Acute-phase inflammatory markers during myocardial infarction: association with mortality and modes of death after 7 years of follow-up.

BACKGROUND: The relationship between acute-phase inflammatory markers in the setting of acute myocardial infarction (AMI) and long-term outcomes is largely unexplored. OBJECTIVES: The aim of the study was to investigate the predictive power of acute-phase inflammatory markers following AMI for short-term and long-term mortality separately and modes of death. METHODS: In 220 unselected patients with AMI [median age 67 (interquartile range 60-74) years, women 26%], blood neutrophil granulocytes, erythrocyte sedimentation rate, C-reactive protein, and alpha1-acid glycoprotein were measured 1, 3 and 7 days after admission. All patients completed 7 years of follow-up. Endpoints were 1-year (short-term) and 2- to 7-year (long-term) mortality and modes of death, classified as nonsudden cardiovascular, sudden, and noncardiovascular death. RESULTS: The short-term mortality rate was 18%. The long-term mortality rate was 26%. The short-term mortality risk was higher in patients in whom the markers were in the upper tertile. Fully adjusted hazard ratios (and 95% confidence interval) were 3.2 (1.4-7.9), 3.5 (1.7-7.9), 3.5 (1.6-8.6), and 6.1 (2.3-19.1) for neutrophil granulocyte, erythrocyte sedimentation rate, C-reactive protein, and alpha1-acid glycoprotein, respectively. The excess mortality was chiefly due to nonsudden cardiovascular mortality [fully adjusted hazard ratios were 4.6 (1.7-14.7), 4.7 (1.9-13.7), 5.9 (2.0-21.3) and 5.5 (2.0-17.6), respectively], whereas no association was found with sudden death or noncardiovascular modes of death. In the long term, the association with mortality and modes of death was no longer significant. CONCLUSION: The acute-phase inflammatory markers tested following AMI are independently and concordantly associated with short-term mortality and their prediction is associated only with nonsudden cardiovascular modes of death. These markers are not associated with long-term mortality.

C-reactive protein in acute myocardial infarction: association with heart failure.

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.