Background-Risk stratification in troponin (cTn)-negative acute coronary syndrome (ACS) remains a clinical challenge.We investigated the predictive value of circulating pregnancy-associated plasma protein A (PAPP-A), a novel marker of atherosclerotic plaque activity, in these patients. Methods and Results-Two hundred consecutive hospitalized ACS patients were included, of whom 136 (69 men and 67 women; meanϮSD age, 66Ϯ16 years) remained cTnI-negative for up to 24 hours. PAPP-A was measured at admission, 6 to 12 hours, and 24 hours. During 6-month follow-up, 26 (19.1%) of the cTnI-negative patients reached a primary end point (cardiovascular death, myocardial infarction, or revascularization). At a cutoff level of 2.9 mIU/L, elevated PAPP-A was an independent predictor of adverse outcome (adjusted risk ratio [RR], 4.6; 95% confidence interval, 1.8 to 11.8; Pϭ0.002). Another independent predictor was admission CRP Ͼ2.0 mg/L (RR, 2.6; Pϭ0.03). Conclusions-Measurement of plasma PAPP-A, a zinc-binding matrix metalloproteinase, is a strong independent predictor of ischemic cardiac events and need of revascularization in patients who present with suspected myocardial infarction but remain troponin negative. (Circulation. 2003;108:1924-1926.)

Background: Elevated cardiac troponin (cTn) levels are relatively common in acute heart failure (AHF). Aims: To evaluate the prevalence and prognostic significance of elevated cTnI and cTnT in AHF. Methods: FINN-AKVA is a prospective, multicenter study in AHF. In this analysis, 364 non-ACS patients with measurements of cTnI and cTnT taken on admission and 48 h thereafter were analyzed. Results: Of the 364 AHF patients, 51.1% had cTnI and 29.7% cTnT levels above the cut-off value. Six-month all-cause mortality was 18.7%. Both cTnI (OR 2.0, 95% CI 1.2-3.5, p = 0.01) and cTnT (OR 2.6, 95% CI 1.5-4.4, p = 0.0006) were associated with adverse outcome. The mortality risk was proportional to the magnitude of cTn release. On multivariable analysis, Cystatin C (OR 6.3, 95% CI 3.2-13, p b 0.0001), logNT-proBNP (OR 1.4, 95% CI 1.0-1.8, p = 0.03) and systolic blood pressure on admission (/10 mm Hg increase, OR 0.9, 95% CI 0.8-0.9, p = 0.0004) were independent risk markers, whereas the troponins were not significantly associated with increased mortality. Conclusions: cTn elevations are frequent in AHF patients without ACS. cTnI is more often elevated than cTnT. Both cTnI and cTnT elevations are associated with increased mortality proportional to the degree elevation but they do not act as independent risk markers.

Background:We recently provided evidence that circulating autoantibodies against cardiac troponin I (cTnI) or the troponin complex cause negative interference in cTnI immunoassays. By comparing three cTnI immunoassays, we further explored the phenomenon of circulating autoantibodies and their consequences in patient samples. Methods: We developed a cTnI immunoassay with a novel assay design using three antibodies, two of which bind epitopes outside the stable, central part of cTnI. Samples from 541 chest pain patients were measured with the new cTnI assay and with a first-generation cTnI assay (Innotrac Aio cTnI) using a conventional midfragment assay design. Using another sample cohort, we also compared the new assay with a second-generation cTnI assay (Access AccuTnI). Results: The analytical detection limit of the new cTnI assay was 0.012 g/L, and the lowest concentration giving a total imprecision (CV) of 10% was 0.060 g/L. The mean difference (95% limits of agreement) between the new cTnI and Aio cTnI assays was larger in admission samples (21.0%; ؊107.8% to 149.7%) than in samples taken 6 -12 h (12.8%; ؊61.5% to 87.2%) and 24 h after admission (3.0%; ؊71.3% to 77.4%; P <0.001). With the lowest concentrations giving 10% CV (0.22 g/L for Aio cTnI) used as cutoffs, 14.3% (n ‫؍‬ 76) of admission samples were positive only with the new assay, whereas 13.5% (n ‫؍‬ 72) were positive with both assays. Of samples taken at 6 -12 and 24 h, 10.2% (n ‫؍‬ 31) and 8.3% (n ‫؍‬ 29) were positive only with the new assay. ROC

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