Table 1.
First author | Year | Ethnicity | Sample size | Gender (M/F) | Age (years) | Disease | Method | Main finding | Mean value (ug/mL) | NOS score | |||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Case | Control | Case | Control | Case | Control | (Case versus control) | |||||||
Kadoglou [20] | 2014 | Caucasians | 95 | 35 | 68/27 | 28/7 | 67.1 ± 6.5 | 65.0 ± 9.5 | CAD | ELISA | ① | 222.00 versus 839 | 7 |
Zhao [10] | 2013 | Asians | 129 | 69 | 67/62 | 35/34 | 63.1 ± 8.9 | 62.9 ± 9.0 | CAD with T2DM | ELISA | ② | 451.14 versus 396.41 | 7 |
129 | 69 | 67/62 | 35/34 | 63.1 ± 8.9 | 62.9 ± 9.0 | CAD with T2DM | ELISA | 451.14 versus 308.3 | |||||
Ballestri [21] | 2013 | Caucasians | 46 | 24 | 35/11 | 13/11 | 67.6 ± 11.4 | 68.9 ± 13.6 | CAD | ELISA | ③ | 374 versus 445.8 | 6 |
Voros [23] | 2012 | Caucasians | 171 | 81 | 120/51 | 46/35 | 62.0 ± 6.0 | 60.0 ± 7.0 | MI | RIA | ④ | 673 versus 673 | 8 |
Afsar [24] | 2012 | Asians | 95 | 81 | 68/27 | 32/49 | 61.8 ± 12.1 | 48.3 ± 9.2 | ACS | ELISA | ⑤ | 760 versus 1100 | 7 |
Basar [19] | 2011 | Asians | 180 | 55 | 152/28 | 46/9 | 57.9 ± 9.4 | 56.7 ± 8.2 | STEMI | ELISA | ⑥ | 286.85 versus 359.8 | 8 |
Bilgir [25] | 2010 | Asians | 34 | 42 | — | — | 60.3 ± 11.8 | 59.6 ± 11.9 | MI | ELISA | ⑦ | 156 versus 179 | 5 |
59.4 ± 8.8 | 59.6 ± 11.9 | SA | ELISA | 167 versus 179 | |||||||||
Weikert [26] | 2008 | Caucasians | 227 | 2198 | 164/63 | 798/1400 | 57.5 ± 0.6 | 49.5 ± 0.2 | MI | ELISA | ⑧ | 253.6 versus 226.9 | 8 |
Lim [22] | 2007 | Caucasians | 284 | 34 | 233/51 | 20/14 | 60.0 ± 14.0 | 67.0 ± 14.0 | STEMI | ELISA | ⑨ | 188 versus 219 | 8 |
Mathews [27] | 2002 | Caucasians | 20 | 44 | 14/6 | 23/21 | 55 (43~69) | 48 (38~62) | AMI | ELISA | ⑩ | 281.3 versus 312.3 | 6 |
FA: fetuin-A; M: male; F: female; CAD: coronary artery disease; MI: myocardial infarction; ACS: acute coronary syndrome; STEMI: ST-elevation myocardial infarction; SA: stable angina; AMI: acute myocardial infarction; NOS: Newcastle-Ottawa Scale; ①: derangements in serum levels of all vascular calcification inhibitors compared with those in healthy controls. Simvastatin treatment for 6 months significantly decreased serum fetuin-A, OPG, and OPN levels; ②: serum fetuin-A levels are independently correlated with the presence and severity of CAD in T2DM patients; ③: high fetuin-A levels are independently associated with NAFLD and a lower risk of chronographically diagnosed CAD; ④: ghrelin level is determined by elevated insulin and decreased adiponectin levels; ⑤: fetuin-A levels decrease in patients with acute coronary syndromes, independent of heart valve calcification; ⑥: low-admission fetuin-A levels are associated with impaired coronary flow in STEMI patients undergoing primary percutaneous coronary intervention; ⑦: fetuin-A levels seem to be decreased in SA and MI patients; ⑧: high plasma fetuin-A levels are correlated with an increased risk of MI and IS; ⑨: fetuin-A is an important predictor of death at 6 months in STEMI patients independent of NT-proBNP, CRP, and CADILLAC risk score; ⑩: Plasmaa2-HSG concentrations start to decrease within a few hours after the onset of AMI and return to near normal concentrations during the recovery period (5–7 days after AMI).