Original title: Relation of C-reactive protein levels to instability of untreated vulnerable coronary plaques (from the PROSPECT study). Reference: Kelly CR et al. Am J Cardiol. 2014;Epub ahead of print.
The original PROSPECT study included 697 patients with acute coronary syndrome (ACS) undergoing culprit artery percutaneous coronary intervention (PCI) followed by intravascular ultrasound (IVUS) to the rest of vessels. At 3.4 year follow up, the combined MACE events rate (death, infarction, or re-hospitalization for unstable angina) was equally attributed to treated culprit lesions (12.9%) and untreated non-culprit lesions (12.6%). Most of non-culprit plaques that later caused events presented a thin-cap by IVUS, large plaque burden (≥70%), minimal luminal area ≤ 4 mm2 or the combination of these characteristics.
This sub analysis included patients with elevated C reactive protein levels (n=571) measured at presentation, 1 month, and 6 months, considering < 3mg/l as a normal value, 3-10 mg/l as elevated, and > 10 mg/l as very elevated. C reactive protein (CRP) values were not associated to the use of aspirin, statins or any other medication, neither were these associated to the number of non-culprit lesions.
For patients with elevated CRP levels at presentation or at 1 month, non-culprit lesions related MACE rates did not vary significantly. However, those with normal values at presentation and at 6 months saw and increase to elevated or very elevated CRP levels; a correlation with non-culprit lesions (NCL) related MACE was observed, both NCL with thin cap (normal CRP, 1.9% events rate; elevated, 4.2%; and very elevated, 13.8%; p=0.002) and with minimal lumen area ≤4% (normal CRP, 2.2%; elevated, 8.3%; and very elevated 15.6%; p=0.0003). Events correlation was not significant for large plaque burden lesions or for those with no risk characteristics.
The multivariable analysis showed that the sole predictor of subsequent NCL-related MACE was CRP values (HR 1.02; IC 95% 1.01-1.03; P =0.0005).
Conclusion
In ACS patients undergoing successful culprit vessel PCI, subsequent NCL-related MACE seem to be associated both to high risk plaque and persistent elevated levels of C reactive protein.
Editorial Comment
The observed relation between C reactive protein and non-culprit lesions is consistent with the change of paradigm from “vulnerable plaque” to “vulnerable patient”.
What remains unclear is whether these elevated levels of C reactive protein are the systemic manifestation of a systemic problem (chronic inflammation) or the systemic manifestation of a local problem (vulnerable plaque). Evidently, having a high risk plaque (e.g. with thin cap) may not be not enough; other factors should combine to cause eventual MACE.
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