Abstract 16948: Local Low Endothelial Shear Stress (ESS) Provides Incremental Prediction of Non-culprit MACE in Addition to Plaque Burden, Minimal Lumen Area, and Plaque Morphology: The PROSPECT Study
Introduction: Low ESS, a pro-inflammatory stimulus, is an important predictor of coronary plaque development/progression. Whether low ESS adds incremental predictive value for future major adverse cardiac events (MACE) in untreated coronary lesions in high-risk patients with an acute coronary syndrome (ACS) is unknown.
Methods: In the PROSPECT study, 697 patients with ACS underwent 3-vessel intracoronary imaging. Independent predictors of non-culprit (nc) lesion MACE from untreated coronary lesions in 3 year followup (f/u) were large plaque burden (PB), small minimum lumen area (MLA), and thin cap fibroatheroma (TCFA) morphology. In the present analysis, all nc-lesions leading to a new MACE in f/u (nc-MACE lesions, n=50) and ~4-fold randomly selected control nc-lesions without f/u MACE (nc-non-MACE lesions) were analyzed. Baseline ESS for each lesion was calculated using computational fluid dynamics. A propensity score for low ESS was determined accounting for PB, MLA, TCFA, artery and location in the artery. Local ESS (lowest ESS in 90o arc around the artery) was then examined for incremental association with MACE.
Results: Imaging was sufficient for analysis in 32 nc-MACE lesions. Two nc-MACE lesions were excluded due to unreliable lesion morphology. Non-fibroatheromas were too few for analysis and excluded. Final dataset included 145 lesions: 13 nc-MACE TCFA, 10 nc-MACE thick cap fibroatheroma (ThCFA), and 122 non-nc-MACE lesions (63 TCFA, 59 ThCFA). Cumulative frequency distribution shows lesions responsible for future nc-MACE frequently exhibited low ESS (Figure). In a propensity-adjusted multivariable model, low ESS was strongly associated with nc-MACE in f/u (odds ratio 0.16 [95% CI 0.06-0.40], p<0.0001).
Conclusions: After accounting for large PB, small MLA, TCFA, and lesion location, low local ESS adds significant and substantial incremental predictive value to identify high-risk untreated lesions likely to cause MACE during 3 year followup.
Author Disclosures: P.H. Stone: None. A. Maehara: None. A.U. Coskun: None. C.C. Maynard: None. I. Andreou: None. G. Siasos: None. M. Zaromitidou: None. D. Fotiadis: None. K. Stefanou: None. M. Papafaklis: None. L. Michalis: None. A.J. Lansky: None. G.S. Mintz: None. P.W. Serruys: None. C.L. Feldman: None. G.W. Stone: None.
- © 2015 by American Heart Association, Inc.