- Email: [email protected]
Vulnerable plaque
THURSDAY 9/30/04 8:00 –10:00
AM
(Hall D and E on Level 2)
Vulnerable Plaque Thursday, September 30, 2004 8:00-10:00 AM Hall D and E on Level 2
TCT 299 In Vivo Detection of a Coronary Artificial Target with a Near Infrared Spectroscopy Catheter. S. Waxman, Tufts- New England Medical Center, Boston, MASS; J. Tang, InfraRedX, Inc.; B.J. Marshik, InfraRedX, Inc.; H. Tan, InfraRedX, Inc.; K.R. Khabbaz, Tufts- New England Medical Center; R.J. Connolly, Tufts-New England Medical Center; T.A. Dunn, InfraRedX, Inc.; A.F. Zuluaga, InfraRedX, Inc.; S. DeJesus, InfraRedX, Inc.; J.D. Caplan, InfraRedX, Inc.; E.J. Muller, InfraRedX, Inc.
(Abstract nos. 298-303)
TCT 298 Influenza Virus in the Atherosclerotic Plaques of Human Aortic Aneurysms and Apo E Deficient Mice. M. Madjid, University of Texas-Houston, Texas Heart Institute; S. Litovsky, University of Texas-Houston, Texas Heart Institute; N. Sadeghi, University of Texas-Houston, Texas Heart Institute; I. Awan, University of TexasHouston, Texas Heart Institute; E.E. Porat, University of TexasHouston, Texas Heart Institute; P.R. Wyde, Baylor College of Medicine, Houston, Texas; W. Casscells, University of TexasHouston, Texas Heart Institute. Background: Influenza can trigger acute coronary syndromes, and influenza vaccination markedly reduces the risk of cardiovascular events. We investigated whether the influenza virus can be recovered from atherosclerotic plaques of humans and mice. Methods: We infected a series of apo E-deficient atherosclerotic mice with influenza A/HK/68 virus and also took aneurysmal aortic samples from 4 asymptomatic patients undergoing surgery for abdominal aortic aneurysm (AAA) repair. Homogenized arterial tissues were cultured for influenza virus. We used the standard titration method using Madin Darby canine kidney cells. We performed immunofluorescence (IF) studies using mouse monoclonal antibody to the nucleoprotein (NP) of influenza A virus and C3 complement. We ran reverse transcriptase polymerase chain reaction (RT-PCR) assays using primers specific for influenza A nucleoprotein. H&E and CD68 and CD3 staining (for macrophages and T lymphocytes) were employed for histopathologic examinations. Results: In mice, we could culture the influenza virus in high titers from lung, aorta, and heart on days 7 and 10. Blood culture was negative, indicating presence of the virus in the plaques in absence of viremia. We also found positive immunofluorescence for influenza antigens and positive RT-PCR assays for influenza NP gene in mice. In human samples, culture for the virus was negative. However, RT-PCR was positive for NP gene of the influenza virus in 3 of the 4 human AAA samples, and IF was positive in those samples. Samples with positive RT-PCR showed histologic features of atherosclerosis while the sample with negative RT-PCR was largely free of atherosclerosis. In mice, plaque influenza was associated with deposition of C3 complement and massive infiltration of inflammatory cells (e.g., macrophages and T cells) in the plaques. Conclusions: We have shown (to our knowledge for the first time) evidence for direct infection of the mouse aortic atherosclerotic and human aneurysmal aortic plaques with influenza virus. This infection was associated with pro-inflammatory changes in the plaque. If confirmed in future studies, the possible chronic influenza infection in the arteries may justify more extensive vaccination and even antiviral therapy to reduce the risk of cardiovascular events.
