Logo image
Evaluations of High-Sensitivity C-Reactive Protein Levels Among Stable Chest Pain and Post–Acute Myocardial Infarction Patients
Conference proceeding   Open access

Evaluations of High-Sensitivity C-Reactive Protein Levels Among Stable Chest Pain and Post–Acute Myocardial Infarction Patients

Xiaomeng Wang, Ching Hui Sia, Philip Adamson, Charlotte Greer, Weimin Huang, Hwee Kuan Lee, Shuang Leng, Yan Ting Loong, Nur Amirah Syahindah Raffiee, Swee Yaw Tan, …
Journal of Molecular and Cellular Cardiology Plus, Vol.15(Supp.), 100645
International Society for Heart Research (ISHR) World Congress, XXV (Nara, Japan, 11/05/2025–14/05/2025)
19/03/2026
Handle:
https://hdl.handle.net/10523/50311

Abstract

Introduction: Inflammation plays a critical role in coronary artery disease (CAD) and acute myocardial infarction (AMI). Although inflammation, commonly measured by high-sensitivity C-reactive protein (hs-CRP), typically declines after AMI, its precise trajectory compared to stable chest pain cohorts remains unclear. This study assessed hs-CRP levels in stable chest pain patients with and without coronary lesions and in post-AMI patients over time. We hypothesized that hs-CRP would initially be elevated in post-AMI patients, compared to stable chest pain cohorts, and decline over time. Methods: This study included 257 stable chest pain and 205 post-AMI patients. Stable patients were classified as no-lesion (n=61) or stable CAD (n=195, with lesions) based on coronary computed tomography angiography. Post-AMI patients were enrolled within two months of the event (Visit 1: 28±13 days) and followed at Visit 2 (62±15 days) and Visit 3 (394±23 days); 96 returned for follow-up. Plasma hs-CRP levels and demographic/clinical data were collected. Group differences were analyzed using Kruskal–Wallis and Dunn’s tests, and longitudinal trends with Friedman and mixed-effects linear models. Multivariate adjustments accounted for demographics (age, sex, BMI), CAD risk factors (hypertension, diabetes, hyperlipidemia, smoking, family CAD history), and medication use. Results: Post-AMI patients had significantly higher hs-CRP levels at Visit 1 (1.43[0.68,3.14] mg/L) compared to no-lesion (0.88[0.35,1.95], p=0.007) and stable CAD (0.84 [0.41,2.11], p<0.001) groups. At Visit 2, hs-CRP (1.40[0.57,2.34] mg/L) remained elevated compared to stable CAD (p=0.022) but was borderline compared to no-lesion (p=0.061). By Visit 3, hs-CRP in post-AMI patients (0.96[0.38,1.55]mg/L) approximated stable cohorts (p>0.05). Longitudinally, hs-CRP declined significantly from Visit 1 to Visit 2 (p=0.038) and Visit 2 to Visit 3 (p<0.001), with the decrease remaining significant after adjustment (Visit 2: β=-2.18±1.00 mg/L, p=0.030; Visit 3: β=-2.35±1.00 mg/L, p=0.019). Cross-sectional differences lost significance after multivariate adjustment (p>0.05). Conclusions: Post-AMI patients exhibited elevated hs-CRP shortly after AMI, which declined to stable chest pain levels within a year. This reduction remains significant after adjusting for clinical factors, highlighting the dynamic nature of post-AMI inflammation. The loss of cross-sectional significance post-adjustment suggests that hs-CRP reflects both inflammation and underlying patient characteristics.
pdf
1-s2.0-S2772976125003642988.88 kBDownloadView
Published (Version of record)CC BY-NC-ND V4.0 Open Access
url
https://doi.org/10.1016/j.jmccpl.2025.100645View
Published (Version of record)CC BY-NC-ND V4.0 Open

Metrics

1 Record Views

Details

Logo image