An acute inflammatory reaction induced by myocardial damage is superimposed on a chronic inflammation in unstable coronary artery disease.
BACKGROUND
Inflammation plays an important role in unstable coronary artery disease (CAD). We assessed the kinetics of inflammatory markers from symptom onset in patients with unstable CAD and their relation to myocardial damage.


METHODS
Serial measurements of inflammatory mediators were performed in consecutive patients with unstable CAD enrolled at selected sites in the FRISC II (n = 558) and the GUSTO IV (n = 404) trials. The time from symptom onset was calculated for every serum sample (total 4400 samples).


RESULTS
Median levels of interleukin 6 and C-reactive protein reached their peaks at 36 to 42 hours and at 48 to 54 hours, respectively, from symptom onset and returned to early postsymptom levels within 6 weeks. The early increase occurred almost exclusively in patients with baseline troponin T elevation (>0.01 microg/L). In contrast, median levels of fibrinogen increased continuously up to 120 hours after symptom onset, independently of myocardial damage. At 6 months, fibrinogen levels were still higher than in the early phase after symptom onset. The median levels of interleukin 6, C-reactive protein, and fibrinogen were still higher at 6 months than in healthy controls matched for age and sex to a population with unstable CAD.


CONCLUSIONS
An early acute inflammatory reaction induced by myocardial damage seems to be superimposed on a chronic inflammatory condition, both of which might influence long-term outcome in unstable CAD.
The Research Group of Cardiology, Department of Medical Sciences, Uppsala University, Uppsala, Sweden. stefan.james@akademiska.se
Stefan K
SK
James
Jonas
J
Oldgren
Johan
J
Lindbäck
Nina
N
Johnston
Agneta
A
Siegbahn
Lars
L
Wallentin
D000077284:Abciximab; D000328:Adult; D000368:Aged; D000789:Angina, Unstable / Q000097:blood / Q000188:drug therapy / Q000473:pathology; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D000925:Anticoagulants / Q000627:therapeutic use; D001241:Aspirin / Q000627:therapeutic use; D002097:C-Reactive Protein / Q000032:analysis*; D016022:Case-Control Studies; D015331:Cohort Studies; D003327:Coronary Disease / Q000097:blood* / Q000473:pathology; D017985:Dalteparin / Q000627:therapeutic use; D005260:Female; D005340:Fibrinogen / Q000032:analysis*; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000627:therapeutic use; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood*; D007700:Kinetics; D008297:Male; D008875:Middle Aged; D015337:Multicenter Studies as Topic; D009206:Myocardium / Q000473:pathology*; D011446:Prospective Studies; D016032:Randomized Controlled Trials as Topic; D020107:Troponin T / Q000097:blood
D000911:Antibodies, Monoclonal; D000925:Anticoagulants; D007140:Immunoglobulin Fab Fragments; D018836:Inflammation Mediators; D015850:Interleukin-6; D020107:Troponin T; D005340:Fibrinogen; D002097:C-Reactive Protein; D001241:Aspirin; D017985:Dalteparin; D000077284:Abciximab