High sensitivity C-reactive protein is associated with vulnerable characteristics in non-culprit plaques in patients with ST-segment elevation myocardial infarction

European Heart Journal

4 February 2022
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ESC Journals

Abstract

AbstractFunding Acknowledgements

Type of funding sources: None.

Background

Higher level of high sensitivity C-reactive protein (hsCRP) is associated with an increased risk of recurrent cardiovascular events in patients with ST-segment elevation myocardial infarction (STEMI). However, the association between hsCRP and the characteristics of non-culprit plaques in patients with STEMI remains to be elucidated.

Purpose

To clarify the morphological characteristics of non-culprit plaque in patients with STEMI according to the hsCRP levels using optical coherence tomography (OCT).

Methods

A total of 79 non-culprit plaques in 76 consecutive patients with STEMI, who underwent OCT imaging of the non-culprit plaques in a culprit vessel were included. The characteristics of non-culprit plaques assessed by OCT were compared between the higher hsCRP group (hsCRP ≥ 0.16 mg/dL, 38 plaques in 38 patients) and the lower hsCRP group (hsCRP < 0.16 mg/dL, 41 plaques in 38 patients).

Results

The prevalence of plaque with macrophage (63.2 vs. 31.7%, p = 0.006), plaque with large lipid (maximal lipid arc > 180 °) (57.9 vs. 31.7%, p = 0.018), healed plaque (50.0 vs. 26.8%, p = 0.045) and cholesterol crystal (18.4 vs. 2.4%, p = 0.045) was significantly higher in the higher hsCRP group than in the lower hsCRP group (Figure). In a multivariate analysis, the higher hsCRP was independently associated with the presence of plaque with macrophage (Odds ratio [OR], 3.031; 95% confidence interval [CI]: 1.112-8.264, p = 0.030), plaque with large lipid (OR, 2.897; 95% CI: 1.122-7.478, p = 0.026) and healed plaque (OR, 2.666; 95% CI: 1.030-6.896, p = 0.040).

Conclusions

Higher level of hsCRP is associated with a higher prevalence of vulnerable characteristics in non-culprit plaques in patients with STEMI. The present results may partly explain the pathogenesis of an increased incidence of recurrent cardiovascular events in patients with STEMI.

Abstract Figure.

Contributors

ESC 365 is supported by