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Updated: Jan 21, 2026

Acute Myocardial Infarction in Rats
Published on: February 16, 2011
Association between temporal changes in C-reactive protein levels and prognosis in patients with previous myocardial
Takuya Oikawa1, Yasuhiko Sakata2, Kotaro Nochioka2
1Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
Insights
Elevated C-reactive protein (CRP) levels after myocardial infarction (MI) predict worse outcomes. Temporal increases in CRP are linked to higher risks of death, emphasizing CRP
Area of Science:
- Cardiology
- Biomarkers
- Inflammation
Background:
- C-reactive protein (CRP) is an inflammatory biomarker known to predict cardiovascular events.
- Previous research established CRP's predictive value independently of low-density lipoprotein cholesterol.
- The association between temporal changes in CRP levels and clinical events in patients with prior myocardial infarction (MI) remained unexamined.
Purpose of the Study:
- To investigate the relationship between temporal changes in C-reactive protein (CRP) levels and clinical outcomes in patients with a history of myocardial infarction (MI).
- To determine if sustained or increased CRP levels post-MI are associated with adverse cardiovascular and all-cause mortality.
Main Methods:
- Analysis of 2184 patients with previous MI from the Chronic Heart Failure Registry and Analysis in the Tohoku district-2 (CHART-2) Study.
- Assessment of C-reactive protein (CRP) levels at baseline and 1-year follow-up.
- Evaluation of all-cause, cardiovascular, and non-cardiovascular deaths during a median 6.4-year follow-up period.
- Statistical analysis using hazard ratios (HR) and inverse probability of treatment weighting (IPTW) models.
Main Results:
- Patients with baseline CRP ≥ 2.0 mg/L had significantly increased risks of all-cause and non-cardiovascular death compared to those with CRP < 2.0 mg/L.
- Temporal increases in CRP levels were strongly associated with prognosis; patients with CRP ≥ 2.0 mg/L at both baseline and 1-year showed significantly higher risks of all-cause, cardiovascular, and non-cardiovascular death.
- Even patients with initially low CRP (< 2.0 mg/L) who showed an increase to ≥ 2.0 mg/L at 1-year had elevated risks of all-cause and cardiovascular death.
Conclusions:
- Temporal increases in C-reactive protein (CRP) levels are significantly associated with an increased incidence of clinical events, including all-cause, cardiovascular, and non-cardiovascular death, in patients with previous myocardial infarction (MI).
- Sustained or rising CRP levels serve as a critical prognostic indicator in post-MI patients, highlighting the importance of monitoring inflammatory markers.
Background:
Several studies have reported that C-reactive protein (CRP), an inflammatory biomarker, predicts cardiovascular events independently of low-density lipoprotein cholesterol levels. However, no study examined whether temporal changes in CRP levels are associated with clinical events in patients with previous myocardial infarction (MI).
Methods And Results:
We examined 2184 consecutive patients with previous MI and CRP data at baseline in the Chronic Heart Failure Registry and Analysis in the Tohoku district-2 (CHART-2) Study. During the median 6.4 years follow-up, 592 all-cause, 245 cardiovascular, and 273 non-cardiovascular deaths occurred. Patients with CRP ≥ 2.0 mg/L at baseline had significantly increased incidence of all-cause (hazard ratio (HR) 1.68, P < 0.001) and non-cardiovascular death (HR 1.86, P < 0.001), compared with those with CRP < 2.0 mg/L. Temporal changes in CRP levels were associated with prognosis; among patients with CRP ≥ 2.0 mg/L at baseline, those with CRP ≥ 2.0 mg/L at 1-year had significantly increased incidence of all-cause (HR 2.12, P < 0.001), cardiovascular (HR 2.31, P < 0.001), and non-cardiovascular death (HR 2.29, P < 0.001). Among patients with CRP < 2.0 mg/L at baseline, those with CRP ≥ 2.0 mg/L at 1-year had significantly increased incidence of all-cause (HR 1.76, P < 0.001) and cardiovascular death (HR 2.10, P = 0.001). These results remained significant after adjusted with the inverse probability of treatment weighted models using propensity sore. Furthermore, as compared with patients with CRP < 2.0 mg/L at both baseline and 1-year, those with CRP ≥ 2.0 mg/L at both baseline and 1-year had increased incidence of all-cause, cardiovascular, and non-cardiovascular death.
Conclusions:
These results provide the evidence that temporal increases in CRP levels are associated with increased clinical events in patients with previous MI.
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