The American Journal of Cardiology姞
Background: Near infrared spectroscopy (NIR-S) can detect lipid-rich coronary plaques by identifying their chemical features ex vivo. However, a catheter-based system for in vivo use must overcome problems of cardiac motion and signal acquisition through blood. We tested whether an NIR-S catheter can distinguish an artificial target (AT) from human coronary arterial wall in a living porcine model. Methods: The human-to-porcine coronary xenograft model was used (JACC 2004;43:73A). Briefly, human coronary segments from fresh autopsy hearts and tubing are used to create a carotid-right atrial conduit in an open-chest anesthetized pig (45–50 kg). The xenograft is fixed to the anterior wall of the heart to simulate motion. An AT (a teflon material with spectral peaks in a range suitable for lipid identification by NIR-S) was secured onto a segment of the xenograft denuded of pericardial fat. The NIR-S catheter was advanced into the xenograft through a hemostatic valve attached to the circuit. Catheter position was confirmed visually and angiographically. NIR spectra were acquired 1) with the catheter stationary in the xenograft aimed at the AT (with and without the AT on the exposed vessel), 2) during 2 pullbacks along the entire length of the xenograft at 5 mm intervals with the AT secured in place, and 3) during 2 pullbacks with no AT. Results: Catheter-based NIR-S correctly identified the presence or absence of the AT through blood and arterial wall with the catheter stationary, using a principal component analysis—Mahalanobis distance algorithm with applied statistics. During pullback 2, the model detected the position of the AT and differentiated between segments with or without the AT. No AT signal was identified during pullback C. Results were reproducible in the different pullbacks. Conclusions: Intravascular NIR-S can detect an artificial target through blood and human coronary arterial wall, despite motion, in the human coronary xenograft porcine model. Our data, coupled with the previously documented ability of NIR-S to identify lipid pools ex vivo, support the potential use of catheter-based NIR-S to detect vulnerable plaques in patients.
TCT 300 High Resolution Micro Computed Tomographic Imaging of Vulnerable Plaques. P. Cherukuri, University of Texas Health Science Center; D. Vela; University of Texas Health Science Center, Houston; D. Cody, Anderson Cancer Center; E. Johnson, Anderson Cancer Center; R. Price, Anderson Cancer Center; J.L. Conyers, University of Texas Health Science Center, Houston; S. Litovsky, University of Texas Health Science Center, Houston; W. Casscells, University of Texas Health Science Center, Houston. Background: Microcalcifications within atherosclerotic plaques are believed to be a major marker of plaque vulnerability but are currently clinically undetectable. X-ray based imaging systems such as multislice and electron beam computed tomography (CT) are ineffective at resolving these microcalcific regions because of each system’s limited spatial resolution (⬃0.625–1 mm). However, high-resolution micro CT of coronary arteries may be capable of both localizing and characterizing these small foci of calcifications, without the aid of exogenous contrast agents or image postprocessing techniques.
SEPTEMBER 30, 2004
TCT ABSTRACTS/Poster
141E
P O S T E R A B S T R A C T S
THURSDAY 9/30/04 8:00 –10:00 Methods: Specimens of left anterior descending (LAD) coronary arteries were obtained from autopsy of individuals with coronary artery disease. GE Medical Systems RS-9 Micro CT system (80 kV, 450 A, 27-m isometric voxel size) imaged the arterial specimens ex vivo, and Hounsfield intensities were calibrated versus air and water standards. Images were corrected and processed using reconstruction software. Following the micro CT protocol, LAD specimens were decalcified, transversely sectioned every 80 to 90 m, and stained with Hematoxylin-Eosin. Histology was correlated with the corresponding crosssectional micro CT images. Results: We found significant correlation between micro CT and histology, in particular the distribution of microcalcifications within lipid-rich plaques. Fibrocalcific plaques were shown to be homogeneous in composition with a dense focus of calcification and were well correlated with histology. However, lipid-rich plaques were variably heterogeneous with ordered distributions of microcalcifications predominantly located deep and lateral to the lipid core(s). Histology of these lipid-rich plaques revealed clusters of microcalcifications, many as small as 10 m in diameter, deep within the arterial wall and peripheral to the lipid core. These microcalcifications were positively identified with the micro CT, and the images strongly indicate that the individual deposits are closely spaced. Conclusions: We believe that this is the first study demonstrating that high-resolution micro CT is capable of identifying microcalcific components of vulnerable plaques. The histological correlation with micro CT clearly reveals that microcalcifications manifest themselves deep from the lumen and peripheral to the lipid cores. Given the abundance of clinical data suggesting that these lipid-rich plaques are more prone to rupture rather than the fibrocalcific plaques, it is highly desirable to characterize the aforementioned plaques to diagnose highrisk patients. Future advances in clinical CT image resolution may someday allow for similar plaque characterization in vivo.
