OCT assessment of thin-cap fibroatheroma distribution in native coronary arteries.

OBJECTIVES We evaluated the geographic distribution of thin-cap fibroatheromas (TCFAs) in the coronary arteries using optical coherence tomography (OCT), a high-resolution imaging modality. BACKGROUND Plaque rupture is the most frequent cause of acute myocardial infarction (AMI). It has been recognized that TCFA is the primary plaque type at the site of plaque rupture. METHODS We performed 3-vessel OCT examinations in 55 patients: 35 AMI and 20 stable angina pectoris patients. The criteria for TCFA in an OCT image was a lipid-rich plaque with fibrotic cap thickness <65 microm. The distance between each TCFA location and the respective coronary artery ostium was measured with motorized OCT imaging pullback. The total length of all 3 coronary arteries imaged by OCT pullbacks was 82 +/- 21 mm in the left anterior descending coronary artery (LAD), 67 +/- 26 mm in the left circumflex coronary artery (LCx), and 104 +/- 32 mm in the right coronary artery (RCA). RESULTS OCT detected 94 TCFAs in 165 coronary arteries. The minimum fibrous-cap thickness of TCFAs was 57.4 +/- 5.4 microm in AMI patients, and 55.9 +/- 7.3 microm in stable angina pectoris patients (p = 0.4). Of the total of 94 TCFAs, 28 were detected in the LAD, 18 in the LCx, and 48 in the RCA. Most LAD TCFAs were located between 0 and 30 mm from the LAD ostium (76%). Conversely, LCx and RCA TCFAs were evenly distributed throughout the entire coronary length. The clustering of the TCFAs was similar in culprit segments as compared with nonculprit segments. In AMI patients, most LAD TCFAs were distributed near side branches, mainly positioned opposite the side branch bifurcation. CONCLUSIONS Three-vessel OCT imaging showed that TCFAs tend to cluster in predictable spots within the proximal segment of the LAD, but develop relatively evenly in the LCx and RCA arteries.

[1]  W. O’Neill,et al.  Multiple complex coronary plaques in patients with acute myocardial infarction. , 2000, The New England journal of medicine.

[2]  J. Badimón,et al.  Atherosclerotic plaque rupture and thrombosis. Evolving concepts. , 1990, Circulation.

[3]  Gary S. Mintz,et al.  The site of plaque rupture in native coronary arteries: a three-vessel intravascular ultrasound analysis. , 2005, Journal of the American College of Cardiology.

[4]  C L Feldman,et al.  Intravascular hemodynamic factors responsible for progression of coronary atherosclerosis and development of vulnerable plaque. , 2000, Current opinion in cardiology.

[5]  G. Getz,et al.  Site Specificity of Atherosclerosis: Site-Selective Responses to Atherosclerotic Modulators , 2004, Arteriosclerosis, thrombosis, and vascular biology.

[6]  E. Boerwinkle,et al.  From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part I. , 2003, Circulation.

[7]  M J Davies,et al.  Thrombosis and acute coronary-artery lesions in sudden cardiac ischemic death. , 1984, The New England journal of medicine.

[8]  R. Virmani,et al.  Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. , 2000, Arteriosclerosis, thrombosis, and vascular biology.

[9]  Y. Neishi,et al.  Measurement of the thickness of the fibrous cap by optical coherence tomography. , 2006, American heart journal.

[10]  Seung‐Jung Park,et al.  Comparison of Coronary Plaque Rupture Between Stable Angina and Acute Myocardial Infarction: A Three-Vessel Intravascular Ultrasound Study in 235 Patients , 2004, Circulation.

[11]  P. Fitzgerald,et al.  Orientation of intracoronary ultrasonography: looking beyond the artery. , 1998, Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography.

[12]  M. Hori,et al.  Extensive development of vulnerable plaques as a pan-coronary process in patients with myocardial infarction: an angioscopic study. , 2001, Journal of the American College of Cardiology.

[13]  G Finet,et al.  Multiple Atherosclerotic Plaque Rupture in Acute Coronary Syndrome: A Three-Vessel Intravascular Ultrasound Study , 2002, Circulation.

[14]  C. Zarins,et al.  Carotid Bifurcation Atherosclerosis: Quantitative Correlation of Plaque Localization with Flow Velocity Profiles and Wall Shear Stress , 1983, Circulation research.

[15]  N. Weissman,et al.  Volumetric intravascular ultrasound quantification of the amount of atherosclerosis and calcium in nonstenotic arterial segments. , 2002, The American journal of cardiology.

[16]  R. Virmani,et al.  The thin-cap fibroatheroma: a type of vulnerable plaque: The major precursor lesion to acute coronary syndromes , 2001, Current opinion in cardiology.

[17]  S. Alper,et al.  Hemodynamic shear stress and its role in atherosclerosis. , 1999, JAMA.

[18]  Sharon-Lise T. Normand,et al.  Coronary Artery Spatial Distribution of Acute Myocardial Infarction Occlusions , 2004, Circulation.

[19]  E. Halpern,et al.  Characterization of Human Atherosclerosis by Optical Coherence Tomography , 2002, Circulation.

[20]  Brett E. Bouma,et al.  In Vivo Characterization of Coronary Atherosclerotic Plaque by Use of Optical Coherence Tomography , 2005, Circulation.

[21]  V. Fuster,et al.  The pathogenesis of coronary artery disease and the acute coronary syndromes (2). , 1992, The New England journal of medicine.

[22]  E. Arbustini,et al.  Eccentric atherosclerotic plaques with positive remodelling have a pericardial distribution: a permissive role of epicardial fat? A three-dimensional intravascular ultrasound study of left anterior descending artery lesions. , 2003, European heart journal.

[23]  A. Gotlieb,et al.  Reduced in vitro repair in endothelial cells harvested from the intercostal ostia of porcine thoracic aorta. , 1999, Arteriosclerosis, thrombosis, and vascular biology.

[24]  P. Serruys,et al.  A new imaging technique to study 3-D plaque and shear stress distribution in human coronary artery bifurcations in vivo. , 2007, Journal of biomechanics.

[25]  K. Cunningham,et al.  The role of shear stress in the pathogenesis of atherosclerosis , 2005, Laboratory Investigation.