Association of midregional proadrenomedullin with coronary artery stenoses, soft atherosclerotic plaques and coronary artery calcium.

Midregional proadrenomedullin (MR-proADM) is elevated in patients with heart failure and myocardial infarction. The aim of this study was to evaluate the association of MR-proADM with the grade of coronary artery stenosis, presence of coronary artery soft plaques and coronary artery calcification score (CACS), determined by 64-multislice computed tomography (MSCT) in patients without known prior cardiovascular disease. This retrospective study included 107 patients undergoing MSCT for confirmation (or exclusion) of coronary artery disease. MR-proADM levels were measured in all patients. The assessment of coronary artery stenoses, CACS and soft coronary plaques was made by MSCT using known criteria. The MR-proADM [median (25th-75th percentiles)] level was 0.33 (0.21-0.43) nmol/l. The MR-proADM level was 0.28 (0.22-0.40) nmol/l in patients with coronary stenoses ≥50% (n = 23) versus 0.33 (0.27-0.40) nmol/l in patients with coronary stenoses <50% (n = 83, P = 0.59), 0.33 (0.26-0.40) nmol/l in patients with soft plaques (n = 56) versus 0.33 (0.25-0.41) nmol/l in patients without soft plaques (n = 50, P = 0.73) and 0.33 (0.25-0.39) nmol/l in patients with CACS <200 (n = 81) versus 0.32 (0.26-0.44) nmol/l in patients with CACS ≥200 (n = 26, P = 0.77). In multivariate analysis, the MR-proADM level was a significant correlate of coronary artery stenoses [odds ratio (OR) = 0.93; 95% confidence interval (CI) 0.86-0.99; P = 0.026] and soft plaques (OR = 0.94; 95% CI 0.90-0.99; P = 0.015) but not of CACS (OR = 0.98; 95% CI 0.93-1.03; P = 0.36). A decreased MR-proADM level is an independent correlate of the presence of coronary artery disease and of soft atherosclerotic plaques. Patients with decreased MR-proADM levels may need invasive examinations to diagnose more severe forms of coronary artery disease.

Relation between plasma fibroblast growth factor-23, serum fetuin-A levels and coronary artery calcification evaluated by multislice computed tomography in patients with normal kidney function.

OBJECTIVE: To examine the correlation of plasma fibroblast growth factor (FGF)-23 and serum fetuin A levels with the coronary artery calcification score (CACS) in patients with normal kidney function. BACKGROUND: Vascular calcification is an active process that may be aggravated by hyperphosphataemia and hypercalcaemia. FGF-23 and human fetuin-A have been associated with calcifying arteriosclerosis in renal failure. Plasma FGF-23 was identified as an independent factor negatively associated with peripheral vascular calcification. Fetuin-A acts as a systemic inhibitor of ectopic calcification in dialysis patients and can be correlated to the survival of these patients. Very few data exists on the role of FGF-23 and fetuin-A in coronary calcification of patients without impaired kidney function. MATERIALS AND METHODS: Sixty-four patients, 21 females and 43 males, were subjected to 64-slice coronary computed tomography (CT) to evaluate coronary artery calcification (CAC). Plasma intact FGF-23 was determined by ELISA. Serum fetuin-A concentration were evaluated nephelometrically. RESULTS: Mean plasma FGF-23 level was 20.4 +/- 9.1 pg/ml and serum fetuin-A was 0.46 +/- 0.09 g/l. There was no correlation between FGF-23 (P = 0.777) and fetuin-A (P = 0.767) levels and the CACS. No correlation was found between the presence of noncalcified plaques and coronary artery stenosis (CAS) >or= 50%, and FGF-23 (P = 0.313 and P = 0.775) and fetuin-A levels (P = 0.601 and P = 0.659). CONCLUSION: Plasma intact FGF-23 and serum fetuin-A concentration do not correlate with the CACS, the grade of stenosis or presence of noncalcified plaques of the coronary arteries in patients with normal kidney function.