Author + information
- Emrah Küçük,
- Turgut Karabağ,
- Muhammet Raşit Sayın,
- İbrahim Akpınar,
- Abdullah Orhan Demirtaş and
- Mustafa Aydın
Stent restenosis still stands out as a major problem despite the developments in the treatment area. A new molecule fetuin-A which is a systemic calcification inhibitor recently conducted many researches about it. It is known that atherosclerotic vessels stores a high rate of fetuin-A in the vesicles of vascular smooth muscle cell. Stent restenosis has multifactorial pathogenesis and it is important to predict it. The aim of this study is to investigate the relationship between serum fetuin-A levels and stent restenosis.
Eighty patients who had previously stent implantation underwent coronary angiography for any reason were included in our study. Thirty-six patients whom stent restenosis detected after coronary angiography (>50% re-narrowing of the stent compared to adjacent normal lumen, loss of >%50 of the lumen diameter gained after implantation, detection of ≥%70 restenosis of the vessel which was remained <%50 after stent implantation) were included to the study (Group 1; 23 M, 13 F, mean age, 59±10 years). Fourty-four patients whom restenosis were not detected after coronary angiography were included to the study as control group (Group 2; 32 M, 12 F, mean age 62±10 years). Detailed histories, demographic data on the cardiovascular and other systemic examinations of all patients were recorded. Characteristics of the stent and procedure at the time of implantation were also recorded. Blood samples of both groups were collected and was stored. Serum fetuin-A levels were measured by competetive ELISA method.
Demographic data and clinical characteristics were similar between group 1 and group 2. Serum fetuin-A levels were significantly higher in group 1 compared to group 2 (78.6±18.3 vs 58.5±10.7 ng/ml; p=000). Although the number of diabetic patients similar between the groups, the fasting blood glucose was significantly higher in group 1 compared to group 2 (110±66.9 vs 102±57.1 g/dl; p=0.03). Other laboratory parameters were similar between groups. There was positive correlation between stent inflation pressure and fetuin-A levels (r:0.641, p<0.05).
Atherosclerotic vascular smooth muscle cells stores high rate of fetuin-A. Fetuin-A is thought to increase neointimal hyperplasia which is the main mechanism of the stent restenosis through several mechanisms like insulin resistance and supression of TGF-ß. According to the results of our study; we consider that, higher fetuin-A levels may play a role in restenosis mechanism.
|Group 1 (n=36)||Group 2 (n=44)||p|
|Gender (F/M) (n)||13/23||12/32||0.54|
|Time from stent implantation (years)||3.5±3.4||3.0±3.8||0.57|
|Systolic blood pressure (mm Hg)||132±20.9||131±21.1||0.69|
|Diastolic blood pressure (mm Hg)||72±11.1||72.5±12.3||0.40|
|Pulse rate (beat/min)||76.0±14.7||72.5±15.5||0.70|
|Fasting blood glucose (mg/dl)||110±67||102±57||0.03|
|Total cholesterol (mg/dl)||167.0±40.5||161.1±35.5||0.48|
Demographic characteristics and laboratory parameters of the groups