P O S T E R A B S T R A C T S
TCT 301 Significance of Fibrous Cap Thickness Measured by Optical Coherence Tomography. Y. Takeda, T. Suzuki, E. Tsuchikane, T. Itoh, M. Ehara, H. Sato, T. Matsubara, I. Shigenori, O. Katoh. Toyohashi Heart Center, Toyohashi, Japan. Background: Recent human histological studies report that fibrous caps (FCs) of vulnerable plaques are thinner (⬍0.065 mm) compared with those of stable plaques. Optical coherence tomography (OCT) may provide in vivo information on fibrous cap thickness. To evaluate the effect of OCT on characterization of FCs in coronary plaques in vivo, we used OCT to measure minimal thickness, maximal thickness, and length of the FCs in stable and vulnerable plaques.
AM
(Hall D and E on Level 2)
Results: OCT detected 7 FCs of 38 culprit lesions (38 patients). The 7 FCs of 7 culprit lesions were divided into 2 lesion subsets, group V (FCs in vulnerable lesions, n ⫽ 4) and group S (FCs in stable lesions, n ⫽ 3), determined by clinical demographics, intracoronary angioscopy, and intracoronary ultrasound. The mean minimal thickness of FC was significantly thinner in group V than in group S (0.03 mm vs 0.07 mm: p ⬍0.05). The mean maximal thickness of FC was 0.31 mm in group V and 0.38 mm in group S. The mean length of FC was 1.8 mm in group V and 2.6 mm in group S, although these differences between the 2 groups did not reach statistical significance. Conclusions: These results indicate that OCT is useful for the detection of vulnerable plaque in terms of the thickness of fibrous caps, although the OCT flushing system should be improved to obtain a stable image of the plaque.
TCT 302 Intravascular Ultrasound Radiofrequency Analysis Identifies Plaque Composition Depending on Risk Factors: In Vivo Virtual Histology. D. Bo¨se, University Essen, Germany; A. Schmermund, University Essen, Germany; P Margolis, Volcano Therapeutics Inc., Orange County, CA; A. Nair, Biomedical Engineering, The Cleveland Clinic Foundation, Ohio; D.G. Vince, Biomedical Engineering, The Cleveland Clinic Foundation, Ohio; H. Eggebrecht, Department of Cardiology, University Essen, Germany; C. Naber, Department of Cardiology, University Essen, Germany; R. Erbel, Department of Cardiology, University Essen, Germany. Background: Ex vivo, intravascular ultrasound (IVUS) radiofrequency (RF) data analysis has been demonstrated to predict coronary plaque composition. Fibrous, fibrolipidic, calcified, and lipid-necrotic areas can be identified within coronary plaques (“virtual histology”). Methods: We examined the first clinically available virtual histology system (Volcano Therapeutics, Orange County, California) in 75 patients (61 ⫾ 11 years, 64 men) undergoing coronary angiography. Using 30-MHz, 3.2-F mechanically rotating IVUS catheters (Boston Scientific). Automated pullback was performed (left anterior descending coronary artery in 43 patients, left circumflex coronary artery in 11, right coronary artery in 21). Results: Average cross-sectional fibrous plaque area was 2.4 ⫾ 1.8 mm2, fibrolipidic 1.1 ⫾ 1.4 mm2, calcified 0.1 ⫾ 0.2 mm2, and lipid-necrotic 0.6 ⫾ 0.6 mm2. Average fibrous plaque volume was 102.1 ⫾ 88.7 mm3, fibrolipidic 56.9 ⫾ 74.7 mm3, calcified 5.5 ⫾ 8.9 mm3, and lipid-necrotic 28.8 ⫾ 29.3 mm3. HDL cholesterol (HDL) was independently associated with overall plaque area (p ⫽ 0.017) and
Methods: The OCT optical fiber was automatically pulled back 1.0 mm per second (15.6 frames per second). A fibrous cap was defined as a thin, homogeneous band overlying a signal-poor region. The thickness of the fibrous cap was measured only in cases in which the fibrous cap was continuously observed in lengths of more than 1 mm by OCT.
