title: Clinical relevance of C-reactive protein during follow-up of patients with acute coronary syndromes in the Aggrastat-to-Zocor Trial.
abstract: BACKGROUND
  Elevated levels of high-sensitivity C-reactive protein (hsCRP) are associated with higher risk of adverse outcomes in patients at risk for or with established coronary artery disease. Retrospective analyses suggest that this risk may be modified with statin therapy. However, a role for hsCRP in monitoring the success of therapy remains uncertain.
  
  
  RESULTS
  We measured the serum concentration of hsCRP at 30 days (n=3813) and 4 months in patients with non-ST-elevation or ST-elevation acute coronary syndrome randomly assigned to an early intensive versus delayed conservative simvastatin strategy in the Aggrastat-to-Zocor Trial. Patients with hsCRP >3 mg/L at 30 days had significantly higher 2-year mortality rates than those with hsCRP 1 to 3 mg/L or hsCRP <1 mg/L (6.1% versus 3.7% versus 1.6%, P<0.0001). Results were similar with hsCRP measured at 4 months. After adjusting for age, gender, diabetes, smoking, cardiovascular history, index event, lipid levels, and randomly assigned treatment, patients with hsCRP >3 mg/L were at more than 3-fold higher risk of death (HR, 3.7; 95% CI, 1.9 to 7.2) compared with those with hsCRP <1 mg/L. "Average" levels of hsCRP (1 to 3 mg/L) were also associated with increased risk compared with those with hsCRP <1 mg/L (HR, 2.3; 95% CI, 1.2 to 4.6). Patients allocated to early intensive statin therapy were more likely to achieve hsCRP levels <1 mg/L at 30 days (P=0.028) and 4 months (P<0.0001).
  
  
  CONCLUSIONS
  Achieved levels of hsCRP at 30 days and 4 months after acute coronary syndrome are independently associated with long-term survival. Patients treated with more aggressive statin therapy are more likely to achieve lower levels of hsCRP.
authors.affiliation: TIMI Study Group, Cardiovascular Division, Brigham and Women's Hospital, 75 Francis St, Boston, Massachusetts 02115, USA. dmorrow@partners.org
authors.forename: David A
authors.initials: DA
authors.lastname: Morrow
authors.forename: James A
authors.initials: JA
authors.lastname: de Lemos
authors.forename: Marc S
authors.initials: MS
authors.lastname: Sabatine
authors.forename: Stephen D
authors.initials: SD
authors.lastname: Wiviott
authors.forename: Michael A
authors.initials: MA
authors.lastname: Blazing
authors.forename: Amy
authors.initials: A
authors.lastname: Shui
authors.forename: Nader
authors.initials: N
authors.lastname: Rifai
authors.forename: Robert M
authors.initials: RM
authors.lastname: Califf
authors.forename: Eugene
authors.initials: E
authors.lastname: Braunwald
mesh_terms: D000208:Acute Disease; D000368:Aged; D002097:C-Reactive Protein / Q000032:analysis*; D003327:Coronary Disease / Q000175:diagnosis* / Q000188:drug therapy* / Q000401:mortality; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D012307:Risk Factors; D019821:Simvastatin / Q000627:therapeutic use*; D016019:Survival Analysis; D000077466:Tirofiban; D014443:Tyrosine / Q000031:analogs & derivatives* / Q000627:therapeutic use
chemical_list: D008077:Lipoproteins, LDL; D014443:Tyrosine; D002097:C-Reactive Protein; D019821:Simvastatin; D000077466:Tirofiban