Literature DB >> 24931291

Relation of C-reactive protein levels to instability of untreated vulnerable coronary plaques (from the PROSPECT Study).

Christopher R Kelly1, Giora Weisz2, Akiko Maehara1, Gary S Mintz1, Roxana Mehran3, Alexandra J Lansky4, Helen Parise1, Bernard de Bruyne5, Patrick W Serruys6, Gregg W Stone7.   

Abstract

C-reactive protein (CRP) levels predict adverse coronary events, but it is uncertain if they predict the burden or stability of vulnerable coronary plaques. In the Providing Regional Observations to Study Predictors of Events in the Coronary Tree study, 697 patients with acute coronary syndromes underwent percutaneous coronary intervention followed by 3-vessel angiography, gray-scale intravascular ultrasound (IVUS), and radiofrequency IVUS. Major adverse cardiac events (MACE) during 3 years of follow-up were adjudicated to initially treated culprit lesions or to untreated nonculprit lesions (NCLs). NCLs at greatest risk of causing subsequent MACE had plaque burden ≥70%, minimal luminal area ≤4.0 mm(2), and/or thin-cap fibroatheroma morphology. Here, we examine the interaction of high-risk NCLs with CRP levels, which were measured at presentation, 1 month, and 6 months, then categorized at each time as normal (<3 mg/L), elevated (3 to 10 mg/L), or very elevated (>10 mg/L). We found that patients with elevated CRP levels at any time did not have more high-risk NCLs; however, untreated high-risk NCLs were more likely to cause subsequent MACE in patients with very elevated compared with normal 6-month CRP levels (for thin-cap fibroatheromas, 13.8% vs 1.9%, p = 0.0003; for lesions with minimal luminal area ≤4.0 mm(2), 15.6% vs 2.2%, p <0.0001). As expected, patients with very elevated 6-month CRP levels had higher rates of subsequent NCL-related MACE (19.0% vs 7.2%, p = 0.039). In conclusion, the higher rates of NCL-related MACE in post-acute coronary syndrome patients with very elevated CRP levels may reflect greater instability of high-risk NCLs, rather than a larger burden of such lesions.
Copyright © 2014 Elsevier Inc. All rights reserved.

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Year:  2014        PMID: 24931291     DOI: 10.1016/j.amjcard.2014.04.048

Source DB:  PubMed          Journal:  Am J Cardiol        ISSN: 0002-9149            Impact factor:   2.778


  7 in total

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  7 in total

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