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Clinical Predictors for Lack of Favorable Vascular Response to Statin Therapy in Patients With Coronary Artery Disease: A Serial Optical Coherence Tomography Study Exercise unmasks distinct pathophysiologic features in heart failure with preserved ejection fraction and pulmonary vascular disease Low shear stress induces endothelial reactive oxygen species via the AT1R/eNOS/NO pathway Difference in basic concept of coronary bifurcation intervention between Korea and Japan. Insight from questionnaire in experts of Korean and Japanese bifurcation clubs Fractional Flow Reserve–Guided PCI for Stable Coronary Artery Disease Optical coherence tomography versus intravascular ultrasound to evaluate coronary artery disease and percutaneous coronary intervention Coronary Atherosclerosis T1-Weighed Characterization With Integrated Anatomical Reference: Comparison With High-Risk Plaque Features Detected by Invasive Coronary Imaging Lipid-rich plaque and myocardial perfusion after successful stenting in patients with non-ST-segment elevation acute coronary syndrome: an optical coherence tomography study Individual Lesion-Level Meta-Analysis Comparing Various Doses of Intracoronary Bolus Injection of Adenosine With Intravenous Administration of Adenosine for Fractional Flow Reserve Assessment Impact of an optical coherence tomography guided approach in acute coronary syndromes: A propensity matched analysis from the international FORMIDABLE-CARDIOGROUP IV and USZ registry

Clinical Trial2012 Jul 10;126(2):172-81.

JOURNAL:Circulation. Article Link

Prediction of progression of coronary artery disease and clinical outcomes using vascular profiling of endothelial shear stress and arterial plaque characteristics: the PREDICTION Study

Stone PH, Saito S, PREDICTION Investigators. Keywords: atherosclerosis; endothelium; natural history; shear stress

ABSTRACT


BACKGROUNDAtherosclerotic plaques progress in a highly individual manner. The purposes of the Prediction of Progression of Coronary Artery Disease and Clinical Outcome Using Vascular Profiling of Shear Stress and Wall Morphology (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, using coronary angiography and intravascular ultrasound, was used to reconstruct each artery and calculate endothelial shear stress and plaque/remodeling characteristics in vivo. Three-vessel vascular profiling (2.7 arteries per patient) was performed at baseline in 506 patients with an acute coronary syndrome treated with a percutaneous coronary intervention and in a subset of 374 (74%) consecutive patients 6 to 10 months later to assess plaque natural history. Each reconstructed artery was divided into sequential 3-mm segments for serial analysis. One-year clinical follow-up was completed in 99.2%. Symptomatic clinical events were infrequent: only 1 (0.2%) cardiac death; 4 (0.8%) patients with new acute coronary syndrome in nonstented segments; and 15 (3.0%) patients hospitalized for stable angina. Increase in plaque area (primary end point) was predicted by baseline large plaque burden; decrease in lumen area (secondary end point) was independently predicted by baseline large plaque burden and low endothelial shear stress. Large plaque size and low endothelial shear stress independently predicted the exploratory end points of increased plaque burden and worsening of clinically relevant luminal obstructions treated with a percutaneous coronary intervention at follow-up. The combination of independent baseline predictors had a 41% positive and 92% negative predictive value to predict progression of an obstruction treated with a percutaneous coronary intervention.

CONCLUSIONS - Large plaque burden and low local endothelial shear stress provide independent and additive prediction to identify plaques that develop progressive enlargement and lumen narrowing.

CLINICAL TRIAL REGISTRATION - URL: http:www.//clinicaltrials.gov. Unique Identifier: NCT01316159.