142E
The American Journal of Cardiology姞
SEPTEMBER 30, 2004
TCT ABSTRACTS/Poster
THURSDAY 9/30/04 8:00 –10:00
AM
(Hall D and E on Level 2)
average % stenosis (p ⫽ 0.007). There was a significant inverse association between HDL cholesterol and lipid necrotic area (p ⫽ 0.001, Figure) and lipid core volume % (p ⫽ 0.02), as well as fibrous plaque area (p ⫽ 0.007); no association was observed with calcified and fibrolipid plaque components. There was a significant positive correlation between total cholesterol and calcified cross-sectional area (p ⬍0.001). Conclusions: Virtual histology IVUS RF analysis allows characterization of plaque composition in vivo and detects differences depending on risk factor profile. This may have implications for prognosis and assessment of treatment effects in patients undergoing invasive diagnostics.
TCT 303 Structural Effects of an Angiotensin-Converting Enzyme Inhibitor on Coronary Atherosclerotic Plaques as Clinically Assessed by Intravascular Ultrasound Radio-Frequency Signal Analysis. M. Yokoyama, Chiba University Hospital, Chiba, Japan; B.K. Courtney, Stanford University Medical Center, Palo Alto, CA; T. Nakayama, Chiba University Hospital, Chiba, Japan; S. Namikawa, Chiba University Hospital, Chiba, Japan, T. Koizumi, Stanford University Medical Center, Palo Alto, CA; M. Nameki, Chiba University Hospital, Chiba, Japan; N. Komiyama, Saitama Medical School, Moroyama, Japan. Background: Many clinical studies have shown that angiotensinconverting enzyme inhibitors (ACE-I) improve the prognosis of patients at high risk for atherothrombotic cardiovascular events. Angiotensin II has been reported to predispose to vascular inflammation and
thrombosis. Suppression of the increased ACE activity within plaque may lead to its stabilization and reduce the risk for rupture and cardiovascular events. Intravascular ultrasound (IVUS) radio-frequency signal (RF) analysis can discriminate among tissue types. IVUS-RF measurements of integrated backscatter (IB) are known to be larger in fibrous tissue than in lipid-rich, degenerated tissue. We clinically assessed by IVUS-RF analysis whether an ACE-I alters the structure of coronary atherosclerotic plaques. Methods: Fourteen consecutive patients undergoing percutaneous coronary intervention (PCI) with plasma total cholesterol (TC) level between 180 and 230 mg/dL were enrolled. We searched for echolucent plaques in non-PCI-influenced coronary regions and acquired IVUS-RF signals. The patients were randomly assigned into two groups: group A (n ⫽ 6) taking enalapril 5 mg/day and group C (n ⫽ 8) as control. In both groups, cholesterol-lowering therapy was diet only. At 6-month follow-up, IVUS-RF signals were sampled at the same plaque sites. Several regions of interest (ROIs) were placed on each plaque. IB was blindly measured in all ROIs (group A, n ⫽ 48; group C, n ⫽ 70) and compared between the paired ROIs at baseline and follow-up. Plaque volumes (PV) including the cross-sections sampled by IVUS-RF were also measured. Results: Although PV did not change over 6 months in either group, IB increased significantly in group A (⫺53.5 ⫾ 3.5 to ⫺49.3 ⫾ 4.9 dB; p ⬍0.0001) but not in group C. Plasma TC and low-density lipoprotein levels were not different between groups and did not change during the follow-up. Conclusions: These results suggest that an ACE-I alters acoustic properties of coronary plaques within 6 months. The plaque stabilization detectable by IVUS-RF analysis may result in improved long-term prognosis of atherosclerotic patients undergoing ACE-I treatment.
