Coronary plaque composition of culprit/target lesions according to the clinical presentation: a virtual histology intravascular ultrasound analysis.

AIMS To evaluate the plaque composition obtained by virtual histology (VH) IVUS according to the clinical presentation and to compare those data to previously published histopathology data. METHODS AND RESULTS VH was performed on 95 de novo significant lesions (>75% stenosis) in 85 patients [28 acute coronary syndrome (ACS) patients, 30 lesions; 57 stable angina pectoris (SAP) patients, 65 lesions]. There were a higher prevalence of positive remodelling (47 vs. 22%, P=0.013), thrombus (20 vs. 1.5%, P=0.0037), and echo-lucent area (23.3 vs. 7.7%, P=0.047) in ACS patients. At the minimal lumen site, fibrous plaque area was significantly larger in ACS lesions than in SAP lesions (66.0+/-10.7 vs. 61.4+/-8.9%, P=0.034), whereas necrotic core and dense calcium plaque area were smaller in ACS lesions (Necrotic core: 6.8+/-6.0 vs. 11.0+/-8.3%, P=0.02; Dense calcium: 2.6+/-3.0 vs. 4.9+/-5.8%, P=0.03). No differences in rate of thin cap fibroatheroma, thick fibrotheroma, or for the presence of multiple necrotic core layers were observed between both groups. CONCLUSION Plaque composition obtained by VH-IVUS shows less necrotic core and more fibrous tissue in ACS compared to SAP lesions, which is in contradiction with previously published histopathologic data.

[1]  R. Virmani,et al.  Accuracy of in vivo coronary plaque morphology assessment: a validation study of in vivo virtual histology compared with in vitro histopathology. , 2006, Journal of the American College of Cardiology.

[2]  S. Nakatani,et al.  Morphology of vulnerable coronary plaque: insights from follow-up of patients examined by intravascular ultrasound before an acute coronary syndrome. , 2000, Journal of the American College of Cardiology.

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

[4]  S E Nissen,et al.  Extent and direction of arterial remodeling in stable versus unstable coronary syndromes : an intravascular ultrasound study. , 2000, Circulation.

[5]  G Baumann,et al.  Angioscopic evaluation of atherosclerotic plaques: validation by histomorphologic analysis and association with stable and unstable coronary syndromes. , 1996, Journal of the American College of Cardiology.

[6]  R. Ross.  Atherosclerosis is an inflammatory disease , 1999 .

[7]  Y. Uchida,et al.  Prediction of acute coronary syndromes by percutaneous coronary angioscopy in patients with stable angina. , 1995, American heart journal.

[8]  Marco Valgimigli,et al.  In vivo intravascular ultrasound-derived thin-cap fibroatheroma detection using ultrasound radiofrequency data analysis. , 2005, Journal of the American College of Cardiology.

[9]  N. Obuchowski,et al.  Assessing spectral algorithms to predict atherosclerotic plaque composition with normalized and raw intravascular ultrasound data. , 2001, Ultrasound in Medicine and Biology.

[10]  M. Davies,et al.  Risk of thrombosis in human atherosclerotic plaques: role of extracellular lipid, macrophage, and smooth muscle cell content. , 1993, British heart journal.

[11]  D. Faxon,et al.  Five-year angiographic follow-up of factors associated with progression of coronary artery disease in the Coronary Artery Surgery Study (CASS). CASS Participating Investigators and Staff. , 1993, Journal of the American College of Cardiology.

[12]  M. Nobuyoshi,et al.  Progression of coronary atherosclerosis: is coronary spasm related to progression? , 1991, Journal of the American College of Cardiology.

[13]  J. Hodgson,et al.  Intracoronary ultrasound imaging: correlation of plaque morphology with angiography, clinical syndrome and procedural results in patients undergoing coronary angioplasty. , 1993, Journal of the American College of Cardiology.

[14]  A. Angelini,et al.  Factors influencing the presence or absence of acute coronary artery thrombi in sudden ischaemic death. , 1989, European heart journal.

