Prediction of Progression of Coronary Artery Disease and Clinical Outcomes Using Vascular Profiling of Endothelial Shear Stress and Arterial Plaque Characteristics: The PREDICTION Study
Background—Atherosclerotic plaques progress in a highly individual manner. The purposes of the PREDICTION Study were to determine the role of local hemodynamic and vascular characteristics in coronary plaque progression and to relate plaque changes to clinical events.
Methods and Results—Vascular profiling (VP), using coronary angiography and intravascular ultrasound, was employed to reconstruct each artery and calculate endothelial shear stress (ESS) and plaque/remodeling characteristics in-vivo. Three-vessel VP (2.7 arteries per patient) was performed at baseline in 506 patients with acute coronary syndrome (ACS) treated with a percutaneous coronary intervention (PCI) and in a subset of 374 (74%) consecutive patients 6-10 months later to assess plaque natural history. Each reconstructed artery was divided into sequential 3-mm segments for serial analysis. One-year clinical followup was completed in 99.2%. Symptomatic clinical events were infrequent: only 1(0.2%) cardiac death; 4(0.8%) patients with new ACS in non-stented segments; 15(3.0%) patients hospitalized for stable angina. Increase in plaque area (primary endpoint) was predicted by baseline large plaque burden; decrease in lumen area (secondary endpoint) was independently predicted by baseline large plaque burden and low ESS. Large plaque size and low ESS independently predicted the exploratory endpoints of increased plaque burden and worsening of clinically relevant luminal obstructions treated with a PCI at followup. The combination of independent baseline predictors had a 41% positive- and 92% negative predictive value to predict progression of obstruction treated with a PCI.
Conclusions—Large plaque burden and low local ESS provide independent and additive prediction to identify plaques that develop progressive enlargement and lumen narrowing.
Clinical Trial Registration Information—clinicaltrials.gov; Identifier: NCT01316159.
- Received January 27, 2012.
- Accepted May 16, 2012.
- Copyright © 2012, American Heart Association, Inc. All rights reserved. Unauthorized use prohibited