Zhongzhao Teng1, Adam J Brown1, Patrick A Calvert1, Richard A Parker1, Daniel R Obaid1, Yuan Huang1, Stephen P Hoole1, Nick E J West1, Jonathan H Gillard1, Martin R Bennett2. 1. From the Department of Radiology (Z.T., Y.H., J.H.G.), Department of Engineering (Z.T.), Division of Cardiovascular Medicine (A.J.B., P.A.C., D.R.O., M.R.B.), and Centre for Applied Medical Statistics, University of Cambridge, Cambridge, UK (R.A.P.); and Department of Interventional Cardiology, Papworth Hospital NHS Trust, Cambridge, UK (S.P.H., N.E.J.W.). 2. From the Department of Radiology (Z.T., Y.H., J.H.G.), Department of Engineering (Z.T.), Division of Cardiovascular Medicine (A.J.B., P.A.C., D.R.O., M.R.B.), and Centre for Applied Medical Statistics, University of Cambridge, Cambridge, UK (R.A.P.); and Department of Interventional Cardiology, Papworth Hospital NHS Trust, Cambridge, UK (S.P.H., N.E.J.W.). mrb@mole.bio.cam.ac.uk.
Abstract
BACKGROUND: Atherosclerotic plaques underlying most myocardial infarctions have thin fibrous caps and large necrotic cores; however, these features alone do not reliably identify plaques that rupture. Rupture occurs when plaque structural stress (PSS) exceeds mechanical strength. We examined whether PSS could be calculated in vivo based on virtual histology (VH) intravascular ultrasound and whether PSS varied according to plaque composition, subtype, or clinical presentation. METHODS AND RESULTS: A total of 4429 VH intravascular ultrasound frames from 53 patients were analyzed, identifying 99 584 individual plaque components. PSS was calculated by finite element analysis in whole vessels, in individual plaques, and in higher-risk regions (plaque burden ≥70%, mean luminal area ≤4 mm(2), noncalcified VH-defined thin-cap fibroatheroma). Plaque components including total area/arc of calcification (R(2)=0.33; P<0.001 and R(2)=0.28; P<0.001) and necrotic core (R(2)=0.18; P<0.001 and R(2)=0.15; P<0.001) showed complex, nonlinear relationships with PSS. PSS was higher in noncalcified VH-defined thin-cap fibroatheroma compared with thick-cap fibroatheromas (median [Q1-Q3], 8.44 [6.97-10.64] versus 7.63 [6.37-9.68]; P=0.002). PSS was also higher in patients with an acute coronary syndrome, where mean luminal area ≤4 mm(2) (8.24 [7.06-9.93] versus 7.72 [6.33-9.34]; P=0.03), plaque burden ≥70% (9.18 [7.44-10.88] versus 7.93 [6.16-9.46]; P=0.02), and in noncalcified VH-defined thin-cap fibroatheroma (9.23 [7.33-11.44] versus 7.65 [6.45-8.62]; P=0.02). Finally, PSS increased the positive predictive value for VH intravascular ultrasound to identify clinical presentation. CONCLUSIONS: Finite element analysis modeling demonstrates that structural stress is highly variable within plaques, with increased PSS associated with plaque composition, subtype, and higher-risk regions in patients with acute coronary syndrome. PSS may represent a novel tool to analyze the dynamic behavior of coronary plaques with the potential to improve prediction of plaque rupture.
BACKGROUND: Atherosclerotic plaques underlying most myocardial infarctions have thin fibrous caps and large necrotic cores; however, these features alone do not reliably identify plaques that rupture. Rupture occurs when plaque structural stress (PSS) exceeds mechanical strength. We examined whether PSS could be calculated in vivo based on virtual histology (VH) intravascular ultrasound and whether PSS varied according to plaque composition, subtype, or clinical presentation. METHODS AND RESULTS: A total of 4429 VH intravascular ultrasound frames from 53 patients were analyzed, identifying 99 584 individual plaque components. PSS was calculated by finite element analysis in whole vessels, in individual plaques, and in higher-risk regions (plaque burden ≥70%, mean luminal area ≤4 mm(2), noncalcified VH-defined thin-cap fibroatheroma). Plaque components including total area/arc of calcification (R(2)=0.33; P<0.001 and R(2)=0.28; P<0.001) and necrotic core (R(2)=0.18; P<0.001 and R(2)=0.15; P<0.001) showed complex, nonlinear relationships with PSS. PSS was higher in noncalcified VH-defined thin-cap fibroatheroma compared with thick-cap fibroatheromas (median [Q1-Q3], 8.44 [6.97-10.64] versus 7.63 [6.37-9.68]; P=0.002). PSS was also higher in patients with an acute coronary syndrome, where mean luminal area ≤4 mm(2) (8.24 [7.06-9.93] versus 7.72 [6.33-9.34]; P=0.03), plaque burden ≥70% (9.18 [7.44-10.88] versus 7.93 [6.16-9.46]; P=0.02), and in noncalcified VH-defined thin-cap fibroatheroma (9.23 [7.33-11.44] versus 7.65 [6.45-8.62]; P=0.02). Finally, PSS increased the positive predictive value for VH intravascular ultrasound to identify clinical presentation. CONCLUSIONS: Finite element analysis modeling demonstrates that structural stress is highly variable within plaques, with increased PSS associated with plaque composition, subtype, and higher-risk regions in patients with acute coronary syndrome. PSS may represent a novel tool to analyze the dynamic behavior of coronary plaques with the potential to improve prediction of plaque rupture.
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