Related Experiment Videos
C-reactive protein in acute myocardial infarction: association with heart failure
Giuseppe Berton1, Rocco Cordiano, Rosa Palmieri
1Department of Internal Medicine and Cardiology, Conegliano General Hospital, Conegliano Veneto, Italy.
Insights
C-reactive protein (CRP) levels predict heart failure (HF) progression and mortality in acute myocardial infarction (AMI) patients. Higher CRP on admission and peak CRP levels indicate increased risk for HF and death within a year.
Area of Science:
- Cardiology
- Biomarkers
- Inflammation
Background:
- High C-reactive protein (CRP) levels are linked to increased mortality in acute myocardial infarction (AMI).
- The role of inflammation, indicated by CRP, in the development of heart failure (HF) post-AMI is unclear.
Purpose of the Study:
- To investigate the relationship between CRP levels and the time-course of heart failure in patients with AMI.
- To determine if CRP can predict HF development and mortality following AMI.
Main Methods:
- Prospective study of 269 subjects with suspected AMI (220 confirmed AMI, 49 controls).
- CRP levels measured on days 1, 3, and 7 post-admission.
- Multivariable regression analysis used to assess predictors of HF progression and mortality.
Main Results:
- CRP levels were significantly higher in AMI patients than controls, peaking on day 3.
- Higher CRP levels correlated with increased HF prevalence and progression.
- First-day CRP predicted HF progression and reduced left ventricular ejection fraction.
- Elevated CRP levels (>85 mg/L) were associated with higher 1-year total and HF-specific mortality.
- Third-day CRP independently predicted 1-year mortality.
Conclusions:
- Admission CRP levels are valuable for predicting the course of heart failure in AMI patients.
- Peak CRP levels serve as a strong independent predictor of overall and heart failure-related mortality within one year post-AMI.
Background:
High C-reactive protein (CRP) levels have been associated with higher mortality rate in patients with acute myocardial infarction (AMI). However, it is not known whether inflammation plays a role in the time-course of heart failure (HF) in this clinical setting. Our aim was to study the nature of the relationship between CRP and HF during AMI.
Methods:
This prospective study was carried out in 269 subjects admitted to the hospital for suspected AMI. Of these, 220 had evidence of AMI. The other 49 subjects were studied as controls. CRP was assessed on the first, third, and seventh day after admission.
Results:
CRP was significantly higher in the patients with AMI than in the control patients (P =.001) and peaked on the third day. Among the patients with AMI, CRP was higher in patients with HF than in patients without HF (adjusted P =.008, P =.02 and P =.03 on 1st, 3rd, and 7th day, respectively). Prevalence of HF on admission was slightly higher in the subjects with first-day CRP >or=15 mg/L than in those with CRP <15 mg/L, and the between-group difference progressively increased from the first to the seventh day (P <.0001). At multivariable regression analysis, first-day log-CRP was shown to be a strong independent predictor of both HF progression (P <.0001) and left ventricular ejection fraction (P <.0001). One-year total mortality and HF-mortality rates turned out to be higher in the patients with CRP >or=85 mg/L than in those with CRP below that level (P <.0001), and log-third-day CRP was independently associated with 1-year mortality at multivariable analysis (P =.0001).
Conclusions:
CRP on admission to hospital is suitable for predicting the time-course of HF in patients with AMI. Peak CRP value is a strong independent predictor of global and HF-mortality during the following year.