From the Division of Cardiology, New York Presbyterian Hospital and Weill Cornell Medical College (P.S.); Cardiac MR PET CT Program, Division of Cardiac Imaging (H.E., S.S., P.M.-H., G.M.-S., Amr Abdelbaky, U.H., A.T.) and Division of Cardiology (A.T.), Massachusetts General Hospital and Harvard Medical School, Boston; MTA-SE Cardiovascular Imaging Research Group, Semmelweis University, Budapest, Hungary (P.M.-H.); Fundacion Cardio-Infantil, Bogota, Colombia (H.M.M.); Merck and Company, Inc, Kenilworth, NJ (Achilles Alon, S.S.S.); Division of Cardiovascular Medicine, University of Cambridge, United Kingdom (J.H.F.R.); and Translational and Molecular Imaging Institute, Icahn School of Medicine at Mount Sinai, New York, NY (Z.A.F.).
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Background—Nonobstructive coronary plaques manifesting high-risk morphology (HRM) associate with an increased risk of adverse clinical cardiovascular events. We sought to test the hypothesis that statins have a greater anti-inflammatory effect within coronary plaques containing HRM.Methods and Results—In this prospective multicenter study, 55 subjects with or at high risk for atherosclerosis underwent 18F-fluorodeoxyglucose positron emission tomographic/computed tomographic imaging at baseline and after 12 weeks of treatment with atorvastatin. Coronary arterial inflammation (18F-fluorodeoxyglucose uptake, expressed as target-to-background ratio) was assessed in the left main coronary artery (LMCA). While blinded to the PET findings, contrast-enhanced computed tomographic angiography was performed to characterize the presence of HRM (defined as noncalcified or partially calcified plaques) in the LMCA. Arterial inflammation (target-to-background ratio) was higher in LMCA segments with HRM than those without HRM (mean±SEM: 1.95±0.43 versus 1.67±0.32 for LMCA with versus without HRM, respectively; P=0.04). Moreover, atorvastatin treatment for 12 weeks reduced target-to-background ratio more in LMCA segments with HRM than those without HRM (12 week-baseline Δtarget-to-background ratio [95% confidence interval]: −0.18 [−0.35 to −0.004] versus 0.09 [−0.06 to 0.26]; P=0.02). Furthermore, this relationship between coronary plaque morphology and change in LMCA inflammatory activity remained significant after adjusting for baseline low-density lipoprotein and statin dose (β=−0.27; P=0.038).Conclusions—In this first study to evaluate the impact of statins on coronary inflammation, we observed that the anti-inflammatory impact of statins is substantially greater within coronary plaques that contain HRM features. These findings suggest an additional mechanism by which statins disproportionately benefit individuals with more advanced atherosclerotic disease.Clinical Trial Registration—URL: http://www.clinicaltrials.gov. Unique identifier: NCT00703261.