P O S T E R A B S T R A C T S
The American Journal of Cardiology姞
SEPTEMBER 30, 2004
TCT ABSTRACTS/Poster
143E
AM
(Hall D and E on Level 2)
Vulnerable Plaque Thursday, September 30, 2004 8:00-10:00 AM Hall D and E on Level 2
TCT 299 In Vivo Detection of a Coronary Artificial Target with a Near Infrared Spectroscopy Catheter. S. Waxman, Tufts- New England Medical Center, Boston, MASS; J. Tang, InfraRedX, Inc.; B.J. Marshik, InfraRedX, Inc.; H. Tan, InfraRedX, Inc.; K.R. Khabbaz, Tufts- New England Medical Center; R.J. Connolly, Tufts-New England Medical Center; T.A. Dunn, InfraRedX, Inc.; A.F. Zuluaga, InfraRedX, Inc.; S. DeJesus, InfraRedX, Inc.; J.D. Caplan, InfraRedX, Inc.; E.J. Muller, InfraRedX, Inc.
(Abstract nos. 298-303)
TCT 298 Influenza Virus in the Atherosclerotic Plaques of Human Aortic Aneurysms and Apo E Deficient Mice. M. Madjid, University of Texas-Houston, Texas Heart Institute; S. Litovsky, University of Texas-Houston, Texas Heart Institute; N. Sadeghi, University of Texas-Houston, Texas Heart Institute; I. Awan, University of TexasHouston, Texas Heart Institute; E.E. Porat, University of TexasHouston, Texas Heart Institute; P.R. Wyde, Baylor College of Medicine, Houston, Texas; W. Casscells, University of TexasHouston, Texas Heart Institute. Background: Influenza can trigger acute coronary syndromes, and influenza vaccination markedly reduces the risk of cardiovascular events. We investigated whether the influenza virus can be recovered from atherosclerotic plaques of humans and mice. Methods: We infected a series of apo E-deficient atherosclerotic mice with influenza A/HK/68 virus and also took aneurysmal aortic samples from 4 asymptomatic patients undergoing surgery for abdominal aortic aneurysm (AAA) repair. Homogenized arterial tissues were cultured for influenza virus. We used the standard titration method using Madin Darby canine kidney cells. We performed immunofluorescence (IF) studies using mouse monoclonal antibody to the nucleoprotein (NP) of influenza A virus and C3 complement. We ran reverse transcriptase polymerase chain reaction (RT-PCR) assays using primers specific for influenza A nucleoprotein. H&E and CD68 and CD3 staining (for macrophages and T lymphocytes) were employed for histopathologic examinations. Results: In mice, we could culture the influenza virus in high titers from lung, aorta, and heart on days 7 and 10. Blood culture was negative, indicating presence of the virus in the plaques in absence of viremia. We also found positive immunofluorescence for influenza antigens and positive RT-PCR assays for influenza NP gene in mice. In human samples, culture for the virus was negative. However, RT-PCR was positive for NP gene of the influenza virus in 3 of the 4 human AAA samples, and IF was positive in those samples. Samples with positive RT-PCR showed histologic features of atherosclerosis while the sample with negative RT-PCR was largely free of atherosclerosis. In mice, plaque influenza was associated with deposition of C3 complement and massive infiltration of inflammatory cells (e.g., macrophages and T cells) in the plaques. Conclusions: We have shown (to our knowledge for the first time) evidence for direct infection of the mouse aortic atherosclerotic and human aneurysmal aortic plaques with influenza virus. This infection was associated with pro-inflammatory changes in the plaque. If confirmed in future studies, the possible chronic influenza infection in the arteries may justify more extensive vaccination and even antiviral therapy to reduce the risk of cardiovascular events.
