Research Article| Volume 328, P191-196, April 01, 2021

Download started.


High sensitivity C-reactive protein is associated with worse infarct healing after revascularized ST-elevation myocardial infarction

Published:December 09, 2020DOI:


      • 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.



      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.


      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.


      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).


      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.


      To read this article in full you will need to make a payment

      Purchase one-time access:

      Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
      One-time access price info
      • For academic or personal research use, select 'Academic and Personal'
      • For corporate R&D use, select 'Corporate R&D Professionals'


      Subscribe to International Journal of Cardiology
      Already a print subscriber? Claim online access
      Already an online subscriber? Sign in
      Institutional Access: Sign in to ScienceDirect


        • Reinstadler S.J.
        • Thiele H.
        • Eitel I.
        Risk stratification by cardiac magnetic resonance imaging after ST-elevation myocardial infarction.
        Curr. Opin. Cardiol. 2015; 30: 681-689
        • de Waha S.
        • et al.
        Prognosis after ST-elevation myocardial infarction: a study on cardiac magnetic resonance imaging versus clinical routine.
        Trials. 2014; 15: 249
        • Klug G.
        • Metzler B.
        Assessing myocardial recovery following ST-segment elevation myocardial infarction: Short- and long-term perspectives using cardiovascular magnetic resonance.
        Expert. Rev. Cardiovasc. Ther. 2013; 11: 203-219
        • Wu E.
        • et al.
        Infarct size by contrast enhanced cardiac magnetic resonance is a stronger predictor of outcomes than left ventricular ejection fraction or end-systolic volume index: prospective cohort study.
        Heart. 2008; 94: 730-736
        • Lonborg J.
        • et al.
        Final infarct size measured by cardiovascular magnetic resonance in patients with ST elevation myocardial infarction predicts long-term clinical outcome: an observational study.
        Eur. Heart J. Cardiovasc. Imaging. 2013; 14: 387-395
        • Ganame J.
        • et al.
        Time course of infarct healing and left ventricular remodelling in patients with reperfused ST segment elevation myocardial infarction using comprehensive magnetic resonance imaging.
        Eur. Radiol. 2011; 21: 693-701
        • Pokorney S.D.
        • et al.
        Infarct healing is a dynamic process following acute myocardial infarction.
        J. Cardiovasc. Magn. Reson. 2012; 14: 62
        • Liehn E.A.
        • et al.
        Repair after myocardial infarction, between fantasy and reality: The role of chemokines.
        J. Am. Coll. Cardiol. 2011; 58: 2357-2362
        • Frangogiannis N.G.
        The mechanistic basis of infarct healing.
        Antioxid. Redox Signal. 2006; 8: 1907-1939
        • Reindl M.
        • et al.
        Relation of inflammatory markers with myocardial and microvascular injury in patients with reperfused ST-elevation myocardial infarction.
        Eur. Heart J. Acute Cardiovasc. Care. 2017; 6: 640-649
        • Frangogiannis N.G.
        The inflammatory response in myocardial injury, repair, and remodelling.
        Nat. Rev. Cardiol. 2014; 11: 255-265
        • Thygesen K.
        • et al.
        Third universal definition of myocardial infarction.
        Eur. Heart J. 2012; 33: 2551-2567
        • Tiller C.
        • et al.
        Biomarker assessment for early infarct size estimation in ST-elevation myocardial infarction.
        Eur. J. Intern. Med. 2019; 64: 57-62
        • Reinstadler S.J.
        • et al.
        Acute kidney injury is associated with microvascular myocardial damage following myocardial infarction.
        Kidney Int. 2017; 92: 743-750
        • Reinstadler S.J.
        • et al.
        Association of copeptin with myocardial infarct size and myocardial function after ST segment elevation myocardial infarction.
        Heart. 2013; 99: 1525-1529
        • Youden W.J.
        Index for rating diagnostic tests.
        Cancer. 1950; 3: 32-35
        • Frangogiannis N.G.
        Inflammation in cardiac injury, repair and regeneration.
        Curr. Opin. Cardiol. 2015; 30: 240-245
        • Frangogiannis N.G.
        Regulation of the inflammatory response in cardiac repair.
        Circ. Res. 2012; 110: 159-173
        • Calabro P.
        • Golia E.
        • Yeh E.T.
        CRP and the risk of atherosclerotic events.
        Semin. Immunopathol. 2009; 31: 79-94
        • Metzler B.
        • et al.
        Mouse model of myocardial remodelling after ischemia: Role of intercellular adhesion molecule-1.
        Cardiovasc. Res. 2001; 49: 399-407
        • Frangogiannis N.G.
        Monomeric C-reactive protein and inflammatory injury in myocardial infarction.
        Cardiovasc. Res. 2012; 96: 4-6
        • Griselli M.
        • et al.
        C-reactive protein and complement are important mediators of tissue damage in acute myocardial infarction.
        J. Exp. Med. 1999; 190: 1733-1740
        • Orn S.
        • et al.
        C-reactive protein, infarct size, microvascular obstruction, and left-ventricular remodelling following acute myocardial infarction.
        Eur. Heart J. 2009; 30: 1180-1186
        • Boljevic D.
        • et al.
        A promising innovative treatment for ST-elevation myocardial infarction: The use of C-reactive protein selective apheresis: Case report.
        Blood Purif. 2020; : 1-5
        • Vanhaverbeke M.
        • et al.
        C-reactive protein during and after myocardial infarction in relation to cardiac injury and left ventricular function at follow-up.
        Clin. Cardiol. 2018; 41: 1201-1206
        • Scholz K.H.
        • et al.
        Impact of treatment delay on mortality in ST-segment elevation myocardial infarction (STEMI) patients presenting with and without haemodynamic instability: Results from the German prospective, multicentre FITT-STEMI trial.
        Eur. Heart J. 2018; 39: 1065-1074