» Articles » PMID: 28883850

C-reactive Protein Levels Predict Systolic Heart Failure and Outcome in Patients with First ST-elevation Myocardial Infarction Treated with Coronary Angioplasty

Overview
Journal Arch Med Sci
Specialty General Medicine
Date 2017 Sep 9
PMID 28883850
Citations 40
Authors
Affiliations
Soon will be listed here.
Abstract

Introduction: There is growing evidence that inflammation plays a pivotal role in the etiology and progression of atherosclerosis. High C-reactive protein (CRP) levels have been associated with high mortality in patients with acute myocardial infarction (AMI). Furthermore, in animal models CRP has been found to significantly increase infarct size. So there is growing evidence that CRP is not only a marker for cardiovascular disease but also might be pathogenic. The aim of our study was to test the hypothesis that peak CRP levels could predict heart failure (HF) in ST-elevation myocardial infarction (STEMI) patients.

Material And Methods: Eighty-one consecutive patients with STEMI were prospectively enrolled in the study. C-reactive protein concentrations were measured on admission and after 6, 12, 24, 30, 48, 72 and 96 h. We assessed the association between the elevation of CRP, heart failure and cardiovascular mortality following the first 12 months after STEMI.

Results: C-reactive protein levels reached a peak after 48 h. Patients with STEMI and signs of HF showed significantly higher peak CRP levels. We found a positive correlation between maximum CK levels and peak CRP and a negative correlation between left ventricular ejection fraction (EF) and peak CRP. One year total mortality and HF mortality rates were found to be higher in patients with peak CRP > 47.5 mg/l than in those with CRP below that level ( < 0.001).

Conclusions: Peak CRP levels in STEMI patients predict emergence of HF. Peak CRP is also a strong predictor of global and cardiovascular mortality during the following year after STEMI.

Citing Articles

Association between lead and circulating markers of inflammation among traffic enforcers in Metro Manila, Philippines: the MMDA traffic enforcer's health study.

Regencia Z, Zhao W, Torres-Roja C, Jones B, Baja E Int Arch Occup Environ Health. 2024; 97(3):303-311.

PMID: 38351350 DOI: 10.1007/s00420-023-02044-w.


Inflammation in Heart Failure-Future Perspectives.

Arvunescu A, Ionescu R, Cretoiu S, Dumitrescu S, Zaharia O, Nanea I J Clin Med. 2023; 12(24).

PMID: 38137807 PMC: 10743797. DOI: 10.3390/jcm12247738.


Cardioprotective Strategies After Ischemia-Reperfusion Injury.

Zhang H, Hu H, Zhai C, Jing L, Tian H Am J Cardiovasc Drugs. 2023; 24(1):5-18.

PMID: 37815758 PMC: 10806044. DOI: 10.1007/s40256-023-00614-4.


Being Eaten Alive: How Energy-Deprived Cells Are Disposed of, Mediated by C-Reactive Protein-Including a Treatment Option.

Sheriff A, Kunze R, Brunner P, Vogt B Biomedicines. 2023; 11(8).

PMID: 37626775 PMC: 10452736. DOI: 10.3390/biomedicines11082279.


Identification of High-Risk Patients for Postoperative Myocardial Injury After CME Using Machine Learning: A 10-Year Multicenter Retrospective Study.

Liu Y, Song C, Tian Z, Shen W Int J Gen Med. 2023; 16:1251-1264.

PMID: 37057054 PMC: 10089277. DOI: 10.2147/IJGM.S409363.


References
1.
KROOP I, SHACKMAN N . Level of C-reactive protein as a measure of acute myocardial infarction. Proc Soc Exp Biol Med. 1954; 86(1):95-7. DOI: 10.3181/00379727-86-21019. View

2.
Pepys M, Hirschfield G, Tennent G, Gallimore J, Kahan M, Bellotti V . Targeting C-reactive protein for the treatment of cardiovascular disease. Nature. 2006; 440(7088):1217-21. DOI: 10.1038/nature04672. View

3.
Berton G, Cordiano R, Palmieri R, Pianca S, Pagliara V, Palatini P . C-reactive protein in acute myocardial infarction: association with heart failure. Am Heart J. 2003; 145(6):1094-101. DOI: 10.1016/S0002-8703(03)00098-X. View

4.
Heinecke J . Chemical knockout of C-reactive protein in cardiovascular disease. Nat Chem Biol. 2006; 2(6):300-1. DOI: 10.1038/nchembio0606-300. View

5.
Jiang H, Robey F, Gewurz H . Localization of sites through which C-reactive protein binds and activates complement to residues 14-26 and 76-92 of the human C1q A chain. J Exp Med. 1992; 175(5):1373-9. PMC: 2119198. DOI: 10.1084/jem.175.5.1373. View