The American Journal of Cardiology姞
Background: Near infrared spectroscopy (NIR-S) can detect lipid-rich coronary plaques by identifying their chemical features ex vivo. However, a catheter-based system for in vivo use must overcome problems of cardiac motion and signal acquisition through blood. We tested whether an NIR-S catheter can distinguish an artificial target (AT) from human coronary arterial wall in a living porcine model. Methods: The human-to-porcine coronary xenograft model was used (JACC 2004;43:73A). Briefly, human coronary segments from fresh autopsy hearts and tubing are used to create a carotid-right atrial conduit in an open-chest anesthetized pig (45–50 kg). The xenograft is fixed to the anterior wall of the heart to simulate motion. An AT (a teflon material with spectral peaks in a range suitable for lipid identification by NIR-S) was secured onto a segment of the xenograft denuded of pericardial fat. The NIR-S catheter was advanced into the xenograft through a hemostatic valve attached to the circuit. Catheter position was confirmed visually and angiographically. NIR spectra were acquired 1) with the catheter stationary in the xenograft aimed at the AT (with and without the AT on the exposed vessel), 2) during 2 pullbacks along the entire length of the xenograft at 5 mm intervals with the AT secured in place, and 3) during 2 pullbacks with no AT. Results: Catheter-based NIR-S correctly identified the presence or absence of the AT through blood and arterial wall with the catheter stationary, using a principal component analysis—Mahalanobis distance algorithm with applied statistics. During pullback 2, the model detected the position of the AT and differentiated between segments with or without the AT. No AT signal was identified during pullback C. Results were reproducible in the different pullbacks. Conclusions: Intravascular NIR-S can detect an artificial target through blood and human coronary arterial wall, despite motion, in the human coronary xenograft porcine model. Our data, coupled with the previously documented ability of NIR-S to identify lipid pools ex vivo, support the potential use of catheter-based NIR-S to detect vulnerable plaques in patients.
TCT 300 High Resolution Micro Computed Tomographic Imaging of Vulnerable Plaques. P. Cherukuri, University of Texas Health Science Center; D. Vela; University of Texas Health Science Center, Houston; D. Cody, Anderson Cancer Center; E. Johnson, Anderson Cancer Center; R. Price, Anderson Cancer Center; J.L. Conyers, University of Texas Health Science Center, Houston; S. Litovsky, University of Texas Health Science Center, Houston; W. Casscells, University of Texas Health Science Center, Houston. Background: Microcalcifications within atherosclerotic plaques are believed to be a major marker of plaque vulnerability but are currently clinically undetectable. X-ray based imaging systems such as multislice and electron beam computed tomography (CT) are ineffective at resolving these microcalcific regions because of each system’s limited spatial resolution (⬃0.625–1 mm). However, high-resolution micro CT of coronary arteries may be capable of both localizing and characterizing these small foci of calcifications, without the aid of exogenous contrast agents or image postprocessing techniques.
SEPTEMBER 30, 2004
TCT ABSTRACTS/Poster
141E
P O S T E R A B S T R A C T S
THURSDAY 9/30/04 8:00 –10:00 Methods: Specimens of left anterior descending (LAD) coronary arteries were obtained from autopsy of individuals with coronary artery disease. GE Medical Systems RS-9 Micro CT system (80 kV, 450 A, 27-m isometric voxel size) imaged the arterial specimens ex vivo, and Hounsfield intensities were calibrated versus air and water standards. Images were corrected and processed using reconstruction software. Following the micro CT protocol, LAD specimens were decalcified, transversely sectioned every 80 to 90 m, and stained with Hematoxylin-Eosin. Histology was correlated with the corresponding crosssectional micro CT images. Results: We found significant correlation between micro CT and histology, in particular the distribution of microcalcifications within lipid-rich plaques. Fibrocalcific plaques were shown to be homogeneous in composition with a dense focus of calcification and were well correlated with histology. However, lipid-rich plaques were variably heterogeneous with ordered distributions of microcalcifications predominantly located deep and lateral to the lipid core(s). Histology of these lipid-rich plaques revealed clusters of microcalcifications, many as small as 10 m in diameter, deep within the arterial wall and peripheral to the lipid core. These microcalcifications were positively identified with the micro CT, and the images strongly indicate that the individual deposits are closely spaced. Conclusions: We believe that this is the first study demonstrating that high-resolution micro CT is capable of identifying microcalcific components of vulnerable plaques. The histological correlation with micro CT clearly reveals that microcalcifications manifest themselves deep from the lumen and peripheral to the lipid cores. Given the abundance of clinical data suggesting that these lipid-rich plaques are more prone to rupture rather than the fibrocalcific plaques, it is highly desirable to characterize the aforementioned plaques to diagnose highrisk patients. Future advances in clinical CT image resolution may someday allow for similar plaque characterization in vivo.
