Prediction of Recurrent Events by D-Dimer and Inflammatory Markers in Patients with Normal Cardiac Troponin I (PREDICT) Study.
BACKGROUND
The independent predictive value of d-dimer and inflammatory markers for the risk of recurrent adverse events in patients with acute chest pain but normal levels of cardiac troponin I (cTnI) remains unclear.


METHODS
We studied 391 patients admitted to the hospital in 1 year with acute ischemic-type chest pain. Creatine kinase-myocardial band isoenzyme (CK-MB) mass and cTnI levels were measured in initial and 12-hour samples. Soluble intercellular adhesion molecule (sICAM)-1, vascular cell adhesion molecule (sVCAM)-1, sP-selectin, sE-selectin, high sensitivity C-reactive protein (hsCRP), interleukin-6 (IL6), fibrinogen, and d-dimer levels were measured in initial samples. A 1-year incidence of death, myocardial infarction (MI), revascularization, or readmission with chest pain was determined (with death/MI as the primary end point).


RESULTS
Patients with normal levels of CK-MB(mass) and cTnI (195/391[50%]) were at a lower risk than patients with elevated levels of CK-MB(mass) or cTnI, but still had an important incidence of events (77/195[39%]). Marker elevation was defined as >75th percentile (upper quartile). Elevated d-dimer levels (>580 ng/mL) was predictive of death/MI (odds ratio, 5.4; 95% CI, 1.5-20.2; P =.005). Elevated sP-selectin levels (>152 ng/mL; odds ratio, 3.2; 95% CI, 0.9-11.6; P =.06) trended to increased death/MI rates, with weaker trends for elevated levels of hsCRP (>7.1 mg/L), IL6 (>10.7 pg/mL), and ST depression. Other markers, other electrocardiogram changes, or classic risk factors were not predictive of death/MI. With a multivariate analysis, d-dimer and sP-selectin were found to be of independent significance for death/MI after adjustment for inflammatory, hemostatic, and electrocardiogram markers and d-dimer after adjustment for classic risk factors.


CONCLUSIONS
Normal cTnI levels after acute chest pain does not confer absence of future risk. Concurrent assessment of d-dimer and inflammatory markers may improve risk stratification.
Menown
Ian B A
IB
Regional Medical Cardiology Centre, Royal Victoria Hospital, Belfast, Northern Ireland, UK. ian@imenown.freeserve.co.uk
Mathew
Thomas P
TP
Gracey
Helen M
HM
Nesbitt
G Selby
GS
Murray
Pamela
P
Young
Ian S
IS
Adgey
A A Jennifer
AA
D000704:Analysis of Variance; D015415:Biomarkers / Q000097:blood*; D002097:C-Reactive Protein / Q000032:analysis; D003402:Creatine Kinase / Q000097:blood; D052279:Creatine Kinase, MB Form; D019040:E-Selectin / Q000097:blood; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D006801:Humans; D007527:Isoenzymes / Q000097:blood; D009203:Myocardial Infarction / Q000097:blood / Q000401:mortality; D017202:Myocardial Ischemia / Q000097:blood*; D016017:Odds Ratio; D019007:P-Selectin / Q000097:blood; D012008:Recurrence; D018570:Risk Assessment; D019210:Troponin I / Q000097:blood; D020107:Troponin T; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
D015415:Biomarkers; D019040:E-Selectin; D005338:Fibrin Fibrinogen Degradation Products; D007527:Isoenzymes; D019007:P-Selectin; D019210:Troponin I; D020107:Troponin T; D019010:Vascular Cell Adhesion Molecule-1; C036309:fibrin fragment D; D002097:C-Reactive Protein; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form