Relationship between coronary arterial remodeling, fibrous cap thickness and high-sensitivity C-reactive protein levels in patients with acute coronary syndrome.

BACKGROUND Thin-capped fibroatheroma (TCFA) is a recognized precursor lesion for acute coronary syndrome (ACS). Positive remodeling (PR) is the predominant pattern of arterial remodeling in patients with ACS. The aim of this study was to evaluate the relationship between coronary arterial remodeling, fibrous cap thickness and high-sensitivity C-reactive protein (hs-CRP) concentration in patients with ACS. METHODS AND RESULTS The 47 consecutive ACS patients were enrolled in this study. Arterial remodeling of culprit plaque was assessed by intravascular ultrasound, and fibrous cap thickness was measured by optical coherence tomography. The remodeling index (RI) was calculated as lesion divided by the reference external elastic membrane cross-sectional area, and PR was defined as RI >1.05 (PR group). TCFA were observed more frequently in the PR group than in the intermediate and negative remodeling (IR/NR) groups (59% vs 17%, P<0.01). RI was inversely correlated with fibrous cap thickness (r=0.47, P=0.02). hs-CRP levels were higher in the PR group than in the IR/NR groups (0.32 +/-0.26 vs 0.18 +/-0.14 mg/dl, P=0.02). CONCLUSIONS Coronary arterial remodeling, fibrous cap thickness and hs-CRP level in patients with ACS are associated with each other. This result suggests that inflammation simultaneously contributes to both plaque growth and plaque instability.

[1]  T. Akasaka,et al.  Safety and usefulness of non-occlusion image acquisition technique for optical coherence tomography. , 2008, Circulation journal : official journal of the Japanese Circulation Society.

[2]  Y. Nishibori,et al.  C‐Reactive Protein and Lesion Morphology in Patients With Acute Myocardial Infarction , 2003, Circulation.

[3]  J. Fujimoto,et al.  Optical coherence tomography for optical biopsy. Properties and demonstration of vascular pathology. , 1996, Circulation.

[4]  K. Shimada,et al.  Multiple plaque rupture and C-reactive protein in acute myocardial infarction. , 2005, Journal of the American College of Cardiology.

[5]  B Hillen,et al.  Relation of arterial geometry to luminal narrowing and histologic markers for plaque vulnerability: the remodeling paradox. , 1998, Journal of the American College of Cardiology.

[6]  A. Newby,et al.  Dual role of matrix metalloproteinases (matrixins) in intimal thickening and atherosclerotic plaque rupture. , 2005, Physiological reviews.

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

[8]  Eiji Toyota,et al.  Visualization of neointima formation by optical coherence tomography. , 2005, International heart journal.

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

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

[11]  Brett E. Bouma,et al.  In vivo association between positive coronary artery remodelling and coronary plaque characteristics assessed by intravascular optical coherence tomography. , 2008, European heart journal.

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

[13]  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.

[14]  E. Falk Plaque rupture with severe pre-existing stenosis precipitating coronary thrombosis. Characteristics of coronary atherosclerotic plaques underlying fatal occlusive thrombi. , 1983, British heart journal.

[15]  T. Kawamoto,et al.  Relationship between coronary remodeling and plaque characterization in patients without clinical evidence of coronary artery disease. , 2008, Atherosclerosis.

[16]  Takashi Akasaka,et al.  Assessment of culprit lesion morphology in acute myocardial infarction: ability of optical coherence tomography compared with intravascular ultrasound and coronary angioscopy. , 2007, Journal of the American College of Cardiology.

[17]  C. Mclachlan,et al.  Are elevations of N-terminal probrain natriuretic peptide in endurance athletes after prolonged strenuous exercise due to systemic inflammatory cytokines? , 2006, American heart journal.

[18]  Jeroen J. Bax,et al.  Evaluation of plaque characteristics in acute coronary syndromes: non-invasive assessment with multi-slice computed tomography and invasive evaluation with intravascular ultrasound radiofrequency data analysis. , 2008, European heart journal.

[19]  K. Seung,et al.  Visualization of coronary atherosclerotic plaques in patients using optical coherence tomography: comparison with intravascular ultrasound. , 2002, Journal of the American College of Cardiology.

[20]  C. Zarins,et al.  Compensatory enlargement of human atherosclerotic coronary arteries. , 1987, The New England journal of medicine.

[21]  A. Yeung,et al.  Impact of coronary artery remodeling on clinical presentation of coronary artery disease: an intravascular ultrasound study. , 2001, Journal of the American College of Cardiology.

[22]  S. Umemura,et al.  C-reactive protein elevation and rapid angiographic progression of nonculprit lesion in patients with non-ST-segment elevation acute coronary syndrome. , 2008, Circulation journal : official journal of the Japanese Circulation Society.

[23]  Eiji Toyota,et al.  Assessment of coronary intima--media thickness by optical coherence tomography: comparison with intravascular ultrasound. , 2005, Circulation journal : official journal of the Japanese Circulation Society.

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

[25]  Eiji Toyota,et al.  Assessment of coronary arterial thrombus by optical coherence tomography. , 2006, The American journal of cardiology.

[26]  S. Umemura,et al.  Serum amyloid A is a better predictor of clinical outcomes than C-reactive protein in non-ST-segment elevation acute coronary syndromes. , 2007, Circulation journal : official journal of the Japanese Circulation Society.

[27]  N. Bruining,et al.  Effect of perindopril on coronary remodelling: insights from a multicentre, randomized study. , 2007, European heart journal.

[28]  C. Tracy,et al.  American College of Cardiology Clinical Expert Consensus Document on Standards for Acquisition, Measurement and Reporting of Intravascular Ultrasound Studies (IVUS). A report of the American College of Cardiology Task Force on Clinical Expert Consensus Documents. , 2001, Journal of the American College of Cardiology.

[29]  G. Stone,et al.  Coronary Plaque Morphology and Frequency of Ulceration Distant From Culprit Lesions in Patients With Unstable and Stable Presentation , 2003, Arteriosclerosis, thrombosis, and vascular biology.

[30]  Hiroto Tsujioka,et al.  Distribution and frequency of thin-capped fibroatheromas and ruptured plaques in the entire culprit coronary artery in patients with acute coronary syndrome as determined by optical coherence tomography. , 2008, The American journal of cardiology.

[31]  Á. Avezum,et al.  Predictors of hospital mortality in the global registry of acute coronary events. , 2003, Archives of internal medicine.

[32]  Antonio Colombo,et al.  Association of plaque characterization by intravascular ultrasound virtual histology and arterial remodeling. , 2005, The American journal of cardiology.

[33]  Kazushi Takemoto,et al.  Morphology of Exertion-Triggered Plaque Rupture in Patients With Acute Coronary Syndrome: An Optical Coherence Tomography Study , 2008, Circulation.

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