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.

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).

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.

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.