Inside ST-elevation myocardial infarction by monitoring concentrations of cardiovascular risk biomarkers in blood.

BACKGROUND: No information is available on the optimal sampling time to catch the highest increase for biomarkers whose elevation after ST-elevation myocardial infarction (STEMI) is prognostic for adverse events. This study aimed to investigate release kinetics and peak times of cardiac troponin I (cTnI), C-reactive protein (CRP), B-type natriuretic peptide (BNP), chromogranin A (CgA) and cystatin C (CyC) in STEMI patients undergoing primary percutaneous coronary intervention (PPCI). METHODS: Blood concentrations of cTnI, CRP, BNP, CgA and CyC were measured before and 6 h, 24 h, and 48 h after PPCI in 84 STEMI patients. The averaged trajectory of marker kinetics was estimated by multivariable regression models adjusted for patient characteristics and orthogonal polynomials were used to describe related releases. RESULTS: From the estimated kinetics cTnI peaked at 10 h from symptoms, BNP at 28 h and CRP within 30 h. CyC concentrations did not change, whereas CgA concentrations increased from 6 to 48 h after PPCI. The amount of BNP release was found to be affected by the interaction between gender and age: females<75 years had BNP concentrations fourfold higher than males. CONCLUSIONS: According to different release kinetics a single blood sampling for measuring all biomarkers is not recommended.

Plasma B-type natriuretic peptide in dialyzed patients: marker of cardiovascular disease or link to plasma refilling.

BACKGROUND: B-type natriuretic peptide (BNP) is released in response to extracellular volume and blood pressure (BP) overload and is a risk factor for cardiovascular diseases (CVD). BNP is increased in dialyzed patients (HDpts). The aim of this study was to evaluate the relationships between BNP and renin, aldosterone and blood volume reduction rate (BV/WL), with the presence of CVD and mortality. METHODS: Fifty-one HDpts aged 70 ± 14 years were enrolled. BP, BV/WL, BNP, aldosterone, renin, C-reactive protein (CRP), troponin I and routine biochemistry were measured. According to the predialytic plasma BNP levels, the patients were divided into group A with higher BNP and group B with lower BNP than the median value of 330 pg/mL. Follow-up was 1 year. RESULTS: After HD, plasma BNP (449.6 ± 582.2 pg/mL vs. 264.1 ± 269.8 pg/mL, p=0.0008) and aldosterone (421.8 ± 573.4 pg/mL vs. 265.1 ± 566.2 pg/mL, p=0.0003) decreased, but not rennin. BNP decreased more after hemodiafiltration than after standard HD (-55.1% ± 28.5% vs. -26.5% ± 19.5%, p=0.002). Patients in group A exhibited more diabetes (58% vs. 28%, p=0.03), ischemic heart disease (42% vs. 16%, p=0.04), left ventricular hypertrophy (88.8% vs. 33.3%, p<0.001), elevated levels of troponin I, CRP (50% vs. 24%, p=0.05), and low BV/BWL in a lower percentage (8% vs. 32%, p=0.03). After 11.2 ± 3.5 months, 8 patients (33.3%) had died in group A and 2 (8%) in group B (p=0.02). CONCLUSION: This study demonstrates that BNP is high in HDpts and decreases after HD. It is correlated with a good capacity for plasma refilling, with diabetes, CVD and short-term mortality risk.

Impact of calibration fitting models on the clinical value of chromogranin A.

BACKGROUND: The clinical relevance of chromogranin A (CgA) concentrations depends on the analytical performance of the assay. The goal of the present study was to define the clinical involvements in CgA calibration models by evaluating the confidence intervals (CIs) for values from patients who were undergoing monitoring for disease. METHODS: Thirty calibration curves for the CgA assay [immunoradiometric assay (IRMA), (CIS-BIO)] were built using linear regression (LR), and four-parameter logistic models were used to estimate CIs for patient concentrations. RESULTS: We reported the inadequacy of the LR curve estimation procedure. We showed: 1) no evidence that the straight calibration line could fit the average responses, 2) non-constant and non-uniform variance of the replicated calibration responses. All tests performed in the analysis of variance and CI calculation for the calibration curve should be invalidated. The four-parameter logistic function yielded results for 16 curves only; this result could be due to the low number and inappropriate concentration of calibrators. This suggests that some aspects of the assay design should be reviewed. However, using the variance function estimated in this model, we could assess the CI for calibration curves and patient samples. CONCLUSIONS: We showed that the four-parameter logistic calibration model with estimated variance function should better support clinical interpretation of marker concentration changes in patients serially tested.

Different patterns of NT-proBNP secretion in acute coronary syndromes.

UNLABELLED: BACKGROUND; The wide variability of NT-proBNP levels in acute coronary syndromes could arise from sympathetic activation and glomerular impairment. The aim of the study was to investigate, in this setting, the dependence of NT-proBNP from Chromogranin A (CgA) and Cystatin C (CC) levels, respectively assessing sympathetic activation and glomerular impairment. METHODS: In 132 patients, 90 ST elevation acute coronary syndrome (STE-ACS) and 42 non ST elevation acute coronary syndrome (NSTE-ACS), within 24 h from symptoms and with creatinine levels lower than 141.4 micromol/L, we measured NT-proBNP, CgA and CC levels. In 41 STE-ACS patients we evaluated the kinetic profiles of the markers. RESULTS: From the multiple regression model, to investigate the dependence of NT-proBNP from CgA, CC levels, time from symptoms, STE-ACS/NSTE-ACS subsets, gender, adjusting for the effect of left ventricular ejection fraction and age we had evidence of: 1) interactions involving the subsets, the first with CgA levels and the second with age; 2) non linear increasing effect of the delay on NT-proBNP secretion. CONCLUSIONS: Our data showed that, in the population studied, sympathetic activation and age could affect NT-proBNP secretion yielding different secretory patterns in STE- or NSTE-ACS. Only for STE-ACS we observed higher marker secretion in older patients.