Usefulness of C-reactive protein as a marker of early post-infarct left ventricular systolic dysfunction

Abstract

ObjectiveTo assess the usefulness of in-hospital measurement of C-reactive protein (CRP) concentration in comparison to well-established risk factors as a marker of post-infarct left ventricular systolic dysfunction (LVSD) at discharge.Materials and methodsTwo hundred and four consecutive patients with ST-segment-elevation myocardial infarction (STEMI) were prospectively enrolled into the study. CRP plasma concentrations were measured before reperfusion, 24 h after admission and at discharge with an ultra-sensitive latex immunoassay.ResultsCRP concentration increased significantly during the first 24 h of hospitalization (2.4 ± 1.9 vs. 15.7 ± 17.0 mg/L; p < 0.001) and persisted elevated at discharge (14.7 ± 14.7 mg/L), mainly in 57 patients with LVSD (2.4 ± 1.8 vs. 25.0 ± 23.4 mg/L; p < 0.001; CRP at discharge 21.9 ± 18.6 mg/L). The prevalence of LVSD was significantly increased across increasing tertiles of CRP concentration both at 24 h after admission (13.2 vs. 19.1 vs. 51.5 %; p < 0.0001) and at discharge (14.7 vs. 23.5 vs. 45.6 %; p < 0.0001). Multivariate analysis demonstrated CRP concentration at discharge to be an independent marker of early LVSD (odds ratio of 1.38 for a 10 mg/L increase, 95 % confidence interval 1.01–1.87; p < 0.04).ConclusionMeasurement of CRP plasma concentration at discharge may be useful as a marker of early LVSD in patients after a first STEMI.

Correlations between severity of coronary atherosclerosis and persistent elevation of circulating C-reactive protein levels 30 days after an acute myocardial infarction

“…In a study published by Swiatkiewicz et al, multivariate analysis demonstrated CRP concentration at discharge to be an independent marker of early postinfarction left ventricular dysfunction (odds ratio of 1.38, 95 % confidence interval 1.01-1.87; p < 0.04), which proves that higher levels of CRP upon admission identifies patients with worse outcomes and suggests that high hsCRP levels may identify patients who will have poorer results after reperfusion, or may be more likely to have ventricular remodeling and enlargement after hospital discharge (20). Similarly, in a recently published study by Perlas et al, high levels of hsCRP upon admission were found to correlate with an increase in cardiovascular risk on short term (21).…”

A Novel Signal-Amplified Immunoassay for the Detection of C-Reactive Protein Using HRP-Doped Magnetic Nanoparticles as Labels with the Electrochemical Quartz Crystal Microbalance as a Detector

“…Ultrasensitive methodologies for detecting free CRP in human serums are required. The most common approaches in analyzing CRP are enzyme-linked immunosorbent assay (ELISA), immunofluorescence, and so forth [3]. However, most of usual methods are time consuming, labor intensive, and hazardous to health or require highly qualified personnel and sophisticated instrumentation [4–6].…”

Enhanced Inflammation is a Marker for Risk of Post-Infarct Ventricular Dysfunction and Heart Failure

“…At present, the potential value of CRP for the prediction of long-term LVSD and HF in patients with STEMI undergoing PCI and guideline-based therapies has not been definitely assessed [14,27]. Previous studies have been limited by heterogenous populations with acute coronary syndromes that were frequently untreated with PCI, small sample size, a lack of multiple high-sensitivity CRP measurements, absence of neurohormonal activation assessment, lack of long-term monitoring of LVEF and HF, and omission of long-term LVSD and HF as clinical endpoints [14,[16][17][18][21][22][23][24][25][26][27][28][29][30][31][32][33][34].The purpose of this study was to assess the value of high-sensitivity CRP in a homogenous population of patients with first STEMI undergoing primary PCI and guideline-based therapies for predicting the risk of: (i) LVSD at 6 months after hospital discharge (LVSD 6M ), which was the primary study endpoint; and (ii) the need for hospitalization for HF in patients with LVSD 6M in long-term multi-year follow-up, which was the secondary study endpoint. This secondary endpoint was chosen because hospitalization for HF is associated with subsequent increase in risk of mortality [8].We performed a single-center prospective cohort study with rigorous selection criteria, adequate sample size, and long-term follow-up data based on multiple assessment time-points: baseline, 24 h, and discharge during index hospitalization for STEMI, 1 month and 6 months after discharge, and long-term multi-year follow-up.…”

“…At present, the potential value of CRP for the prediction of long-term LVSD and HF in patients with STEMI undergoing PCI and guideline-based therapies has not been definitely assessed [14,27]. Previous studies have been limited by heterogenous populations with acute coronary syndromes that were frequently untreated with PCI, small sample size, a lack of multiple high-sensitivity CRP measurements, absence of neurohormonal activation assessment, lack of long-term monitoring of LVEF and HF, and omission of long-term LVSD and HF as clinical endpoints [14,[16][17][18][21][22][23][24][25][26][27][28][29][30][31][32][33][34].…”