthe severity of stenosis (Fig. 2C) and a repeat ICUS studyalso revealed a decrease in the plaque size as well as anincrease in the echo density (Fig. 2D). Figure 3 demon-strates serial changes in the cross-sectional MPR images ofthe proximal reference site (6mm distal to the bifurcation ofthe first diagonal artery), the center of the stenotic lesion,and the distal reference site (4mm distal to the seconddiagonal artery). The external vessel area was greater at thestenotic site than at the proximal reference site, a findingindicating the positive vascular remodeling. The decrementin the size of the CT-low-signal mass during the follow-upperiod was demonstrated by the increment in the luminalarea (from 7 to 14mm2) without any change in the externalvessel areas (40mm2) in serial MSCT studies.

Discussion

Coronary artery plaque disruption with subsequent throm-bus formation leads to acute coronary syndrome, includingacute myocardial infarction and unstable angina pectoris.6,7

Therefore, the detection of coronary artery plaques is ofutmost importance in individuals with multiple coronaryrisk factors. At present, ICUS is the most reliable methodfor detecting early plaque formation and changes in theplaque size.8 In addition, ICUS provides information onplaque echogenicity, which represents plaque composition.9

In the latter report, a favorable effect of 3-hydroxy-3-

Fig. 1. Multislice spiral computed tomography (MSCT) images before(A–C) and after (D–F) lipid-lowering therapy. Significant stenosis(arrows) is noted at the proximal portion of the left anterior descend-ing artery on volume-rendering images (A,D). A plaque (arrows) isdocumented on curved multiplanar reconstruction (MPR; B,E) andaxial images (C,F). #9-1, first diagonal artery; #9-2, second diagonalartery

Fig. 2. Coronary angiograms (A,C) and intracoronary ultrasoundimages (B,D) before and after the lipid-lowering therapy. Arrows in Aand C indicate the site of the stenosis, and arrows in B and D indicatethe plaque

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methylglutaryl coenzyme A reductase on the ICUS-docu-mented plaque size has been demonstrated. Nevertheless,ICUS requires invasive procedures in the catheter labora-tory and high medical expenses and, therefore, has limita-tions for widespread clinical use. The recent introduction ofMSCT has enabled the noninvasive detection and tissuecharacterization of coronary artery plaques.4 To our knowl-edge, this is the first report describing plaque regression byserial MSCT examinations. There was an increase in the CTsignal of the plaque, which corresponded to the increase inthe echogenicity observed in the serial ICUS studies. Thesefindings may represent the changes in plaque compositionfollowing the lipid-lowering therapy with pravastatin. An-other major finding in the present report was the depictionof vascular remodeling by MSCT. Assessment of vascularremodeling, which is at present a domain of ICUS,10 can beassessed noninvasively by MSCT.

Finally, our present observation may initiate a random-ized large-scale clinical trial concerning the progressionor regression of the coronary artery plaque and vascularremodeling by means of MSCT.

References

1. Achenbach S, Ulzheimer S, Baum U, Kachelriess M, Ropers D,Giesler T, Bautz W, Daniel WG, Kalender WA, Moshage W(2000) Noninvasive coronary angiography by retrospectivelyECG-gated multislice spiral CT. Circulation 102:2823–2828

2. Achenbach S, Giesler T, Ropers D, Ulzheimer S, Derlien H,Schulte C, Wenkel E, Moshage W, Bautz W, Daniel WG, Kalender

Fig. 3. Cross-sectional images atthe proximal reference site,center, and distal reference siteof the stenotic lesion before (A)and after (B) the lipid-loweringtherapy. The external vessel areawas greater at the stenotic sitethan at the proximal referencesite, a finding indicating thepositive vascular remodeling.The decrement in the size of thecomputed tomography low-signal mass was demonstrated bythe increment in the luminalarea (from 7 to 14 mm2) withoutchange in the external vesselarea (40 mm2) in serial MSCTstudies

WA, Baum U (2001) Detection of coronary artery stenoses bycontrast-enhanced, retrospectively electrocardiographically-gated,multislice spiral computed tomography. Circulation 103:2535–2538

3. Nieman K, Rensing BJ, van Geuns R-JM, Munne A, LigthartJMR, Pattynama PMT, Krestin GP, Serruys PW, de Feyter PJ(2002) Usefulness of multislice computed tomography for detect-ing obstructive coronary artery disease. Am J Cardiol 89:913–918

4. Schroeder S, Kopp AF, Baumbach A, Meisner C, Kuettner A,George C, Ohnesorge B, Herdeg C, Claussen CD, Karsch KR(2001) Noninvasive detection and evaluation of atheroscleroticcoronary plaques with multislice computed tomography. J Am CollCardiol 37:1430–1435

5. Sato Y, Kanmatsuse K, Inoue F, Horie T, Kato M, Kusama J,Yoshimura A, Imazeki T, Furuhashi S, Takahashi M (2003)Noninvasive coronary artery imaging by means of multislice spiralcomputed tomography: a novel approach for retrospectively ECG-gated reconstruction technique. Circ J 67:107–111

6. Falk E, Shah PK, Fuster V (1995) Coronary plaque disruption.Circulation 92:657–671

7. Davies MJ (1996) Stability and instability: two faces of coronaryatherosclerosis. Circulation 94:2013–2020

8. von Birgelen C, Slager JS, Di Mario C, deFeyter PJ, SerruysPW (1995) Volumetric intracoronary ultrasound: a new maxi-mum confidence approach for the quantitative assessment ofprogression-regression of atherosclerosis? Atherosclerosis118(suppl):S103-S113

9. Schartl M, Bocksch W, Koschyk DH, Voelker W, Karsch KR,Kreuzer J, Hausmann D, Beckmanm S, Gross M, for the GermanAtrovastatin Intravascular Ultrasound Study Investigators(GAIN) (2001) Use of intravascular ultrasound to compare effectsof different strategies of lipid-lowering therapy on plaque volumeand composition in patients with coronary artery disease. Circula-tion 104:387–392

10. Schoenhagen P, Ziada KM, Vince G, Nissen SE, Tuzcu EM (2001)Arterial remodeling and coronary artery disease: the concept of“dilated” versus “obstructive” coronary atherosclerosis. J Am CollCardiol 38:297–306