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.)

This large real-world prospective registry of catheter-based LAAO using the AMPLATZER Amulet device reports a high implant success rate and a low periprocedural complication rate in a population with a high risk of stroke and bleeding. Transoesophageal echo data confirm good closure rates during follow-up and low rates of device-associated thrombus.

This is the first systematic study to quantify venous changes after PM or ICD implantation. Our study shows that venous anomalies rendering PM implantation difficult are not infrequent. The incidence of new venous obstruction was 14%. Atrial fibrillation and biventricular PM implantation were independent predictors of venous obstruction.

The development of mucosal immunity is presumed to be the most important marker of rotavirus infection. The practical difficulties of obtaining small-bowel secretions stimulated this study of the antibody response to acute rotavirus infection at other sites. Forty-four infants admitted to the hospital with rotavirus gastroenteritis had serum, saliva, and feces collected at the acute phase (median, 5.5 days), during convalescence (median, 33.5 days), and 4 months later (median, 12.2 weeks). A subgroup of 19 children also had duodenal juice collected in parallel. Rotavirus-specific immunoglobulin G (IgG), IgA, secretory immunoglobulin, and IgM were measured and compared in all samples. The results showed that the estimation of antirotavirus serum IgM, serum IgG, duodenal juice IgA, and duodenal juice IgM by an enzyme immunoassay indicated an immune response to severe primary rotavirus infection in all children. Four months iater, the levels of serum IgG and IgA served as the most sensitive markers of the preceding rotavirus infection. The predictive accuracies of immune responses at different sites in relation to a positive IgA immune response in the duodenum were calculated. Fecal IgA predicted duodenal IgA rotavirus antibodies with accuracies of 86% at 1 month and 92% at 4 months. The high sensitivity of serum IgM and IgG in detecting rotavirus infection and the high predictive accuracy of fecal IgA as an indicator of duodenal IgA abrogates the need for duodenal intubation to detect (or monitor) an immune response to rotavirus infection. This finding has important practical implications for epidemiological studies of acute diarrhea in children and in rotavirus vaccine trials.

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Pacemaker implantation induces a transient hypercoagulable state, but its degree does not predict subsequent venous thromboembolism, and neither did the grade of endothelial damage as reflected by plasma markers. The aetiology of these lesions seems to be multifactorial, and clustering of classic thrombotic risk factors plays a role in the pathogenesis.

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