P O S T E R A B S T R A C T S
TCT 301 Significance of Fibrous Cap Thickness Measured by Optical Coherence Tomography. Y. Takeda, T. Suzuki, E. Tsuchikane, T. Itoh, M. Ehara, H. Sato, T. Matsubara, I. Shigenori, O. Katoh. Toyohashi Heart Center, Toyohashi, Japan. Background: Recent human histological studies report that fibrous caps (FCs) of vulnerable plaques are thinner (⬍0.065 mm) compared with those of stable plaques. Optical coherence tomography (OCT) may provide in vivo information on fibrous cap thickness. To evaluate the effect of OCT on characterization of FCs in coronary plaques in vivo, we used OCT to measure minimal thickness, maximal thickness, and length of the FCs in stable and vulnerable plaques.
AM
(Hall D and E on Level 2)
Results: OCT detected 7 FCs of 38 culprit lesions (38 patients). The 7 FCs of 7 culprit lesions were divided into 2 lesion subsets, group V (FCs in vulnerable lesions, n ⫽ 4) and group S (FCs in stable lesions, n ⫽ 3), determined by clinical demographics, intracoronary angioscopy, and intracoronary ultrasound. The mean minimal thickness of FC was significantly thinner in group V than in group S (0.03 mm vs 0.07 mm: p ⬍0.05). The mean maximal thickness of FC was 0.31 mm in group V and 0.38 mm in group S. The mean length of FC was 1.8 mm in group V and 2.6 mm in group S, although these differences between the 2 groups did not reach statistical significance. Conclusions: These results indicate that OCT is useful for the detection of vulnerable plaque in terms of the thickness of fibrous caps, although the OCT flushing system should be improved to obtain a stable image of the plaque.
TCT 302 Intravascular Ultrasound Radiofrequency Analysis Identifies Plaque Composition Depending on Risk Factors: In Vivo Virtual Histology. D. Bo¨se, University Essen, Germany; A. Schmermund, University Essen, Germany; P Margolis, Volcano Therapeutics Inc., Orange County, CA; A. Nair, Biomedical Engineering, The Cleveland Clinic Foundation, Ohio; D.G. Vince, Biomedical Engineering, The Cleveland Clinic Foundation, Ohio; H. Eggebrecht, Department of Cardiology, University Essen, Germany; C. Naber, Department of Cardiology, University Essen, Germany; R. Erbel, Department of Cardiology, University Essen, Germany. Background: Ex vivo, intravascular ultrasound (IVUS) radiofrequency (RF) data analysis has been demonstrated to predict coronary plaque composition. Fibrous, fibrolipidic, calcified, and lipid-necrotic areas can be identified within coronary plaques (“virtual histology”). Methods: We examined the first clinically available virtual histology system (Volcano Therapeutics, Orange County, California) in 75 patients (61 ⫾ 11 years, 64 men) undergoing coronary angiography. Using 30-MHz, 3.2-F mechanically rotating IVUS catheters (Boston Scientific). Automated pullback was performed (left anterior descending coronary artery in 43 patients, left circumflex coronary artery in 11, right coronary artery in 21). Results: Average cross-sectional fibrous plaque area was 2.4 ⫾ 1.8 mm2, fibrolipidic 1.1 ⫾ 1.4 mm2, calcified 0.1 ⫾ 0.2 mm2, and lipid-necrotic 0.6 ⫾ 0.6 mm2. Average fibrous plaque volume was 102.1 ⫾ 88.7 mm3, fibrolipidic 56.9 ⫾ 74.7 mm3, calcified 5.5 ⫾ 8.9 mm3, and lipid-necrotic 28.8 ⫾ 29.3 mm3. HDL cholesterol (HDL) was independently associated with overall plaque area (p ⫽ 0.017) and
Methods: The OCT optical fiber was automatically pulled back 1.0 mm per second (15.6 frames per second). A fibrous cap was defined as a thin, homogeneous band overlying a signal-poor region. The thickness of the fibrous cap was measured only in cases in which the fibrous cap was continuously observed in lengths of more than 1 mm by OCT.
