High sensitivity C-reactive protein is associated with worse infarct healing after revascularized ST-elevation myocardial infarction. (1st April 2021)

• Record Type: Journal Article
• Authors: Tiller, Christina; Reindl, Martin; Holzknecht, Magdalena; Lechner, Ivan; Simma, Felix; Schwaiger, Johannes; Mayr, Agnes; Klug, Gert; Bauer, Axel; Reinstadler, Sebastian Johannes; Metzler, Bernhard
• Is Part Of: International journal of cardiology. Volume 328(2021)
• Page Start: 191
• Page End: 196
• Publication Date: 2021-04-01
• Subjects: ST-elevation myocardial infarction -- C-reactive protein -- Infarct healing -- Cardiac magnetic resonance imaging; Cardiology -- Periodicals; Electronic journals; 616.12
• DOI: 10.1016/j.ijcard.2020.12.006
• Languages: English
• ISSNs: 0167-5273

Abstract

Abstract: Background: The inflammatory response due to myocardial tissue injury in the setting of acute ST-elevation myocardial infarction (STEMI) is essential for proper local infarct healing. However, an excessive inflammatory response may aggravate myocardial damage and hampers infarct healing processes. The present study aimed to investigate the association of systemic inflammatory biomarkers with infarct size (IS) dynamics post-STEMI, using cardiac magnetic resonance (CMR) imaging. Methods: This prospective observational study included 245 STEMI patients treated with primary percutaneous coronary intervention (pPCI). Peak values of high-sensitivity C-reactive protein (hs-CRP), white blood cell count (WBCc) and fibrinogen were determined serially until 96 h after pPCI. Infarct healing, defined as relative IS reduction from baseline to 4 months after STEMI, was assessed using late gadolinium enhanced CMR imaging. Results: IS significantly decreased from 16% of left ventricular mass (LVM) (Interquartile range [IQR]:8–24) at baseline to 10% (IQR:5–17) at 4 months ( p < 0.001). Relative IS reduction was 35% (IQR:8–50). Whereas peak WBCc ( p = 0.926) and peak fibrinogen ( p = 0.161) were not significantly associated with relative IS reduction, peak hs-CRP showed a significant association with IS reduction ( p = 0.003). In multivariable logistic regression analysis, the association between peak hs-CRP and relative IS reduction remained significant after adjustment for baseline IS, hypertension, hs-cardiac troponin T and N-terminal pro B-type natriuretic peptide (odds ratio:0.35 [95% confidence interval:0.19–0.63]; p = 0.001). Conclusions: In STEMI patients treated with pPCI, hs-CRP was independently associated with 4 months IS reduction as determined by CMR, suggesting a pathophysiological interplay between inflammation and adverse infarct healing in survivors of acute STEMI. Highlights: Hs-CRP is significantly associated acute and chronic IS. Hs-CRP is independently associated with IS reduction after 4 months post-STEMI. Inflammation plays an essential role in infarct healing dynamics after acute STEMI.