[15]  J. Deckers,et al.  Anatomical Progression of Coronary Artery Disease in Humans as Seen by Prospective, Repeated, Quantitated Coronary Angiography: Relation to Clinical Events and Risk Factors , 1992, Circulation.

[16]  E. Topol,et al.  Comparison of histopathologic coronary lesions obtained from directional atherectomy in stable angina versus acute coronary syndromes. , 1994, The American journal of cardiology.

[17]  P. Serruys,et al.  Histologic characteristics of tissue excised during directional coronary atherectomy in stable and unstable angina pectoris. , 1993, The American journal of cardiology.

[18]  B Meier,et al.  Relation of the site of acute myocardial infarction to the most severe coronary arterial stenosis at prior angiography. , 1992, The American journal of cardiology.

[19]  Elena Bonanno,et al.  Diffuse and active inflammation occurs in both vulnerable and stable plaques of the entire coronary tree: a histopathologic study of patients dying of acute myocardial infarction. , 2005, Journal of the American College of Cardiology.

[20]  M J Davies,et al.  Stability and instability: two faces of coronary atherosclerosis. The Paul Dudley White Lecture 1995. , 1996, Circulation.

[21]  V. Fuster,et al.  Angiographic progression of coronary artery disease and the development of myocardial infarction. , 1988, Journal of the American College of Cardiology.

[22]  W. Roberts,et al.  Morphometric analysis of the composition of atherosclerotic plaques in the four major epicardial coronary arteries in acute myocardial infarction and in sudden coronary death. , 1989, Circulation.

[23]  R. Detrano,et al.  The dynamics of progression of coronary atherosclerosis studied in 168 medically treated patients who underwent coronary arteriography three times. , 1989, American heart journal.

[24]  V. Fuster,et al.  Coronary plaque disruption. , 1995, Circulation.

[25]  Weifeng Shen,et al.  Relationship between coronary arterial remodeling and clinical presentation. , 2003, Chinese medical journal.

[26]  W. Laskey,et al.  Clinical Progression of Incidental, Asymptomatic Lesions Discovered During Culprit Vessel Coronary Intervention , 2005, Circulation.

[27]  R. Virmani,et al.  Coronary plaque erosion without rupture into a lipid core. A frequent cause of coronary thrombosis in sudden coronary death. , 1996, Circulation.

[28]  E. Tuzcu,et al.  Coronary Plaque Classification With Intravascular Ultrasound Radiofrequency Data Analysis , 2002, Circulation.

[29]  H. Fujita,et al.  Assessment of vulnerable plaques causing acute coronary syndrome using integrated backscatter intravascular ultrasound. , 2006, Journal of the American College of Cardiology.

[30]  K. Channon,et al.  Differential Expression of Tissue Factor Protein in Directional Atherectomy Specimens From Patients With Stable and Unstable Coronary Syndromes , 1995 .

[31]  R. Virmani,et al.  Pathology of the Vulnerable Plaque , 2006 .

[32]  高野 雅充.  Mechanical and structural characteristics of vulnerable plaques : analysis by coronary angioscopy and intravascular ultrasound , 2002 .

[33]  Renu Virmani,et al.  Vulnerable plaque: the pathology of unstable coronary lesions. , 2002, Journal of interventional cardiology.

[34]  C von Birgelen,et al.  Plaque distribution and vascular remodeling of ruptured and nonruptured coronary plaques in the same vessel: an intravascular ultrasound study in vivo. , 2001, Journal of the American College of Cardiology.

[35]  K. Channon,et al.  Differential expression of tissue factor protein in directional atherectomy specimens from patients with stable and unstable coronary syndromes. , 1995, Circulation.

[36]  P. Serruys,et al.  Coronary plaque composition of nonculprit lesions, assessed by in vivo intracoronary ultrasound radio frequency data analysis, is related to clinical presentation. , 2006, American heart journal.

[37]  V. Fuster,et al.  Macrophage Infiltration in Acute Coronary Syndromes: Implications for Plaque Rupture , 1994, Circulation.