142E
The American Journal of Cardiology姞
SEPTEMBER 30, 2004
TCT ABSTRACTS/Poster
THURSDAY 9/30/04 8:00 –10:00
AM
(Hall D and E on Level 2)
average % stenosis (p ⫽ 0.007). There was a significant inverse association between HDL cholesterol and lipid necrotic area (p ⫽ 0.001, Figure) and lipid core volume % (p ⫽ 0.02), as well as fibrous plaque area (p ⫽ 0.007); no association was observed with calcified and fibrolipid plaque components. There was a significant positive correlation between total cholesterol and calcified cross-sectional area (p ⬍0.001). Conclusions: Virtual histology IVUS RF analysis allows characterization of plaque composition in vivo and detects differences depending on risk factor profile. This may have implications for prognosis and assessment of treatment effects in patients undergoing invasive diagnostics.
TCT 303 Structural Effects of an Angiotensin-Converting Enzyme Inhibitor on Coronary Atherosclerotic Plaques as Clinically Assessed by Intravascular Ultrasound Radio-Frequency Signal Analysis. M. Yokoyama, Chiba University Hospital, Chiba, Japan; B.K. Courtney, Stanford University Medical Center, Palo Alto, CA; T. Nakayama, Chiba University Hospital, Chiba, Japan; S. Namikawa, Chiba University Hospital, Chiba, Japan, T. Koizumi, Stanford University Medical Center, Palo Alto, CA; M. Nameki, Chiba University Hospital, Chiba, Japan; N. Komiyama, Saitama Medical School, Moroyama, Japan. Background: Many clinical studies have shown that angiotensinconverting enzyme inhibitors (ACE-I) improve the prognosis of patients at high risk for atherothrombotic cardiovascular events. Angiotensin II has been reported to predispose to vascular inflammation and
thrombosis. Suppression of the increased ACE activity within plaque may lead to its stabilization and reduce the risk for rupture and cardiovascular events. Intravascular ultrasound (IVUS) radio-frequency signal (RF) analysis can discriminate among tissue types. IVUS-RF measurements of integrated backscatter (IB) are known to be larger in fibrous tissue than in lipid-rich, degenerated tissue. We clinically assessed by IVUS-RF analysis whether an ACE-I alters the structure of coronary atherosclerotic plaques. Methods: Fourteen consecutive patients undergoing percutaneous coronary intervention (PCI) with plasma total cholesterol (TC) level between 180 and 230 mg/dL were enrolled. We searched for echolucent plaques in non-PCI-influenced coronary regions and acquired IVUS-RF signals. The patients were randomly assigned into two groups: group A (n ⫽ 6) taking enalapril 5 mg/day and group C (n ⫽ 8) as control. In both groups, cholesterol-lowering therapy was diet only. At 6-month follow-up, IVUS-RF signals were sampled at the same plaque sites. Several regions of interest (ROIs) were placed on each plaque. IB was blindly measured in all ROIs (group A, n ⫽ 48; group C, n ⫽ 70) and compared between the paired ROIs at baseline and follow-up. Plaque volumes (PV) including the cross-sections sampled by IVUS-RF were also measured. Results: Although PV did not change over 6 months in either group, IB increased significantly in group A (⫺53.5 ⫾ 3.5 to ⫺49.3 ⫾ 4.9 dB; p ⬍0.0001) but not in group C. Plasma TC and low-density lipoprotein levels were not different between groups and did not change during the follow-up. Conclusions: These results suggest that an ACE-I alters acoustic properties of coronary plaques within 6 months. The plaque stabilization detectable by IVUS-RF analysis may result in improved long-term prognosis of atherosclerotic patients undergoing ACE-I treatment.
P O S T E R A B S T R A C T S
The American Journal of Cardiology姞
SEPTEMBER 30, 2004
TCT ABSTRACTS/Poster
143E